Chapter 19. HIV INFECTION

Chapter 19. HIV INFECTION

HIV infection is a chronic progressive human disease caused by a retrovirus, in which the immune system is affected and an immunodeficiency state is formed, leading to the development of opportunistic and secondary infections, as well as malignant tumors.

19.1. ETIOLOGY

The causative agent of this disease was isolated in 1983 and named human immunodeficiency virus - HIV (Human Immunodeficiency Virus - HIV). The virus belongs to the retrovirus family.

There are currently 2 known strains of the human immunodeficiency virus: HIV-1 and HIV-2.

The viral particle is about 100 nm in size and consists of a core surrounded by an envelope. The core contains RNA and a special enzyme (reverse transcriptase, or revertase), due to which the genetic material of the virus is integrated into the DNA of the host cell, which leads to further reproduction of the virus and cell death. The shell of the viral particle contains the glycoprotein gp120, which determines the tropism of the virus towards cells of the human body that have CD4 + receptors.

Like all retroviruses, HIV is unstable in the external environment, is completely inactivated by heating at a temperature of 56 ° C for 30 minutes, dies by boiling or by changing the reaction of the environment (pH below 0.1 and above 13), as well as when exposed to traditional disinfectants ( solutions of 3-5% chloramine, 3% bleach, 5% Lysol, 70% ethyl alcohol etc.). In biological fluids (blood, semen), the virus can persist for a long time in a dried or frozen state.

19.2. EPIDEMIOLOGY

The incubation period lasts about 1 month.

The source of infection is an HIV-infected person, both in the stage of asymptomatic carriage and in advanced clinical manifestations of the disease.

The virus is found in the greatest quantities in blood, semen, cerebrospinal fluid, breast milk, vaginal and cervical secretions, as well as in biopsies of various tissues. In small quantities, insufficient for infection, it is found in saliva, tear fluid, and urine.

Routes of HIV transmission: sexual contact and parenteral.

The contact-sexual route of transmission is characterized by the penetration of the virus into the body through damaged skin and mucous membranes (which are abundantly supplied with blood and have a high absorption capacity). The unaffected epidermis is practically impenetrable to viral particles.

Sexual transmission is observed during sexual contacts (hetero- and homosexual) and is apparently associated with microtraumas of the mucous membranes, which is especially great with anogenital and orogenital contacts, as well as in the presence of inflammatory diseases genitals.

The parenteral route of transmission is characterized by the virus entering directly into the bloodstream and occurs during blood transfusions of contaminated blood or its components, injections using contaminated instruments, especially when using drugs, transplantation of organs and tissues of donors.

Child infection most often occurs transplacentally during pregnancy or during childbirth. It has been noted that in children born to HIV-infected mothers, the disease develops only in 25-40% of cases, which is associated with the condition of the mother and obstetric interventions. Thus, a high concentration of the virus in the blood or AIDS in the mother, prematurity of the child, natural birth and contact of the child with maternal blood increase the risk of HIV transmission, but none of these factors predicts the likelihood of infection of the child. Infection of a child can also occur when feeding HIV-infected mother breasts and expressed breast milk.

At-risk groups(most frequently infected persons): drug addicts, homosexuals and bisexuals, prostitutes, as well as persons prone to frequent changes of sexual partners.

19.3. PATHOGENESIS

Having penetrated the body, the virus, with the help of the gp120 glycoprotein, is fixed on the membrane of cells that have CD4 + receptors. These receptors are located primarily on T-helper lymphocytes, which play a major role in the development of the immune response, as well as on monocytes, macrophages and some other cells. The RNA of the virus penetrates deep into the cells from the surface, is transformed by the reverse transcriptase enzyme into the DNA of the cell, and new viral particles are synthesized, leading to the death of T-lymphocytes. Infected monocytes, unlike lymphocytes, do not die, but serve reservoir latent infection.

During HIV infection, the ratio of T-helpers and T-suppressors in the body is disrupted. The defeat of T-helper cells leads to a decrease in the activity of macrophages and natural killer cells, the production of antibodies by B-lymphocytes decreases, which results in a pronounced weakening of the immune response.

The result of an immunodeficiency state is the development of various opportunistic infections, secondary infections, and malignant neoplasms.

19.4. CLASSIFICATION OF HIV INFECTION

According to the classification of V.I. Pokrovsky, since 1989, 5 stages of HIV infection have been distinguished.

Incubation period

The incubation period is 2-8 weeks. There are no clinical manifestations, but an HIV-infected person can be a source of infection. Antibodies to the virus have not yet been detected.

Primary manifest (acute) period

In 50% of patients, the disease begins with nonspecific clinical manifestations: fever, myalgia and arthralgia, lymphadenopathy, nausea, vomiting, diarrhea, skin rashes, etc.

In some patients, this period of the disease is asymptomatic.

The virus in the blood is detected using PCR. Antibodies to HIV may not yet be detected.

Latent period

The latent period lasts several years (from 1 year to 8-10 years). There are no clinical manifestations, the immune status does not change, but the person is the source of infection (virus carriage is noted). Antibodies to HIV are detected using the method ELISA and reactions immunoblotting.

At the end of the latent period, generalized lymphadenopathy develops. Diagnostic value has an enlargement (more than 1 cm) of two or more lymph nodes (except inguinal) in unrelated areas for more than 3 months.

AIDS (stage of secondary diseases)

The main clinical manifestations of AIDS are fever, night sweats, fatigue, weight loss (before cachexia), diarrhea, generalized lymphadenopathy, hepatosplenomegaly, Pneumocystis pneumonia, progressive neurological disorders, candidiasis of internal organs, lymphomas, Kaposi's sarcoma, opportunistic and secondary infections.

Terminal stage

Cachexia, general intoxication, dementia are increasing, and intercurrent diseases are progressing. The process ends in death.

19.5. SKIN MANIFESTATIONS IN AIDS

Distinctive features of skin diseases in AIDS are a long-term relapsing course, a widespread nature of the rashes, atypical localization, an unusual age period, and poor effectiveness of conventional therapy.

Mycoses

The development of fungal diseases in HIV-infected patients is an early clinical symptom of an immunodeficiency state.

Candidiasis of the skin and mucous membranes

Candidiasis of the skin and mucous membranes occurs in almost all AIDS patients. Most often it manifests itself as candidiasis of the mucous membranes of the oral cavity, cheilitis, esophagitis, candidiasis of large folds (yeast diaper rash), damage to the anogenital area, candidiasis of the external auditory canal, damage to the nail folds (candidal paronychia), and nail plates.

Features of the course of candidiasis in AIDS are damage to young people, especially men, a tendency to form large lesions, a tendency to erosion and ulceration.

Rubrophytia

Rubrophytia is a common form of mycosis of smooth skin in patients with AIDS. During the course of the disease, attention is drawn to the prevalence of rashes, the appearance of infiltrated elements, and upon microscopic examination, the abundance of mycelium.

Seborrheic dermatitis and pityriasis versicolor

Seborrheic dermatitis and pityriasis versicolor - diseases belonging to the group of malacezioses and caused by yeast-like lipophilic flora Malassezia furfur.

Seborrheic dermatitis

Seborrheic dermatitis is detected in more than half of HIV-infected people in the early stages. Typically, the disease begins with seborrheic areas (face, scalp, ears, etc.), and later spreads to the skin of the torso, upper and lower extremities (up to erythroderma). The rashes are accompanied by abundant peeling, the formation of crusts, erosions occur in the folds, and hair falls out.

Tinea versicolor

Lichen versicolor in HIV-infected people is characterized by the appearance of large infiltrated spots on the skin that transform into plaques.

Viral skin diseases

Herpes simplex

Herpes simplex is a typical disease in HIV-infected patients and occurs with frequent relapses, almost without remissions. It is characterized by an abundance of elements, up to disseminated lesions, as well as a tendency to erosion and ulceration, accompanied by severe pain. Scars often form at the sites of rashes. With repeated use of acyclovir, viral resistance to this drug quickly develops.

Herpes zoster

Herpes zoster against the background of HIV infection acquires a recurrent course, which is extremely rare in young patients and is an early marker of an immunosuppressive state. The recurrent form of herpes zoster in people under 60 years of age is currently considered as one of the HIV indicator diseases (especially if patients have persistent lymphadenopathy).

Clinically, the disease is characterized by prevalence, frequent development of gangrenous (necrotic) forms, severe pain, prolonged neuralgia, and scar formation.

Molluscum contagiosum

Molluscum contagiosum - a viral disease, more typical for younger children, is very common among HIV-infected patients, in whom it acquires a disseminated recurrent nature. The most common localization of rashes is the face, neck, scalp, where the elements become large (more than 1 cm), confluent.

Oral hairy leukoplakia

Oral hairy leukoplakia - the disease, described only in HIV-infected patients, is caused by the Epstein-Barr virus and papillomavirus. Clinically it is a thickening

mucous membrane of the lateral surface of the tongue in the form of a whitish plaque, covered with thin keratotic hairs, the length of which is several millimeters.

Warts

Warts are caused by different types of human papillomavirus. In HIV-infected patients, common forms of vulgar, palmoplantar and anogenital (genital warts) warts are found more often than in the general population.

Pyoderma

Pyoderma is common in AIDS patients. They are characterized by a severe course and often lead to the development of sepsis. The most typical development is folliculitis, furunculosis, ecthyma, rupoid pyoderma, chronic diffuse streptoderma, ulcerative vegetative pyoderma and other forms. In some cases, atypical pyoderma caused by gram-negative flora is observed.

Scabies

Scabies against the background of an immunodeficiency state is very severe - in the form of Norwegian scabies, which is characterized by high contagiousness to others, and clinically by widespread localization of rashes, massive cortical deposits, and a violation of the general condition.

Skin tumors

Kaposi's sarcoma - a malignant tumor of blood vessels - is a reliable clinical manifestation of HIV infection. The disease is considered an AIDS-defining disease. It is characterized by the appearance of dark cherry or black vascular nodules on the skin, mucous membranes, and internal organs. Unlike the classic type of Kaposi's sarcoma (which occurs in elderly patients, is characterized by a slow development of the clinical picture, rare involvement of internal organs in the process and a typical initial localization on the feet and legs), AIDS-associated Kaposi's sarcoma, on the contrary, affects young and middle-aged people age, characterized by a malignant course with meta-

stasis of the tumor in the internal organs (lungs, bones, brain, etc.), and primary rashes can appear not only on the legs, but also on the face, scalp, ears, oral mucosa (Fig. 19- 1, 19-2).

Drug toxicoderma

Drug-induced toxicoderma in HIV-infected patients usually develops during co-trimoxazole therapy and proceeds according to the measles-like type. This reaction develops in 70% of patients.

Rice. 19-1. Kaposi's sarcoma on the foot

Rice. 19-2. Kaposi's sarcoma on the leg

19.6. FEATURES OF HIV INFECTION IN CHILDREN

Infection of children occurs mainly through vertical transmission (from an HIV-infected mother to her child): in utero, during childbirth or during breastfeeding.

Children born to HIV-infected mothers become ill in 25-40% of cases. When children are born to seropositive mothers, deciding whether the child has HIV infection can be difficult, since newborns are usually seropositive (maternal antibodies in the child’s blood persist for up to 18 months), regardless of whether they are infected or not. In children under one and a half years of age, the diagnosis of HIV is confirmed by detecting viral nucleic acids using the PCR method.

The first clinical manifestations of HIV infection in a child with perinatal infection occur no earlier than 4 months of age. For most children, the asymptomatic period lasts longer - on average about 5 years.

The most typical skin lesions in children are candidiasis of the oral mucosa and esophagus, seborrheic dermatitis, as well as staphyloderma, herpetic gingivostomatitis, common giant molluscum contagiosum, and onychomycosis. Children often develop a hemorrhagic rash (petechial or purpuric) that develops against the background of thrombocytopenia.

Kaposi's sarcoma and other malignant neoplasms are not typical for childhood.

