UNPUNCHED
A certain number of Russians are carriers of a genetic mutation that makes them immune to the immunodeficiency virus
The analysis is not scary at all. Ilya Kofiadi, Researcher, Laboratory of Human Histocompatibility Genetics, Institute of Immunology, Federal Medical and Biological Agency of Russia, hands me a carefully sealed sterile probe. Now I will open the package and scrape the cheek with a stick - with my own hand, so that someone else's DNA does not get on the probe. Then the scientist will lower the probe into a test tube with a special reagent. You will need to wait a little. In just two hours I will find out if I am among the lucky ones. On the eve of December 1 - World AIDS Day - that would be welcome. Scientists have found that about one percent of the inhabitants of the Old World, due to genetic mutation