19.7. LABORATORY RESEARCH

Methods for determining the presence of antibodies to HIV

The screening method is the enzyme-linked immunosorbent assay (ELISA), in which antibodies to HIV are detected in 90-95% of patients 3 months after infection. In the terminal stage, the number of antibodies may decrease until they disappear completely.

To confirm ELISA data, the method is used immunoblotting, which detects antibodies to certain viral proteins. This method rarely gives false positive results.

Methods for determining the presence of viral particles in the blood

The PCR method allows you to determine the number of copies of HIV RNA in 1 μl of blood plasma. The presence of any number of viral particles in serum

A mouthful of blood proves HIV infection. This method is also used to determine the effectiveness of antiviral treatment.

Methods to assess the state of immunity

The number of T-helpers (CD4) and T-suppressors (CD8), as well as their ratio, is determined. Normally, T helper cells are more than 500 cells per μl, and the CD4/CD8 ratio is 1.8-2.1. With HIV infection, the number of T-helper cells is significantly reduced and the ratio is less than 1.

19.8. DIAGNOSTICS

Diagnosis is based on characteristic complaints (weight loss, increased fatigue, cough, diarrhea, prolonged fever, etc.), clinical picture (detection of drug addiction stigmas, lymphadenopathy, the presence of AIDS-associated dermatoses and other infectious and opportunistic infections), as well as laboratory data.

19.9. TREATMENT

Three classes of antiretroviral drugs are used to treat HIV infection.

Nucleoside reverse transcriptase inhibitors (zidovudine 200 mg orally 4 times a day, for children the dose is calculated based on 90-180 mg/m2 orally 3-4 times a day; didanosine 200 mg orally

2 times a day, for children - 120 mg/m2 orally 2 times a day; as well as stravudine, lamivudine, etc.

Non-nucleoside reverse transcriptase inhibitors (zalcitabine 0.75 mg orally 3 times a day, for children - 0.01 mg/kg orally

3 times a day; abacavir 300 mg orally 2 times a day, for children - 8 mg/kg orally 2 times a day.

HIV protease inhibitors (nelfinavir 750 mg orally 3 times a day, for children - 20-30 mg/kg 3 times a day; ritonavir 600 mg 2 times a day, for children - 400 mg/m2 orally 2 times per day, as well as saquinavir, amprenavir, etc.

The most effective treatment regimens are those that include 2 nucleoside reverse transcriptase inhibitors in combination with an inhibitor

protease or with a non-nucleoside reverse transcriptase inhibitor.

HIV-infected patients are treated for malignant tumors and opportunistic infections.

19.10. CONSULTING

Preventive measures include the promotion of protected sex, the fight against drug addiction, compliance with the sanitary and anti-epidemic regime in medical institutions, examination of donors, etc.

To prevent infection of children, routine screening of pregnant women for HIV infection is necessary. If a disease is detected in a pregnant woman, she should be prescribed antiviral treatment, which reduces the risk of illness in the child to 8%. Delivery of HIV-infected women is carried out by caesarean section. Breastfeeding a child should be avoided.

Dermatovenerology: a textbook for higher education students educational institutions/ V. V. Chebotarev, O. B. Tamrazova, N. V. Chebotareva, A. V. Odinets. -2013. - 584 p. : ill.

HIV is an acronym that stands for human immunodeficiency virus, which attacks the human immune system, causing HIV infection.

The last stage of HIV infection is AIDS (acquired immunodeficiency syndrome).

HIV infection and AIDS: what is the fundamental difference between these two conditions?

HIV infection
Incurable infectious disease. It belongs to the group of slow viral infections with a long-term course that affects the immune system.

That is, the virus, having entered the body of a healthy person from a sick person, may not manifest itself in any way for many years.

However, HIV gradually destroys the cells of the immune system, which is designed to protect the human body from all kinds of infections and negative influences.
Therefore, over time, the immune system “loses its ground.”

AIDS
A condition in which the human immune system is practically unable to fight infections, resist the development of cancer cells and various harmful environmental factors. At this stage, any infection, even the most harmless one, can lead to the development of a serious illness, and subsequently the death of the patient from complications, encephalitis or a tumor.

Facts about the disease

Perhaps now there is not a single adult who has never heard of HIV infection. It’s not for nothing that it’s called the “plague of the 20th century.” And even in the 11th century, it moves forward by leaps and bounds, claiming about 5,000 human lives all over the world every day. Although, As a disease, HIV has a not so long history.

It is believed that HIV infection began its “triumphant march” across the planet back in the 70s of the last century, when the first mass cases of infection with symptoms similar to AIDS were described.

However, they started talking about HIV infection officially only in the early 80s of the last century:

• In 1981, two articles were published that described the development of an unusual pneumocystis pneumonia (caused by a yeast-like fungus) and Kaposi's sarcoma (a malignant skin tumor) in homosexual men.
• In July 1982, the term “AIDS” was coined to describe the new disease.
• The human immunodeficiency virus was discovered in 1983 simultaneously in two independent laboratories:
  • In France at the Institute. Louis Pasteur under the direction of Luc Montagnier
  • In the USA at the National Cancer Institute under the leadership of Gallo Robert
• In 1985, a technique was developed that determined the presence of antibodies to HIV in the blood of patients - an enzyme-linked immunosorbent assay.
• In 1987, the first case of HIV infection in the USSR was diagnosed. The patient is a homosexual man who worked as a translator in African countries.
• In 1988, the World Health Organization declared International AIDS Day on December 1st.

Where did HIV come from? There is no clear answer to this question. However, there are several hypotheses.

The most common theory is that man became infected from a monkey. It is based on the fact that in apes (chimpanzees) living in Central Africa (Congo), a virus was isolated from the blood that can cause the development of AIDS in humans. It is likely that human infection occurred through accidental injury during butchering of a monkey carcass or a human being bitten by a monkey.

However, monkey HIV is a weak virus and the human body copes with it within one week. But for the virus to harm the immune system, it must be transmitted from one person to another within a short time. Then the virus mutates (changes), acquiring properties characteristic of human HIV.

There is also an assumption that HIV existed for a long time among the tribes of Central Africa. However, it was only with the onset of increased migration in the 20th century that the virus spread throughout the world.

Statistics

Every year, a huge number of people around the world become infected with HIV.

Number of HIV-infected people

• Worldwide as of 01/01/2013 amounted to 35.3 million people
• In Russia at the end of 2013 - about 780,000 people, with 51,190 thousand identified between 01/01/13 and 08/31/13
• By CIS countries(data as of the end of 2013):
  • Ukraine - about 350,000
  • Kazakhstan - about 16,000
  • Belarus - 15,711
  • Moldova - 7,800
  • Georgia - 4,094
  • Armenia - 3,500
  • Tajikistan - 4,700
  • Azerbaijan - 4,171
  • Kyrgyzstan - about 5,000
  • Turkmenistan - officials say HIV infection does not exist in the country
  • Uzbekistan - about 7,800

Mortality

Since the beginning of the epidemic, about 36 million people have died from AIDS. Moreover, the mortality rate of patients is decreasing year by year - thanks to successful highly active antiretroviral therapy (HAART or ART).

Celebrities who died from AIDS

• Gia Carangi- American supermodel. She died in 1986. She suffered from a severe form of drug addiction.
• Freddie Mercury- lead singer of the legendary rock band Queen. Died in 1991.
• Michael Wastphal- famous tennis player. He died at the age of 26.
• Rudolf Nureyev- a legend of world ballet. Died in 1993.
• Ryan White- the first and most famous child with HIV infection. He suffered from hemophilia and contracted HIV through a blood transfusion at age 13. The boy, together with his mother, fought for the rights of HIV-infected people all his life. Ryan White died of AIDS in 1990 at the age of 18, but did not lose: he proved to the whole world that HIV-infected people do not pose a threat if basic precautions are taken, and have the right to an ordinary life.

AIDS virus

In addition, there are several varieties of the virus itself.

HIV: structure

• HIV-1or HIV-1(discovered in 1983) is the main causative agent of infection. It is very aggressive, causing typical manifestations of the disease. Most often found in Western Europe and Asia, South and North America, Central Africa.

• HIV-2 or HIV-2(discovered in 1986) is a less aggressive analogue of HIV-1, so the disease is milder. Not so widespread: found in western Africa, Germany, France, Portugal.

Structure

HIV- a spherical (spherical) particle having a size from 100 to 120 nanometers. The virus shell is dense, formed by a double lipid (fat-like substance) layer with “spikes”, and under it is a protein layer (p-24 capsid).

Under the capsule are:

• two strands of viral RNA (ribonucleic acid) - a carrier of genetic information
• viral enzymes: protease, intergrase and transcriptase
• p7 protein

The most important feature of retroviruses is the presence of a special enzyme: reverse transcriptase. Thanks to this enzyme, the virus converts its RNA into DNA (a molecule that ensures the storage and transmission of genetic information to subsequent generations), which it then introduces into the host cells.

HIV: properties

• quickly dies under the influence of a 5% solution of hydrogen peroxide, ether, chloramine solution, 70 0 C alcohol, acetone
• outside the body in the open air dies within a few minutes
• at +56 0 C - 30 minutes
• when boiling - instantly

HIV: features of the life cycle

What are the cells of the immune system responsible for?

T lymphocytes-helpers activate the work of almost all cells of the immune system, and also produce special substances that fight foreign agents: viruses, microbes, fungi, allergens. That is, in fact, they control the functioning of almost the entire immune system.

Monocytes and macrophages - cells that absorb foreign particles, viruses and microbes, digesting them.

The HIV life cycle includes several phases

• Once in the body, the virus binds to special receptors on the surface of the T-lymphocyte - CD4 cells. Next, it penetrates the host cell and sheds the outer membrane.

• Using reverse transcriptase a DNA copy (one chain) is synthesized on the viral RNA (template). The copy is then completed into double-stranded DNA.
• Double-stranded DNA moves into the T-lymphocyte nucleus, where it is integrated into the DNA of the host cell. At this stage, the active enzyme is integrase.
• The DNA copy remains in the host cell from several months to several years, “sleeping,” so to speak. At this stage, the presence of the virus in the human body can be detected using tests with specific antibodies.
• Any secondary infection provokes the transfer of information from the DNA copy to the template (viral) RNA, which leads to further replication of the virus.
• Next, the host cell's ribosomes (protein-producing particles) synthesize viral proteins on the viral RNA.
• Then from viral RNA and newly synthesized viral proteins assembly of new parts of viruses occurs, which leave the cell, destroying it.
• New viruses attach to receptors on the surface of other T lymphocytes - and the cycle begins again.

HIV infection

Anyone can become infected, regardless of social status, financial income, gender, age and sexual orientation. The source of infection is an HIV-infected person at any stage of the infectious process.

HIV doesn't just fly through the air. It is found in biological fluids of the body: blood, semen, vaginal secretions, breast milk, cerebrospinal fluid. For infection, an infectious dose of about 10,000 viral particles must enter the bloodstream.

Routes of transmission of HIV infection

1. Heterosexual contacts- unprotected vaginal sex.

The risk of infection after one sexual contact with ejaculation ranges from 0.1 to 0.32% for the passive partner (the “receiving” side), and 0.01-0.1% for the active partner (the “introducing” side).

However, infection can occur after one sexual contact if there is any other sexually transmitted disease (STD): syphilis, gonorrhea, trichomoniasis and others. Because the number of helper T-lymphocytes and other cells of the immune system increases in the inflammatory focus. And then HIV “enters the human body on a white horse.”

In addition, with all STDs, the mucous membrane is prone to injury, so its integrity is often compromised: cracks, ulcers, and erosions appear. As a result, infection occurs much faster.

The likelihood of infection increases with prolonged sexual intercourse: if the husband is sick, then within three years in 45-50% of cases the wife becomes infected, if the wife is sick - in 35-45% of the cases the husband becomes infected. A woman’s risk of infection is higher because a large amount of infected sperm enters the vagina, it stays in contact with the mucous membrane for longer, and the contact area is larger.

1. Intravenous drug use

Since drug addicts often use shared non-sterile medical syringes or shared containers for preparing the solution when administering drugs intravenously. The probability of infection is 30-35%.

In addition, drug addicts often engage in promiscuous sex, which several times increases the likelihood of infection for both themselves and others.

1. Unprotected anal sex regardless of sexual orientation

1. Unprotected oral sex

However, the risk of infection increases if there are jams in the corners of the mouth, and wounds and ulcers in the cavity.

1. Children born from HIV-infected mothers

It is possible for a healthy mother to become infected when breastfeeding a sick child, if the woman has cracked nipples and the baby’s gums bleed.

1. Accidental injuries with medical instruments, subcutaneous and intramuscular injections

1. Blood transfusion and organ transplantation

On a note

The likelihood of infection depends on the initial state of the person’s immune system: the weaker it is, the faster infection occurs, and the more severe the disease. In addition, it matters what the viral load of an HIV-infected person is; if it is high, then the risk of infection increases several times.

Diagnosis of HIV infection

Methods for diagnosing HIV infection

Available three main stages of diagnosis HIV infections in adults:

1. Preliminary- screening (sorting), which serves to select presumably infected individuals
2. Referential

1. Confirming- expert

Some concepts in the context of diagnosing HIV infection:

• Antigen- the virus itself or its particles (proteins, fats, enzymes, capsule particles, and so on).
• Antibody- cells produced by the immune system in response to HIV entering the body.
• Seroconversion- immune response. Once in the body, HIV multiplies rapidly. In response, the immune system begins to produce antibodies, the concentration of which increases over the next few weeks. And only when their number reaches a certain level (seroconversion), they are detected by special test systems. Then the level of the virus drops, and the immune system calms down.
• "Window period"- the interval from the moment of infection to the appearance of seroconversion (on average 6-12 weeks). This is the most dangerous period, since the risk of HIV transmission is high, and the test system gives a false negative result

Screening stage

It is preferable to use fourth generation test systems. They have one feature - in addition to antibodies, they also detect the HIV antigen - p-24-Capsid, which makes it possible to identify the virus even before the development of a sufficient level of antibodies, reducing the “window period”.

However, in most countries, outdated third or even second generation test systems (only detect antibodies) are still used, because they are cheaper.

However, they are more often give false positive results: if there is an infectious disease during pregnancy, autoimmune processes (rheumatism, systemic lupus erythematosus, psoriasis), the presence of the Epstein-Bar virus in the body and some other diseases.

If the ELISA result is positive, then the diagnosis of HIV infection is not made, but proceeds to the next stage of diagnosis.

Reference stage

Expert stage - immunoblotting

Consists of several stages:

• HIV is broken down into antigens using electrophoresis.
• using the blotting method (in a special chamber), they are transferred to special strips on which proteins characteristic of HIV are already applied.
• The patient's blood is applied to the strips; if it contains antibodies to the antigens, a reaction occurs that is visible on the test strips.

Therefore there are two options for conducting the expert stage laboratory diagnosis of HIV infection:

Diagnosis in children born from HIV-infected mothers

Diagnostic tactics

• up to 1 month - PCR, since the virus does not multiply intensively during this period
• older than a month - determination of p24-Capsid antigen
• laboratory diagnostic examination and observation from birth to 36 months

Symptoms and signs of HIV in men and women

Stages of HIV infection

HIV infection symptoms

• The first stage is incubation

  The virus is actively reproducing. Duration - from the moment of infection to 3-6 weeks (sometimes up to one year). In case of weakened immunity - up to two weeks.

  Symptoms
  None. You can be suspicious if there was a dangerous situation: unprotected casual sexual contact, blood transfusion, and so on. Test systems do not detect antibodies in the blood.

• The second stage - primary manifestations

  The body's immune response to the introduction, reproduction and massive spread of HIV. The first symptoms appear within the first three months after infection; they may precede seroconversion. Duration is usually 2-3 weeks (rarely several months).

  Flow options

• 2A - Asymptomatic There are no manifestations of the disease. There is only the production of antibodies.

• 2B - Acute infection without secondary diseases It is observed in 15-30% of patients. It occurs as an acute viral infection or infectious mononucleosis.

• Increased body temperature 38.8C and above is a response to the introduction of the virus. The body begins to produce an active biological substance - interlekin, which “gives a signal” to the hypothalamus (located in the brain) that there is a “stranger” in the body. Therefore, energy production increases and heat transfer decreases.
• Enlarged lymph nodes- reaction of the immune system. In the lymph nodes, the production of antibodies by lymphocytes against HIV increases, which leads to working hypertrophy (increase in size) of the lymph nodes.
• Skin rashes in the form of red spots and compactions, small hemorrhages up to 10 mm in diameter, prone to merging with each other. The rash is located symmetrically, mainly on the skin of the torso, but sometimes on the face and neck. It is a consequence of direct damage by the virus to T-lymphocytes and macrophages in the skin, which leads to disruption of local immunity. Therefore, there is subsequently an increased susceptibility to various pathogens.
• Diarrhea(frequent loose stools) develops due to the direct effect of HIV on the intestinal mucosa, which causes changes in the local immune system and also impairs absorption.
• Sore throat(sore throat, pharyngitis) and oral cavity This is due to the fact that HIV affects the mucous membranes of the mouth and nose, as well as lymphoid tissue (tonsils). As a result, swelling of the mucous membrane appears, the tonsils become enlarged, which causes a sore throat, painful swallowing and other symptoms characteristic of a viral infection.
• Enlarged liver and spleen associated with the reaction of the immune system to the introduction of HIV into the body.
• Sometimes autoimmune diseases develop(psoriasis, seborrheic dermatitis and others). The cause and mechanism of formation are not yet clear. However, most often these diseases occur in later stages.
• 2B - Acute infection with secondary diseases

  It is observed in 50-90% of patients. It occurs against the background of a temporary decrease in CD4 lymphocytes, so the immune system is weakened and cannot fully resist “strangers.”

  Secondary diseases occur caused by microbes, fungi, viruses: candidiasis, herpes, respiratory tract infections, stomatitis, dermatitis, sore throat and others. As a rule, they respond well to treatment. Then the state of the immune system stabilizes, and the disease moves to the next stage.

• The third stage is long-term widespread enlargement of the lymph nodes

  Duration - from 2 to 15-20 years, since the immune system inhibits the reproduction of the virus. During this period, the level of CD4 lymphocytes gradually decreases: at approximately a rate of 0.05-0.07x109/l per year.

  There is only an increase in at least two groups of lymph nodes (LNs) that are not connected to each other for three months, with the exception of the inguinal ones. The size of the lymph nodes in adults is more than 1 cm, in children - more than 0.5 cm. They are painless and elastic. Gradually, the lymph nodes decrease in size, remaining in this state for a long time. But sometimes they can increase again and then decrease - and so on for several years.

• Stage four - secondary diseases (pre-AIDS)

  Develops when the immune system is depleted: the level of CD4 lymphocytes, macrophages, and other cells of the immune system drops significantly.

  Therefore, HIV, having practically no response from the immune system, begins to multiply intensively. It affects more and more healthy cells, leading to the development of tumors and severe infectious diseases - opurtonic infections (the body can easily cope with them under normal conditions). Some of them occur only in HIV-infected people, and some - in ordinary people, only in HIV-positive people they are much more severe.

  The disease can be suspected if there are at least 2-3 diseases or conditions listed at each stage.

  Has three stages

  1. 4A. Develops 6-10 years after infection with a CD4 lymphocyte level of 350-500 CD4/mm3 (in healthy people it ranges from 600-1900CD4/mm3).
     • Losing body weight up to 10% of initial weight in less than 6 months. The reason is that the viral proteins invade the body’s cells, suppressing protein synthesis in them. Therefore, the patient literally “dries out before our eyes,” and absorption is also impaired. nutrients in the intestines.
     • Repeated damage to the skin and mucous membranes by bacteria (ulcers, boils), fungi (candidiasis, lichen), viruses (herpes zoster)
     • Pharyngitis and sinusitis (more than three times a year).

1. 4B. Occurs 7-10 years after infection with a CD4 lymphocyte level of 350-200 CD4/mm3.

   Characterized by diseases and conditions:

   • Loss of body weight more than 10% in 6 months. There is weakness.
   • Increase in body temperature to 38.0-38.5 0 C for more than 1 month.
   • Chronic diarrhea (diarrhea) for more than 1 month develops as a result of both direct damage to the intestinal mucosa by the virus and the addition of a secondary infection, usually mixed.
   • Leukoplakia is the growth of the papillary layer of the tongue: white thread-like formations appear on its lateral surface, sometimes on the mucous membrane of the cheeks. Its emergence - bad sign for disease prognosis.
   • Deep lesions of the skin and mucous membranes (candidiasis, lichen simplex, molluscum contagiosum, rubrophytia, lichen versicolor and others) with a protracted course.
   • Repeated and persistent bacterial (tonsillitis, pneumonia), viral (cytomegalovirus, Epstein-Bar virus, herpes simplex virus) infections.
   • Repeated or widespread shingles caused by the varicella zoster virus.
   • Localized (non-spread) Kaposi's sarcoma is a malignant skin tumor that develops from the vessels of the lymphatic and circulatory system.
   • Pulmonary tuberculosis.

1. 4B. Develops 10-12 years after infection when the CD4 lymphocyte level is less than 200 CD4/mm3. Life-threatening diseases arise.

   Characterized by diseases and conditions:

   • Extreme exhaustion, lack of appetite and severe weakness. Patients are forced to spend more than a month in bed.
   • Pneumocystis pneumonia (caused by a yeast-like fungus) is a marker of HIV infection.
   • Often recurrent herpes, manifested by non-healing erosions and ulcers on the mucous membranes.
   • Protozoal diseases: cryptosporidiosis and isosporosis (affect the intestines), toxoplasmosis (focal and diffuse brain lesions, pneumonia) - markers of HIV infection.
   • Candidiasis of the skin and internal organs: esophagus, respiratory tract, etc.
   • Extrapulmonary tuberculosis: bones, meninges, intestines and other organs.
   • Common Kaposi's sarcoma.
   • Mycobacterioses that affect the skin, lungs, gastrointestinal tract, central nervous system and other internal organs. Mycobacteria are present in water, soil, and dust. They cause disease only in HIV-infected people.
   • Cryptococcal meningitis is caused by a fungus that is present in the soil. It usually does not occur in a healthy body.
   • Diseases of the central nervous system: dementia, movement disorders, forgetfulness, decreased ability to concentrate, slowed thinking abilities, gait disturbance, personality changes, clumsiness in the hands. It develops both due to the direct impact of HIV on nerve cells for a long time, and as a result of complications that develop after illness.
   • Malignant tumors of any location.
   • Damage to the kidneys and heart caused by HIV infection.

• Fifth stage - terminal

  Develops when the CD4 cell count is below 50-100 CD4/mm3. At this stage, all existing diseases progress; treatment of secondary infections is ineffective. The patient’s life depends on HAART, but, unfortunately, it, as well as the treatment of secondary diseases, are ineffective. Therefore, patients usually die within a few months.

  There is a classification of HIV infection according to WHO, but it is less structured, so mostly specialists prefer to work according to Pokrovsky’s classification.

The given data on the stages and their manifestations of HIV infection are averaged. Not all patients go through the stages sequentially, sometimes “skipping” through them or staying at a certain stage for a long time.

Therefore, the course of the disease can be quite long (up to 20 years) or short-lived (cases of fulminant course are known, when patients died within 7-9 months from the moment of infection). This is associated with the characteristics of the patient’s immune system (for example, some have few CD4 lymphocytes or initially reduced immunity), as well as the type of HIV.

HIV infection in men

HIV infection in women

Women have a slightly higher risk of developing malignant tumors on the cervix.

In addition, in them, inflammatory processes of the female genital organs occur more often (more than three times a year) than in healthy women, and are more severe.

HIV infection in children

Treatment of HIV infection

Moreover, these drugs are so effective that when proper treatment CD4 cells are growing, and HIV itself is difficult to detect in the body even with the most sensitive methods.

To achieve this you The patient must have self-discipline:

• taking medication at the same time
• compliance with dosage and diet
• continuity of treatment

Main directions of treatment

• Prevent and delay the development of life-threatening conditions
• Ensure longer preservation of the quality of life of infected patients
• With the help of HAART and prevention of secondary diseases, achieve remission (absence of clinical symptoms)
• Emotional and practical support for patients
• Providing free drugs

First stage

No treatment is prescribed. However, if there was contact with an HIV-infected person, then chemoprophylaxis is recommended in the first three days after contact.

Second stage

2A. No treatment unless the CD4 count is less than 200 CD4/mm3

2B. Treatment is prescribed, but if the CD4 lymphocyte count is more than 350 CD4/mm3, it is withheld.

2B. Treatment is prescribed if the patient has manifestations characteristic of stage 4, but with the exception of cases when the level of CD4 lymphocytes is more than 350 CD4/mm3.

Third stage

HAART is prescribed if the CD4 lymphocyte count is less than 200 CD4/mm3, and the HIV RNA level is more than 100,000 copies, or the patient actively wishes to begin therapy.

Fourth stage

Treatment is prescribed if the CD4 count is less than 350 CD4/mm3 or the HIV RNA number is more than 100,000 copies.

Fifth stage

Treatment is always prescribed.

On a note

HAART is prescribed to children regardless of the stage of the disease.

These are the existing standards for the treatment of HIV infection today. But recent studies have shown that starting HAART earlier produces better results. Therefore, it is likely that these recommendations will be revised soon.

Medicines used to treat HIV

• Nucleoside inhibitors of viral reverse transcriptase (Didanosine, Lamivudine, Zidovudine, Abacovir, Stavudine, Zalcitabine)
• Non-nucleoside reverse transcriptase inhibitors (Nevirapine, Ifavirenz, Delavirdine)
• Viral protease (enzyme) inhibitors (Saquinavir, Indinavir, Nelfinavir, ritonavir, nelfinavir)

However, it will soon hit the market new drug -Quad, which promises to radically change the lives of people living with HIV. Because it works faster, it has fewer side effects. In addition, it solves the problem of HIV drug resistance. And patients will no longer have to swallow handfuls of pills. Because the new medicine combines the effects of several drugs to treat HIV infection, and is taken once a day.

Prevention of HIV infection

There is probably not a person who disagrees with this statement. This also applies to HIV/AIDS. Therefore, most countries are implementing various programs to reduce the rate of spread of this infection.

However, we will talk about what everyone can do. After all, it doesn’t take much effort to protect yourself and your loved ones from this plague.

Preventing HIV/AIDS among people at increased risk

• The surest way is to have one sexual partner whose HIV status is known.

• Engage in casual sexual intercourse (vaginal, anal) only using a condom. The most reliable are latex ones with standard lubricant.

But the likelihood of infection is still reduced to almost zero if you use a condom correctly: you must put it on before sexual intercourse, make sure that there is no air left between the latex and the penis (there is a risk of rupture), and always use a condom in accordance with the size.

Almost all condoms made from other materials do not protect against HIV at all.

Intravenous drug use

Drug addiction and HIV often go hand in hand, so the most reliable way is to stop taking intravenous drugs.

However, if you still choose this path, you must take precautions:

• Individual and single use of sterile medical syringes
• Preparation of solution for injection in sterile individual containers

• using a self-insemination kit (HIV-negative partner)

• sperm purification followed by insemination (both partners are HIV positive)

• in vitro fertilization

Taking medications:

• HAART (if necessary) for therapeutic or prophylactic purposes depending on the stage of pregnancy
• multivitamins
• iron supplements and others

It is important to take all the necessary tests on time: determine the viral load, CD4 cell level, smears, and so on.

Medical staff

There is a risk of infection if the activity involves penetration through natural barriers (skin, mucous membranes) and manipulations during which they come into contact with biological fluids.

Prevention of infection

• use of protective equipment: glasses, gloves, mask and protective clothing

• promptly dispose of the used needle in a special puncture-proof container

• contact with HIV-infected biological fluid - chemoprophylaxis - taking complex HAART according to the regimen

• contact with a suspected infected body fluid:
  • skin injury (puncture or cut) - the bleeding does not need to be stopped for a few seconds, then treat the injury site with 700C alcohol

• contact with biological fluid on undamaged areas of the body - wash with running water and soap, then wipe with 700C alcohol

• contact with eyes - rinse with running water

• in the mouth - rinse with 700C alcohol

• on clothes - remove them and soak them in one of the disinfectants (chloramine and others), and wipe the skin underneath with 70% alcohol

• for shoes - wipe twice with a rag soaked in one of the disinfectant solutions

• on walls, floors, tiles - pour disinfectant solution for 30 minutes, then wipe

How is HIV transmitted?

Methods of transmission of the virus

• Unprotected sexual intercourse with an HIV-infected person (heterosexual and homosexual contacts). Most often - in people who are promiscuous. The risk increases with anal sex, regardless of sexual orientation.

• When using intravenous drugs: sharing a non-sterile syringe or container for preparing a solution with an HIV-infected person.

• From an HIV-infected woman to her child during pregnancy, childbirth and breastfeeding.

• When healthcare workers come into contact with contaminated biological fluid: contact with mucous membranes, injections or cuts.

• Blood transfusions or organ transplants from HIV-infected people. Of course, the donor organ or blood is tested before medical procedures. However, if it falls during the window period, the test produces a false negative result.

Where can you donate blood for HIV?

There are two types of free blood donation for HIV infection:

• Anonymous The person does not give his name, but is assigned a number by which you can find out the result (for many this is more comfortable).

• Confidential Laboratory staff become aware of the person's first and last name, but they maintain medical confidentiality.

• at any regional AIDS center

• in a city, regional or district clinic in anonymous and voluntary testing rooms, where blood is drawn to detect HIV infection.

In addition, you can get tested at a private medical center, which is equipped with special equipment, but most likely for a fee.

Depending on the capabilities of the laboratory, the result can be obtained on the same day, after 2-3 days or after 2 weeks. Considering that testing is stressful for many people, it is better to clarify the timing in advance.

What should you do if you test positive for HIV?

• course of the disease itself

• what research still needs to be done?

• how to live with this diagnosis

• what treatment to take if necessary, and so on

Must be determined:

• CD4 cell level

• presence of viral hepatitis (B, C, D)

• in some cases, p-24-Capsid antigen

How can you avoid becoming infected with HIV?

• when coughing or sneezing
• for insect or animal bites
• through shared tableware and cutlery
• during medical examinations
• when swimming in a pool or pond
• in the sauna, steam room
• through a handshake, hug and kiss
• when using a shared toilet
• in public places

Who are HIV dissidents?

Their beliefs are based on the following:

• HIV has not been identified clearly and indisputably

In fact, there are plenty of photographs taken under an electron microscope.

• From treatment antiviral drugs sick people die faster than from illness

  This is partly true, since the very first drugs did cause a large number of side effects. However, modern medicines are much more effective and safer. In addition, science does not stand still, inventing more effective and safe means.

• Considered a global conspiracy of pharmaceutical companies

  If this were so, then pharmaceutical companies would disseminate information not about the disease itself and its treatment, but about some kind of miracle vaccine, which, by the way, does not exist to this day.

• They say that AIDS is a disease of the immune system, not caused by a virus

  They say it is a consequence of immunodeficiency that developed as a result of stress, after strong radiation, exposure to poison or strong drugs, and some other reasons.

  Here we can contrast the fact that as soon as an HIV-infected patient starts taking HAART, his condition improves significantly.

  All these statements mislead patients, therefore they refuse treatment. Whereas, when started on time, HAART slows down the course of the disease, prolonging life and allowing HIV-infected people to be full-fledged members of society: to work, give birth to healthy children, live in a normal rhythm, and so on. Therefore, it is so important to detect HIV in time and, if necessary, begin HAART.

Mature human immunodeficiency virus virions They have a spherical shape, their sizes do not exceed 100-120 mm in diameter. Human immunodeficiency virus genome form two strands +RNA; they are bound by proteins pb and p7 (the number corresponds to the molecular weight in kDa).

Human immunodeficiency virus capsid forms p24 protein. The core of the human immunodeficiency virus virion is cylindrical or cone-shaped; it is formed by proteins p18 and p24.

At the core of the human immunodeficiency virus RNA, internal proteins (p7 and p9), reverse transcriptase (a dimer of proteins p66 and p51) and endonuclease (p31) are located. The matrix protein p17 forms a layer between the virion core and the outer envelope.

Human immunodeficiency virus supercapsid formed by a double lipid layer, which is penetrated by glycoprotsin spines. Each spine is composed of the proteins gp41 and gp 120. The gpl20 glycoproteins are localized in the protruding part of the spine and interact with CD4 molecules on cell membranes.

gp41 glycoproteins (fusion proteins) human immunodeficiency virus are located inside the membrane and ensure its fusion with the cell membrane.

Antigenic structure of human immunodeficiency virus

In human immunodeficiency virus the main antigens are group- and species-specific antigens [core (gag-) proteins p24; type-specific antigens [envelope (env-) proteins gp41 and gp120].

According to their structure, two types and more than 10 are distinguished human immunodeficiency virus serovars. The human immunodeficiency virus is characterized by high antigenic variability, and as a result of reverse transcriptase failures, serologically different viruses can be isolated from the patient's body.

The main antigens of the human immunodeficiency virus- surface gp41 and gpl20, as well as core (nuclear) gp24.

Pathological anatomy of AIDS (HIV infection): Guidelines/ Avtsyn A.P., Permyakov N.K., Kazantseva I.A., Parkhomenko O.G. - M., 1989. - 18 p.

Compiled by: Academician of the USSR Academy of Medical Sciences prof. A.P. Avtsyn, academician of the USSR Academy of Medical Sciences prof. N.K. Permyakov, prof. I.A. Kazantseva, Doctor of Medical Sciences O.G. Parkhomenko

Instructions of the USSR Ministry of Health dated March 20, 1989 No. 269-U

Pathological anatomy of AIDS (HIV infection): Guidelines

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MINISTRY OF HEALTH OF THE USSR

PATHOLOGICAL ANATOMY OF AIDS (HIV infection)

RESEARCH INSTITUTE OF HUMAN MORPHOLOGY USSR Academy of Medical Sciences ALL-UNION RESEARCH AND METHODOLOGY CENTER OF PATHOLOGICAL-ANATOMICAL SERVICE

INTRODUCTION

Acquired immune deficiency syndrome (AIDS) is an infectious disease that causes a severe defect in cellular immunity in previously healthy people. First described in 1981. By 1987, the Center for Disease Control (USA) had information on more than 50 thousand AIDS patients aged 28 days to 60 years. Currently, according to WHO, in 144 countries of the world there are about 140 thousand such patients and from 5 to 10 million people infected with the AIDS pathogen.

The causative agent of AIDS is a human T-lymphotropic virus, which belongs to the retrovirus family. It was abbreviated as HTlv - III (or Hiv), in Russian - HIV (human immunodeficiency virus) in contrast to HTlv - I, which causes T-cell lymphomas, and HTlv - II, which is the etiological factor of the so-called hairy cell leukemia.

To identify people infected with the virus, an ELISA test (enzyme-linked immunoserbent assay) is used, which determines the presence of serum antibodies to HIV. It is believed that the ELISA test should be confirmed by a more specific test - immunoblotting. Serum antibodies to HIV were found in 90% of patients with AIDS and in 50% with a high risk of developing AIDS (homosexuals, drug addicts, prostitutes, people with a history of blood transfusions, children born from infected mothers).

Birion HIV is a spherical particle with a diameter of about 1000 A. Its core contains genetic material, which is RNA. Birion is covered with a membrane from which protein particles protrude. The first stage of cell infection

HIV, like any other virus, is the binding of the viral particle to a special component of the cell membrane (receptor). For HIV, such a receptor is a protein called the Cd 4 antigen, which binds to a glycoprotein (GP-120), the viral envelope protein. Consequently, the distribution of Cd 4 determines the spectrum of cells and tissues affected by HIV, i.e. determines the tropism of the virus. These are, first of all, T4 - halper lymphocytes, which during AIDS practically disappear from the lymphocyte population.

In addition to T4 - helper lymphocytes, the CD 4 antigen is contained by approximately 40% of monocytes (macrophages), the so-called dendritic antigen - representing cells of lymphoid organs and skin, as well as 5% of all B-lymphocytes of the body. Some cells, in particular glial and neuroendocrine intestinal (enterochromaffin) cell elements, become infected with HIV in culture, but Cd 4 cannot be detected in them. This is explained by the fact that these cells contain traces of messenger RNA encoding the Cd 4 protein, i.e. they are capable of synthesizing this protein. It appears that very little Cd4 protein is required to infect a cell with HIV. HIV infection causes severe immunosuppression with a predisposition to so-called opportunistic infections and tumors (see below). Damage to the immune system primarily occurs as a result of infection and death of T4 halper lymphocytes. However, with the selective elimination of T4 lymphocytes, which are of paramount importance for the generation of a specific immune response, severe changes develop throughout the entire immune system. These changes are induced by opportunistic infections (especially herpes viruses) in immunosuppressed patients and are manifested by a decrease in delayed-type hypersensitivity reactions and blast transformation reactions of lymphocytes to antigens and metogens, polyclonal B-cell activation, a decrease in monocyte/macrophage hematoxin, and a decrease in the occurrence of specific and nonspecific cytotoxicity of immune cells. It is likely that the full spectrum of diseases associated with HIV infection has not yet been fully established. However, it is already known that the causative agents of opportunistic infections in AIDS can be viruses, bacteria, fungi and protozoa, which persist in the body of a person with a normal immune system, without causing clinical and morphological manifestations of the disease. After the body is infected with HIV, these pathogens are activated and the disease can become generalized.

Tumors characteristic of AIDS are also, because their occurrence is associated with viruses of the Herpes group, primarily the cytomegaly virus (for example, Kaposi's sarcoma) and the Epstein-Barr virus (for example, malignant B-cell lymphomas). The development of tumors is explained by a decrease in the body's antitumor resistance.

AIDS SYNDROMOLOGY

Currently there are:

1. Fully developed AIDS, meeting the criteria of the North American Disease Notification System, with the presence of opportunistic infections and/or tumors.

2. AIDS - associated complex - AIDS without signs of opportunistic infections and/or tumors.

3. Chronic lymphadenopathy syndrome: the presence of lymphadenopathy in homosexual men for more than 3 months involving 2 or more areas (excluding the groin).

The range of diseases in patients infected with HIV is extremely wide; they can be divided into separate syndromes. Although AIDS causes damage to many organs and systems, most patients die as a result of diseases of the lungs or central nervous system.

The clinical syndromes observed in AIDS can be grouped according to the organ system that is most often affected:

pulmonary syndrome;

neurological syndrome;

intestinal syndrome;

damage to the skin and mucous membranes;

lymphadenopathy;

fever of unknown origin;

retinal syndrome.

PULMONARY SYNDROME

Pulmonary syndrome in AIDS is clinically manifested by fever, dry cough, and scanty ascultative data.

With bilateral lung damage and the predominance of interstitial pneumonia, one should think about the following etiological factors: Pneumocystis carinii pnemoniae, cytomegalovirus infection; Logionella species; Micobakterium avium intracellulare (atypical mycobacterial infection) and/or Micobacterium tuberculosis; Toxoplasma gondii; pathogenic fungi (candidiasis, blestomycosis, actinomycosis, coccidioidosis, histoplasmosis).

With bilateral lesions with predominant involvement of the alveoli, the following is most often found:

a) atypical or typical mycobacterial infection;

b) pulmonary form of Kaposi's sarcoma (especially if the process is accompanied by hemorrhagic pleural effusion);

c) bacterial (usually staphylococcal) pneumonia.

Pneumocystis pneumonia is the most common opportunistic infection in AIDS, occurring in 85% of patients. Microscopically, Pneumocystis pneumonia is characterized by foamy eosinophilic exudate in the alveoli; the number of alveolar macrophages is usually small; occasionally, foci of granulomatous inflammation are observed; in long-term cases, interstitial pulmonary fibrosis develops, and calcifications may occur. The pathogen persists in lung tissue for up to 5-6 weeks. Pneumocystis are detected in lung tissue and bronchoalveolar lavage (BAL). Using Homus silver impregnation, toluidine blue staining, or Giemsa staining, oval, round, or collapsed pneumocystis can be identified in histological sections and impressions of lung tissue from BAL fluid. The detection of foamy exudate in the BAL fluid is the basis for a presumptive diagnosis of Pneumocystis pneumonia. A quick method for detecting pneumocystis is the fluorescent antibody method. The detection rate of pneumocystis in the study of transbronchial biopsy and BAL is 65-10..... Cytomegalovirus infection is the most frequently detected generalized opportunistic infection in autopsy and microscopic examination, including the lungs. However, intravital diagnosis of cytomegaly is rarely made. Cytomegalovirus-containing large cells (with typical intranuclear inclusions) are unevenly distributed in the lung tissue, and the inflammatory response is minimal or absent. In severe pulmonary infection, diffuse interstitial pneumonia, hyaline membranes, and even areas of necrosis of the lung tissue are observed. Detection of cytomegalovirus by the immunoperoxidase method using monoclonal antibodies in BAL fluid is very effective, but a positive result often indicates carriage of the virus rather than an active infection. With transbronchial biopsy, the detection rate of cytomegalovirus pneumonia is 50-85%%.

Mycobacterial pneumonia, including atypical pneumonia, may not be diagnosed in AIDS due to a minimal and atypical tissue reaction. Disseminated pulmonary tuberculosis has been described only in drug addicts and residents of the island of Haiti. An atypical mycobacterial infection is characterized by accumulations of foamy (granular) macrophages with PAS - positive cytoplasm, in which mycobacteria are detected. Epithelioid cell granulomas are rare. In all cases of AIDS, histological preparations of lung tissue should be stained with Ziehl-Neelsen to detect acid-fast flora. With transbronchial biopsy, atypical mycobacterial infection is detected in 62-87% of cases.

NEUROLOGICAL SYNDROME

HIV can primarily affect the nervous system. In addition, opportunistic infections involving the central nervous system and malignant brain lymphomas often develop. It is necessary to carry out differential diagnosis between these processes Pathological changes in the central nervous system in AIDS based on materials from 153 people who died from AIDS Infections

Normal, metabolic encephalopathy, or nonspecific changes 23.6%

Progressive spinal symptoms can be caused by damage to the spinal cord: a) HIV itself; b) HIV in combination with herpetic and/or cytomegalovirus infection (for diagnosis, material for detecting the virus should be obtained from the cerebrospinal fluid). Damage to the peripheral nerves of the so-called. peripheral neuropathy can be caused by both HIV infection and complications of chemotherapy, especially during treatment with vincristine. Sometimes polymyopathy occurs due to autoimmune muscle damage by antisarcolemmal auto-antibodies. Encephalopathy caused directly by HIV is clinically characterized by personality changes, amnesia, social isolation, and progressive dementia. Pathomorphological changes develop mainly in the white matter and subcortical structures, the cortex is relatively preserved. There is a correlation between the severity of dementia and the severity of pathomorphological changes in the brain. Macroscopically, the pathology of the white matter and subcortical formations of the brain is characterized by areas of blanching and areas of softening.

Histologically, HIV encephalomyelitis can be characterized as a subacute encephalitis with multinucleated cells, small or larger accumulations of microglia (monocytes/macrophages), which are especially numerous in subcortical structures, including the basal ganglia and centrum semiovale. These microglial nodules can also be found in the brain stem, brainstem, spinal cord, and less commonly in the cerebral cortex. For HIV infection in the central nervous system, the formation of multinucleated cells of the symplast type, which can be located alone or in combination with microglial nodules and nodes, is pathognomic. Microscopically, foci of demyelination, perivascular inflammatory infiltrates, macrophages containing brown pigment (siderophages) and (i.e., impregnated with iron salts) neurons are also characteristic. Neuronal changes are not specific to HIV.

Characteristic manifestations of HIV encephalomyelitis include vacuolation of white matter. Vacuolar myelopathy with damage to the lateral and posterior columns of the spinal cord is especially common, but not specific. During vacuolation, the white matter appears holey (this process is also called). When differentially diagnosing HIV encephalitis, it should be taken into account that microglial nodules are also characteristic of cytomegalovirus encephalitis, however, in the latter, the degree of dementia does not correlate with the severity of damage to the brain substance.

Progressive multifocal leukoencephalopathy (PML), characteristic of AIDS, was previously considered a very rare disease. It was first described in people with oncological lymphoproliferative diseases, especially chronic lymphocytic leukemia, as well as in patients with sarcoidosis. It is believed that PLM is caused by slow viruses (not HIV itself) and only in patients with severe immune deficiency. Fixed macroscopic specimens of PML reveal multiple grayish foci in the white matter of the brain and spinal cord, which are slightly sunken and have a granular appearance. In lesions, viruses destroy oligodendroids, the nuclei of which can be moderately hyperchronic, with homogeneous chromatin. The nuclei of many astrocytes surrounding the lesion are enlarged, polymorphic, and very reminiscent of the early stage of neoplastic transformation. In half of the described cases, perivascular infiltrates of lymphocytes and plasma cells were encountered. The most common opportunistic infections in the central nervous system in AIDS are cytomegalovirus encephalitis, cryptococcosis and toxiplasmosis. These infections differ from HIV encephalitis in the presence of the corresponding microorganisms and the absence of characteristic multinucleated cells.

Encephalitis caused by cytomegalovirus is characterized by the presence of foci of necrosis and specific large cells with a large basophilic intranuclear inclusion surrounded by a light rim and small cytoplasmic inclusions (cells resembling). These cells are usually mononuclear, but may have 2-3 nuclei; typical inclusions distinguish them from multinucleated cells, pathognomonic for HIV encephalitis.

Xyptococcosis (fungal infection) can cause massive damage to the brain with the development of foci of necrosis, macroscopically and in consistency resembling jelly. Clusters of rounded forms of the fungus are clearly visible in histological sections with the PHIK reaction.

Brain toxoplasmosis is manifested by the development of foci of necrosis of varying sizes against the background of severe microcirculation disorders and hemorrhages. Toxoplasmosis in histological sections can be identified by Giemsa staining; they are characterized by their arrangement in groups.

All of the listed causative agents of opportunistic reactions of the central nervous system can be identified by electron microscopic examination.

Pediatric encephalopathy with AIDS is characterized by the following features:

1. reduction in brain weight;

2. inflammatory infiltrates (more typical are diffuse or microglial nodules);

3. multinucleated cells, multinucleated giant cells;

4. calcifications of small vessels, perivascular infiltrates;

5 . changes in white matter: demyelization, proliferation of astrocytes (astrocytosis) with relative preservation of axons; absence of vacuolar myelopathy;

6. rare association with opportunistic infections;

7. During electron microscopy, the so-called multinucleated giant cells are found to be represented by clusters of mitochondria surrounded by lipid vacuoles (retrovirus particles are shown in and outside the mitochondria).

INTESTINAL SYNDROME

Diarrhea and wasting syndrome associated with HIV infection has been described for the first time in the Republic of Uganda. The incidence of diarrhea in patients with AIDS in the United States ranges from 30 to 50%, and in Africa and Haiti it is 70 to 90%. Diarrhea is usually caused by opportunistic infections, most often caused by the following pathogens: a) Shigella, Campylobakter, Blastocystis hominis; b) cryptosporidium; c) clostridia.

In addition, with AIDS, a disease resembling Sprue is described, without an established etiology. In biopsies of the small intestine, flattening of the villi, necrosis and desquamation of the epithelium, and signs of chronic inflammation are noted. It has not been conclusively established whether these changes are the primary manifestation of HIV infection or whether they are associated with another, as yet unverified pathogen.

Immunological and immunomorphological study of the cells of the infiltrate of the mucous membrane of the small intestine in AIDS indicates severe depletion (reduction) of the population of T-4 lymphocytes, a sharp decrease in the number of plasma cells containing Ig A. These changes may explain the tendency to relapse of intestinal infections when appropriate therapy is stopped in patients AIDS; they probably play an important role in the pathogenesis of enteropathy in AIDS and in the development of opportunistic infections as a result of local impairment of cell-mediated immunity.

Intestinal biopsy in patients with AIDS ranks second in frequency after lung biopsy; their informative value in terms of the possibility of establishing a diagnosis of a pathological process characteristic of AIDS is about 40%.

Characteristic manifestations of AIDS include diarrhea and proctitis in homosexuals, the causative agents of which are the most common intestinal pathogens, the most common sexually transmitted pathogens, as well as random intestinal flora for which the individual is found to be idiosyncratic.

In AIDS patients, the intestines are mainly affected by 4 infections; candidiasis, cytomegaly, mycobacteria (M.avium intracellulare) and cryptosporidiosis. Rarely, but still found in the intestines of AIDS are histoplasmosis, toxoplasmosis, pneumocystis infection, and botryomycosis. Tuberculosis of the ileocecal zone, colon, and stomach is also rare. Opportunistic infections and intestinal tumors in AIDS differ from their counterparts in patients in the pre-AIDS period in particular prevalence and severity. Thus, cryptosporidiosis, previously known as a common cause of diarrhea in calves, causes severe diarrhea and can affect the biliary tract and liver in patients with AIDS. With abdominal syndrome without diarrhea in patients with AIDS, cytomegalovirus infection, cryptosporidiosis, and tumors are most often detected: Kaposi's sarcoma and malignant lymphoma. Candidiasis in patients with AIDS is often limited to the oral mucosa and esophagus, but can affect the entire gastrointestinal tract.

Candidal ulcers are usually not deep; with the PHIK reaction, numerous threads of pseudomycelium are revealed in their bottom.

Cytomegalovirus infection primarily affects the large intestine, especially the cecum, but penetrating ulcers can also occur in the small intestine. Sometimes there is mild gastritis, esophagitis, and occasionally cholecystitis. Macroscopically, the mucous membrane looks hyperemic with small whitish depressions, which are ulcers. Microscopically, inflammation is often absent; intestinal crypts in a special plate contain typical viral inclusions. Most virus-infected cells are of mesenchymal origin.

In the small intestine, cytomegaly causes deep ulcers that reach the serosa and can perforate, causing a more severe inflammatory reaction. Microscopically, granulation tissue with numerous plasma cells, lymphocytes, and histiocytes is visible at the edges of the ulcer; in some of the latter, viral inclusions are detected. They can also be found in fibroblasts, smooth muscle cells and endothelium. Cytomegalovirus infection may not be accompanied by ulceration of the mucosa and may manifest itself as focal or segmental productive inflammation, simulating Crohn's disease.

Another common opportunistic infection of the gastrointestinal tract in patients with AIDS is an atypical microbacterial infection caused by M. Avium intracellulare. This infection affects the small intestine. Macroscopically, the mucous membrane appears swollen and thickened. Microscopically, flattened villi are visible, shortened and expanded due to the infiltrate of histocytes. These histocytes are similar to those found in Whipple's disease. With the CHIC reaction, abundant cytoplasm is detected in them. When stained for acid-fast microorganisms according to Ziehl-Nielson, many mycobacteria are detected in histocytes. If the process is widespread, then clinically the patients are diagnosed with malabsorption syndrome. Damage to the small intestine is often combined with enlargement of the mesenteric lymph nodes. The colon in atypical mycobacterial infection is involved secondarily and moderately. Biopsies from the colon look almost normal, and acid-fast bacilli are detected only in single histocytes. Intestinal tuberculosis in AIDS can occur without typical granulomatosis and manifest itself with changes that mimic nonspecific ulceration.

Cryptosporidiosis. Pathogens do not invade tissue, but adhere to the surface of the epithelium of the small and large intestine. They may be visible on conventional staining (hematoxylin and eosin) as small blue-stained structures. Several intestinal infections can be combined in AIDS patients.

Kaposi's sarcoma occurs quite often in the stomach and intestines of AIDS patients. In most cases, this is combined with skin lesions, but the intestine may be the only organ in which foci of Kaposi's sarcoma develop. The tumor is localized submucosally and is usually not diagnosed with a superficial biopsy.

Malignant lymphomas in AIDS occur in the stomach, small intestine and colon. Their localization in the oral cavity and anal area is also typical. The most common are B-cell (lymphoblastic, immunoblastic) lymphosarcoma with poor prognosis. Cases of lymphogranulomatosis with damage to the gastrointestinal tract have also been described.

PATHOLOGICAL CHANGES IN OTHER ORGANS.

Liver pathology in AIDS. The most typical pathological processes are:

1. infection: atypical mycobacterial infection, cryptococcosis, cytomegalovirus infection and viral hepatitis B;

2. Kaposi's sarcoma;

3. nonspecific changes.

Atypical mycobacterial infection is characterized by accumulations of histocytes both along the portal tracts and inside the lobules. If granulomas form, they also consist of histiocytes, the lymphocytic reaction is weak or absent. Histocytes have light granular cytoplasm, are PAS-positive and can be confused with those of Upla disease. Ziehl Nielson staining reveals M. Avium intracellulare in these cells.

Cryptococcal infection can severely affect the entire liver. Fungi are detected in sinusoids (single or in the form of clusters), the inflammatory reaction is very weak.

In approximately 25% of AIDS cases, viral hepatitis B occurs. The diagnosis is confirmed by immunomorphological detection of the hepatitis B virus antigen.

Kaposi's sarcoma can primarily affect the liver; it is characterized by localization in the hilum of the liver and along the portal tracts. Nonspecific changes in the liver in patients with AIDS occur as a result of massive therapy with antibiotics, cytostatics and corticosteroids.

Damage to the esophagus in patients with AIDS is usually caused by candidomycosis, cytomegaly, mycobacteria, and herpes simplex virus. The skin and mucous membranes of the mouth, pharynx, and external genitalia are often affected by Kaposi's sarcoma. Candida ulcers are also characteristic; necrotizing gingivitis, often herpetic; Herpes zoster; seborrheic dermatitis occurs.

Other skin syndromes are also described in AIDS: psoriasis, herpes, molluscum contagiosum (don't miss syphilis!). Kaposi's sarcoma in AIDS patients is characterized by infiltrative-plaque pale red lesions, which are located not only on lower limbs, but also on the face, external genitals and other areas of the skin.

Nodular formations are rare. A histological examination reveals foci of chaotic antiogenesis with the formation of thin-walled sucky cavities, proliferation of spindle-shaped cells, lymphoid-plasma cell and macrophage infiltration, hemosiderosis, erythrophagy.

Retinal damage in AIDS can develop as a reaction to the antigen of Pneumocystis in Pneumocystis pneumonia or is caused by cytomegalovirus.

Heart pathology in AIDS.

In patients with AIDS, the epicardial form of Kaposi's sarcoma and lymphosarcoma occur; Pericardial hemorrhage, myocarditis and pericarditis caused by opportunistic viral-bacterial, fungal or protozoal infection are common. Chronic lymphohistiocytic () myocarditis was found in more than 50% of autopsies of people who died from AIDS.

Kidney pathology in AIDS.

HIV-associated nephropathy is described. The most common morphological findings are focal segmental glomerulosclerosis with deposits of immune complexes in the glomeruli, microcystic tubules, the so-called tubulo-interstitial nephritis. By electron microscopy, tubuloreticular structures resembling viral particles are detected in the glomerular endothelium and cells of the stromal infiltrate. The kidneys do not decrease in size throughout the entire illness until the development of uremia. The disproportion of changes in nephrons and the severity of interstitial fibrosis may explain the preservation of normal kidney sizes.

LYMPHADENOPATHY

The primary manifestation of AIDS may be generalized lymphadenopathy. The reaction of lymph nodes in AIDS is divided into several types, which represent successive stages of a dynamic process, starting with hyperplasia and ending with atrophy. The following types of lymphadenopathy are distinguished:

1. follicular hyperplasia;

2. hypervascular follicular type;

3. mixed follicular type;

4. follicular involution with lymphoid depletion.

With follicular hyperplasia, the follicles are very large, irregular in shape, sometimes spreading over almost the entire node. The hyperplastic centers are surrounded by mantle zones, which often appear discontinuous and lose the characteristic concentric arrangement of lymphocytes, the latter of which can penetrate into the germinal centers. As the follicles enlarge within the germinal centers, the number of centroblasts increases, and numerous mitoses are visible. A study using monoclonal antibodies showed an increase in the subpolation of T8 suppressor lymphocytes. The parafollicular sinuses contain many monocytoid cells with slightly eosinophilic cytoplasm. Electron microscopic and immunomorphological data show that dendritic cells and T-4 lymphocytes in the germinal centers are infected with HIV, and activation of viral RNA is detected in them.

The paracortical zone is also usually hyperplastic, represented predominantly by small lymphocytes, immunoblasts, and neutrophilic leukocytes.

Characteristic is a decrease in the ratio of T-halpers and T-suppressors due to a decrease in the number of T4-halper lymphocytes.

The pathomorphological picture is complemented by plasma cells, a large number of dilated and full-blooded vessels, hemophagocytic macrophages, small accumulations of polymorphonuclear leukocytes, multinucleated giant cells similar to those found in viral infections, multinuclear immunoblasts.

Hypervascular follicular lymphadenopathy in patients with AIDS is often associated with Kaposi's sarcoma; characterized by changes resembling angiofollicular hyperplasia. In the tissues of the lymph nodes, the number of plasma cells and many small tree-like branching blood vessels are increased; the range of changes in follicles is wide - from large ones with hyperplastic germinal centers to hyalinized ones.

The mixed follicular type of lymphadenopathy is characterized by the presence of both hyperplastic and involuted follicles with the colonization of the paracortical zone by plasma cells. These changes are frequent in the case of opportunistic infections. A reduction in T4 lymphocytes is characteristic.

Follicular involution with lymphoid depletion is characterized by the complete absence of various follicles and germinal centers. Two morphological variants of this stage are described: the first is characterized by a large number of immunoblasts, plasma cells and proliferating blood vessels (reminiscent of angioimmunoblastic lymphadenopathy); the second - an almost complete reduction of lymphocytes, an abundance of non-mophagocytic macrophages; the remaining lymphocytes are represented by T8 suppressors.

Lymph nodes in AIDS can become massively infected with various opportunistic infections, Kaposi's sarcoma, and malignant lymphomas. Granulomatous processes are common in opportunistic infections. Infections are extremely aggressive, quickly generalize, and are resistant to therapy.

With rapid local enlargement of the lymph nodes in a patient with AIDS, one should think about Kaposi's sarcoma or malignant lymphoma; Damage to the femoral, para-aortic, and retroperitoneal lymph nodes by these tumors is especially typical. Buboes are usually seen with malignant lymphoma, tuberculosis, or atypical mycobacterial infection.

In cases of fever of unknown origin with anemia, splenomegaly, and liver dysfunction in a patient with AIDS, one should first of all think about disseminated atypical mycobacterial infection, as well as malignant lymphoma.

PRINCIPLES OF PATHOLOGANATOMIC DIAGNOSIS OF AIDS

Before, after and during autopsy, AIDS may be suspected if the manifestations of opportunistic infections and tumors described above are present, especially if these processes are combined or generalized. In the case when a patient's clinical diagnosis of AIDS was confirmed during his lifetime by the detection of antibodies to HIV in the blood serum, the interpretation of autopsy data, as a rule, does not cause difficulties. If AIDS was suspected based on a combination of pathological processes only at autopsy, at least 5 ml of blood from the femoral vein should be sent (with a special order) to the appropriate regional laboratory. Blood is drawn into a dry sterile tube, closed with a rubber stopper, placed in a plastic bag, treated with a 3-5% chloramine solution and placed in a container.

It is believed that detection of serum HIV antibodies is possible up to 24 hours after death, but the study is complicated by hemolysis of cadaveric blood. Therefore, a negative result does not mean that there was no HIV infection in this case. However, a pathological diagnosis of AIDS can only be made if it is confirmed by a test for antibodies to HIV.

In each case suspected of AIDS, a careful comparison of clinical, anatomical and pathological data should be carried out. It should be remembered that opportunistic infections and Kaposi's sarcoma are not specific manifestations of HIV infection and can be observed with severe secondary immune deficiencies of various origins, in particular those associated with long-term use of antibiotics, cytostatics, corticosteroids or other drugs that have an immunosuppressive effect.

When formulating a pathological diagnosis in cases of confirmation of HIV infection, the following should be indicated at the head of the diagnosis: AIDS (positive reaction to antibodies to HIV in the blood serum). Next, opportunistic infections and/or tumors are listed in a sequence reflecting the severity of the pathological process and its role in thanatogenesis.

The epicrisis should indicate which disease played a role in the death.

For example: the death of an AIDS patient (the presence of antibodies to HIV in the blood serum) resulted from bilateral Pneumocystis pneumonia (or Kaposi's sarcoma with damage to the skin, lymph nodes, lungs and intestines). If the diagnosis of AIDS is not confirmed serologically or there was no opportunity to conduct research, but the case is extremely suspicious for AIDS, then this should be indicated and justified in the pathological epicrisis.

For pathological examination in cases suspected of AIDS, the brain should be taken (necessarily from the area of ​​the subcortical ganglia and white matter of the hemispheres), spinal cord, lungs (even in the absence of macroscopically visible inflammatory changes), organs of the gastrointestinal tract (pieces from all sections of the intestine should be examined microscopically after careful macroscopy), organs of immunogenesis (bone marrow, thymus, lymph nodes, spleen), liver, kidneys, heart, if indicated - retina, skin, oral mucosa, external genitalia. The pieces are placed in conventional fixatives (formalin, Carnoy's liquid, 80% alcohol, etc.).

It must be remembered that all infections with AIDS tend to generalize and can occur as sepsis. Therefore, in all cases of intravitally confirmed AIDS or if AIDS is suspected, send blood from the heart cavity for bacteriological testing.

As noted above, the role of pathological examination of diagnostic biopsies and surgical material (especially lymph nodes, skin, lungs, intestines) in identifying cases of disease suspected of AIDS is very great.

If opportunistic infections and/or tumors characteristic of AIDS are detected in a biopsy specimen in persons under 60 years of age, the pathologist is obliged to reflect in his conclusion the need to examine the patient for antibodies to HIV or directly inform the attending physician about this. When drawing up a conclusion, caution should be exercised and unjustified overdiagnosis of AIDS should be avoided, given that this can cause serious ethical problems for the relatives of the deceased and all persons who were in contact with him.

ANNEX 1

DIRECTION OF THE USSR MINISTRY OF HEALTH dated March 20, 1989 No. 269-U (addition to the Directive of the USSR Ministry of Health dated December 22, 1987 No. 460-U.

In order to streamline the system of collecting and transmitting information on registering those who died from AIDS, a special record of cases of AIDS diagnosis during a pathological or forensic examination of a corpse based on a set of pathological changes confirmed by a serological test of cadaveric blood for antibodies to HIV is being introduced. For each such case, the health care institution fills out (form No. 058/u) and sends it to the territorial sanitary-epidemiological station at the place of registration.

In cases where, based on the results of a pathoanatomical or forensic autopsy of a corpse, a suspicion of AIDS arises, but a study of cadaveric blood for antibodies to HIV gave a negative result or it was not possible to conduct it, the institution is also obliged to notify the sanitary-epidemiological station at the location. detection of a disease suspicious for AIDS.

Information about this person is also entered into the journal, on a separate sheet for recording infectious diseases (form 060/у). First Deputy Minister I.N. DENISOV

APPENDIX 2

COMPREHENSIVE PLAN OF ACTIONS FOR BODIES AND HEALTH CARE INSTITUTIONS WHEN PROVIDING PATHOLOGANATOMICAL AUTOPSIES IN CASES OF AIDS.

1. Determination of the procedure for informing a higher health authority when a corpse with an established (or suspected) diagnosis of AIDS is identified.

2. Designation of a pathology department for autopsy of those who died from AIDS.

3. Determining the procedure for delivering corpses to the pathology department, where the autopsy will be performed.

4. ensuring the delivery of corpses by special vehicles.

5. provision of a supply of disinfectants and protective suits, incl. gloves

6. ensuring the referral of fixed samples of organs and tissues to the Institute of Human Morphology of the USSR Academy of Medical Sciences, which performs the functions of a consultative and methodological center on the pathological anatomy of AIDS.

7. determination of laboratory facilities for serological testing of cadaveric blood for antibodies to HIV.

8. compliance with the anti-epidemic regime for pathogens of group II pathogenicity when working with biopsy and autopsy materials.

APPENDIX 3

PRECAUTIONARY MEASURES FOR PERSONS PERFORMING OPTIONS AND EXAMINATIONS OF BIOPSY (SURGICAL) MATERIAL FROM PATIENTS AND DEAD FROM AIDS, AND FUNERAL HOME PERSONNEL.

The AIDS virus (HIV) is classified in pathogenicity group II, along with the viruses listed in Appendix 8 (approved by the USSR Ministry of Health on June 29, 1978).

1. In the case of AIDS or if it is suspected, a special tag with a warning inscription should be attached to the body of the deceased.

2. All personnel involved in the autopsy must wear a type I suit: double gloves, oversleeves, waterproof aprons, boots or galoshes, shoe covers. Tools and surfaces contaminated during opening must be treated with a 3% chloramine solution. The discharge of wastewater into the sewer system is stopped. Rinse water is collected in buckets or other containers containing disinfected solutions. A mat moistened with a disinfectant solution is placed at the entrance to the sectional room.

3. When handling fabric material and biological fluids or, if necessary, coming into contact with surfaces that may be contaminated with them, rubber gloves should be worn.

4. Clothing used during autopsy, soaked in blood or other biological fluids, must be placed in a waterproof bag with a warning label. Contaminated material can also be placed in color-coded plastic bags designed to collect and dispose of infectious waste. Before removing the suit, wipe the oilcloth apron with a cotton swab, generously moistened with a disinfectant solution, remove it, folding it from the outside inward; remove the second pair of gloves and sleeves; boots or galoshes are wiped from top to bottom with cotton swabs generously moistened with a disinfectant solution (a separate swab is used for each boot).

5. For handling all liquids in laboratories, only mechanical pipettes with a rubber bulb should be used. Pipetting by mouth is prohibited!

6. All skin lesions on the hands must first be covered with adhesive tape or fingertips.

7. All procedures and manipulations with potentially infected material should be performed carefully to avoid the formation of droplets and aerosols. If hands or other parts of the body are contaminated with blood or other biological fluids, they should be treated with a disinfectant solution or 70o alcohol. If there is a suspicion that contaminated material has entered the mucous membranes, they are immediately treated with a 0.5% solution of potassium permanganate, the eyes are washed with a 1% solution of boric acid or a stream of water or a few drops of a 1% solution of silver nitrate are instilled, a 1% solution of protargol is instilled into the nose, the mouth and throat are additionally rinsed with 70° alcohol or a 0.05% solution of potassium permanganate or a 1% solution of boric acid.

8. In case of accidental splashing of infected material and upon completion of work, the working surfaces of laboratory shafts must be disinfected with a 3% chloramine solution.

9. On sterile jars with material sent for research (blood, biopsies or surgical material), it is necessary to make warning labels, for example; . If the outer surface of the jar is dirty, it must be wiped with an aqueous solution of sodium hypochlorite (5.25%) diluted 1:10 or 3% chloramine solution. During transportation, all cans of material must be hermetically sealed with a rubber stopper and rubber film (from gloves) and placed in a second container or tight bag, which must be carefully inspected to ensure there is no mechanical damage. The outer surfaces of containers or bags are treated with a 3% chloramine solution. An accompanying document is attached to the parcel, which indicates the full name, age, diagnosis, date of collection of the material, nature of the material, name and position of the medical worker sending the material. All materials are sent by express. Fixed autopsy material is stored in a specially designated room. The procedure for recording, storing, handling, releasing and sending materials containing the AIDS virus (HIV) is carried out in accordance with those approved by the USSR Ministry of Health on May 18, 1979.

10. When working with potentially infected material, you should wear protective clothing (gowns or suits), which must be removed before leaving the laboratory premises.

11. All personnel must wash their hands thoroughly after completing work, removing clothing and before leaving the laboratory (sectional room).

12. After the autopsy, the corpse is irrigated with a disinfectant solution (3% solution of chloramine B or bleach), wrapped in a sheet soaked in a disinfectant solution, and placed in a metal coffin or wooden one, lined with oilcloth inside. A layer of at least 10 cm of bleach is poured onto the bottom. The corpse is transported to the cemetery or crematorium by an evacuation team, accompanied by specialists from the department of especially dangerous infections of the torportorial SES.

13. Funeral home personnel should be aware of the potential hazards and take appropriate precautions to prevent skin or mucous membranes from being exposed to body fluids from a corpse.

14. All potentially contaminated materials used for pathomorphological (cytological) studies must be disinfected (see clause 15) and only after that sent for disposal.

15. Disinfection modes for ongoing disinfection of various objects:

APPENDIX 4

HIV INACTIVATION

Laboratory studies show that to inactivate HIV, the concentrations of disinfectants calculated to inactivate retroviruses are quite sufficient: 40% ethyl alcohol, 30% isopropyl alcohol, 1% Lysol, 5% phenol, 2% formaldehyde, 200 mg sodium hypochloride.

The infectivity of the virus completely disappeared after incubation for 1 minute with 0.5% sodium hypochloride or 70% ethyl alcohol. A widely used fixative mixture of ethyl alcohol and acetone in a 1:1 ratio completely inactivated HIV within 10 minutes.

The thermostability of HIV was compared with the thermostability of other RNA-containing enveloped viruses. Incubation at 60° in the presence of 5% human albumin leads to the destruction of the virus within 20 minutes. The addition of a stabilizer (50% sucrose with 2 glycine at pH 7.0), used to prevent denaturation of some proteins during concentration and purification, increases the duration of incubation at elevated temperatures necessary to inhibit HIV infectivity. It is important that even in the presence of stabilizing additives, HIV retains fairly high thermolability: heating at 60° for 1-3 hours completely inactivates it.

The rate of HIV inactivation in the culture fluid depends on the incubation temperature and the presence of human serum or plasma. The infectivity of the virus remains at 25° for 15 days, at 37° for 11 days. At room temperature, HIV remains infectious in a liquid or dried state for at least 4-7 days. This stability was demonstrated in laboratory conditions when virus-containing preparations were stored under sterile conditions. Nevertheless, these results indicate the ability of the virus to maintain biological activity in environmental objects for quite a long time. Inactivation of HIV in the presence of various disinfectants.

The time of HIV inactivation in the examined autopsy and biopsy material during its fixation depends on the volume of the examined piece of tissue. The fixation procedure is as follows: cut out pieces of organs measuring no more than 1x1x0.5 cm are placed in a fixing liquid in a clean container. A piece of cotton wool (gauze) is first placed at the bottom. The volume of fixing liquid should be 7-10 times greater than the volume of the material being tested. Fixation time: 1-2 days or more at room temperature. The material is stored in a specially designated place.

It is a disease caused by the human immunodeficiency virus, characterized by acquired immunodeficiency syndrome, which contributes to the occurrence of secondary infections and malignancies due to the profound inhibition of the body's protective properties. HIV infection has a varied course. The disease can last only a few months or last up to 20 years. The main method for diagnosing HIV infection remains the identification of specific antiviral antibodies, as well as viral RNA. Currently, patients with HIV are treated with antiretroviral drugs that can reduce viral reproduction.

General information

It is a disease caused by the human immunodeficiency virus, characterized by acquired immunodeficiency syndrome, which contributes to the occurrence of secondary infections and malignancies due to the profound inhibition of the body's protective properties. Today, the world is experiencing a pandemic of HIV infection; the incidence of the disease in the world's population, especially in Eastern Europe, is steadily growing.

Characteristics of the pathogen

The DNA-containing human immunodeficiency virus belongs to the Lentivirus genus of the Retroviridae family. There are two types: HIV-1 is the main causative agent of HIV infection, the cause of the pandemic, the development of AIDS. HIV-2 is a less common type, found mainly in West Africa. HIV is an unstable virus, it dies quickly outside the host’s body, is sensitive to temperature (reduces infectious properties at a temperature of 56 ° C, dies after 10 minutes when heated to 70-80 ° C). It is well preserved in blood and its preparations prepared for transfusion. The antigenic structure of the virus is highly variable.

The reservoir and source of HIV infection is a person: an AIDS sufferer and a carrier. No natural reservoirs of HIV-1 have been identified; it is believed that the natural host in nature is wild chimpanzees. HIV-2 is carried by African monkeys. Susceptibility to HIV has not been observed in other animal species. The virus is found in high concentrations in blood, semen, vaginal secretions and menstrual fluid. It can be isolated from human milk, saliva, tear secretion and cerebrospinal fluid, but these biological fluids pose less of an epidemiological danger.

The likelihood of transmitting HIV infection increases in the presence of damage to the skin and mucous membranes (injuries, abrasions, cervical erosion, stomatitis, periodontal disease, etc.) HIV is transmitted using the blood-contact and bio-contact mechanism naturally (through sexual contact and vertically: from mother to child) and artificial (mainly realized through the hemopercutaneous transmission mechanism: during transfusions, parenteral administration of substances, traumatic medical procedures).

The risk of contracting HIV from a single contact with a carrier is low; regular sexual contact with an infected person significantly increases it. Vertical transmission of infection from a sick mother to a child is possible both in the prenatal period (through defects in the placental barrier) and during childbirth, when the child comes into contact with the mother’s blood. In rare cases, postnatal transmission through breast milk has been recorded. The incidence among children of infected mothers reaches 25-30%.

Parenteral infection occurs through injections using needles contaminated with the blood of HIV-infected individuals, through blood transfusions of infected blood, and non-sterile medical procedures (piercing, tattoos, medical and dental procedures performed with instruments without proper treatment). HIV is not transmitted through household contact. Human susceptibility to HIV infection is high. The development of AIDS in people over 35 years of age, as a rule, occurs within a shorter period of time from the moment of infection. In some cases, immunity to HIV is noted, which is associated with specific immunoglobulins A present on the mucous membranes of the genital organs.

Pathogenesis of HIV infection

When the human immunodeficiency virus enters the bloodstream, it invades macrophages, microglia and lymphocytes, which are important in the formation of the body’s immune responses. The virus destroys the ability of immune bodies to recognize their antigens as foreign, colonizes the cell and begins reproduction. After the multiplied virus is released into the blood, the host cell dies, and the viruses invade healthy macrophages. The syndrome develops slowly (over years), in waves.

At first, the body compensates for the massive death of immune cells by producing new ones; over time, compensation becomes insufficient, the number of lymphocytes and macrophages in the blood decreases significantly, the immune system is destroyed, the body becomes defenseless against both exogenous infection and bacteria inhabiting organs and tissues. normal (which leads to the development of opportunistic infections). In addition, the mechanism of protection against the proliferation of defective blastocytes - malignant cells - is disrupted.

The colonization of immune cells by the virus often provokes various autoimmune conditions, in particular, neurological disorders are characteristic as a result of autoimmune damage to neurocytes, which can develop even before the clinical manifestations of immunodeficiency appear.

Classification

In the clinical course of HIV infection, there are 5 stages: incubation, primary manifestations, latent, stage of secondary diseases and terminal. The stage of primary manifestations can be asymptomatic, in the form of primary HIV infection, and can also be combined with secondary diseases. The fourth stage, depending on the severity, is divided into periods: 4A, 4B, 4C. The periods go through phases of progression and remission, varying depending on the presence of antiretroviral therapy or its absence.

Symptoms of HIV infection

Incubation stage (1)– can range from 3 weeks to 3 months, in rare cases it extends to a year. At this time, the virus is actively multiplying, but there is no immune response to it yet. The incubation period of HIV ends either with the clinical manifestation of acute HIV infection or with the appearance of HIV antibodies in the blood. At this stage, the basis for diagnosing HIV infection is the detection of the virus (antigens or DNA particles) in the blood serum.

Stage of primary manifestations (2) characterized by the manifestation of the body's reaction to active replication of the virus in the form of a clinic of acute infection and an immune reaction (production of specific antibodies). The second stage can be asymptomatic; the only sign of developing HIV infection will be a positive serological diagnosis for antibodies to the virus.

Clinical manifestations of the second stage occur according to the type of acute HIV infection. The onset is acute, observed in 50-90% of patients three months after infection, often preceding the formation of HIV antibodies. An acute infection without secondary pathologies has a fairly varied course: fever, various polymorphic rashes on the skin and visible mucous membranes, polylymphadenitis, pharyngitis, linear syndrome, and diarrhea may be observed.

In 10-15% of patients, acute HIV infection occurs with the addition of secondary diseases, which is associated with a decrease in immunity. These can be tonsillitis, pneumonia of various origins, fungal infections, herpes, etc.

Acute HIV infection usually lasts from several days to several months, on average 2-3 weeks, after which in the vast majority of cases it enters a latent stage.

Latent stage (3) characterized by a gradual increase in immunodeficiency. The death of immune cells at this stage is compensated by their increased production. At this time, HIV can be diagnosed using serological tests (antibodies to HIV are present in the blood). A clinical sign may be enlargement of several lymph nodes from different, unrelated groups, excluding the inguinal lymph nodes. At the same time, no other pathological changes in the enlarged lymph nodes (pain, changes in surrounding tissues) are noted. The latent stage can last from 2-3 years to 20 or more. On average it lasts 6-7 years.

Stage of secondary diseases (4) characterized by the occurrence of concomitant (opportunistic) infections of viral, bacterial, fungal, protozoal origin, malignant tumors against the background of severe immunodeficiency. Depending on the severity of secondary diseases, 3 periods of progression are distinguished.

• 4A – loss of body weight does not exceed 10%, infectious (bacterial, viral and fungal) lesions of the integumentary tissues (skin and mucous membranes) are noted. Performance is reduced.
• 4B - weight loss of more than 10% of total body weight, prolonged temperature reaction, prolonged diarrhea without an organic cause is possible, pulmonary tuberculosis may occur, infectious diseases recur and progress, localized Kaposi's sarcoma, hairy leukoplakia are detected.
• 4B - general cachexia is noted, secondary infections acquire generalized forms, candidiasis of the esophagus, respiratory tract, Pneumocystis pneumonia, extrapulmonary tuberculosis, disseminated Kaposi's sarcoma, and neurological disorders are noted.

Substages of secondary diseases undergo phases of progression and remission, varying depending on the presence or absence of antiretroviral therapy. In the terminal stage of HIV infection, secondary diseases that have developed in the patient become irreversible, treatment measures lose their effectiveness, and death occurs several months later.

The course of HIV infection is quite diverse; all stages do not always occur; certain clinical signs may be absent. Depending on the individual clinical course, the duration of the disease can range from several months to 15-20 years.

Peculiarities of the HIV clinic in children

HIV in early childhood contributes to delayed physical and psychomotor development. Recurrence of bacterial infections in children is observed more often than in adults; lymphoid pneumonitis, enlarged pulmonary lymph nodes, various encephalopathies, and anemia are not uncommon. Common cause The leading cause of infant mortality due to HIV infections is hemorrhagic syndrome, which is a consequence of severe thrombocytopenia.

The most common clinical manifestation of HIV infection in children is a delay in the rate of psychomotor and physical development. HIV infection received by children from mothers ante- and perinatally is noticeably more severe and progresses faster, in contrast to that in children infected after one year.

Diagnostics

Currently, the main diagnostic method for HIV infection is the detection of antibodies to the virus, which is carried out primarily using the ELISA technique. In case of a positive result, the blood serum is examined using the immunoblotting technique. This makes it possible to identify antibodies to specific HIV antigens, which is a sufficient criterion for final diagnosis. Failure to detect a characteristic molecular mass using antibody blotting, however, does not exclude HIV. During the incubation period, the immune response to the introduction of the virus has not yet been formed, and in the terminal stage, as a result of severe immunodeficiency, antibodies cease to be produced.

If HIV is suspected and there are no positive immunoblotting results effective method detection of RNA virus particles is PCR. HIV infection diagnosed by serological and virological methods is an indication for dynamic monitoring of the immune status.

Treatment of HIV infection

Therapy for HIV-infected individuals involves constant monitoring of the body’s immune status, prevention and treatment of secondary infections that arise, and control over the development of tumors. Often, people living with HIV require psychological help and social adaptation. Currently, due to the significant spread and high social significance of the disease on a national and global scale, support and rehabilitation of patients is being provided, access to social programs is expanding, providing patients with medical care, facilitating the course and improving the quality of life of patients.

Today, the predominant etiotropic treatment is the prescription of drugs that reduce the reproductive abilities of the virus. Antiretroviral drugs include:

• NRTIs (nucleoside transcriptase inhibitors) of various groups: zidovudine, stavudine, zalcitabine, didanosine, abacavir, combination drugs;
• NTRTIs (nucleotide reverse transcriptase inhibitors): nevirapine, efavirenz;
• protease inhibitors: ritonavir, saquinavir, darunavir, nelfinavir and others;
• fusion inhibitors.

When deciding to start antiviral therapy, patients should remember that the drugs are used for many years, almost for life. The success of therapy directly depends on strict adherence to recommendations: timely, regular intake medicines in the required dosages, adherence to the prescribed diet and strict adherence to the regimen.

Emerging opportunistic infections are treated in accordance with the rules of effective therapy against the causative agent (antibacterial, antifungal, antiviral agents). Immunostimulating therapy is not used for HIV infection, since it contributes to its progression; cytostatics prescribed for malignant tumors suppress the immune system.

Treatment of HIV-infected people includes general strengthening and body-supporting agents (vitamins and biological active substances) and methods of physiotherapeutic prevention of secondary diseases. Patients suffering from drug addiction are recommended to undergo treatment in appropriate dispensaries. Due to significant psychological discomfort, many patients undergo long-term psychological adaptation.

Forecast

HIV infection is completely incurable; in many cases, antiviral therapy gives little effect. Today, on average, HIV-infected people live 11-12 years, but careful therapy and modern medications will significantly extend the life of patients. The main role in containing the developing AIDS is played by the psychological state of the patient and his efforts aimed at complying with the prescribed regimen.

Prevention

Currently, the World Health Organization is carrying out general preventive measures to reduce the incidence of HIV infection in four main areas:

• education on safe sexual relations, distribution of condoms, treatment of sexually transmitted diseases, promotion of a culture of sexual relations;
• control over the production of drugs from donor blood;
• managing the pregnancy of HIV-infected women, providing them with medical care and providing them with chemoprophylaxis (in the last trimester of pregnancy and during childbirth, women receive antiretroviral drugs, which are also prescribed to newborn children for the first three months of life);
• organization of psychological and social assistance and support for HIV-infected citizens, counseling.

Currently, in world practice, special attention is paid to such epidemiologically important factors in relation to the incidence of HIV infection as drug addiction, disorderly sex life. As a preventive measure, many countries provide free distribution of disposable syringes and methadone substitution therapy. As a measure to help reduce sexual illiteracy, courses on sexual hygiene are being introduced into educational programs.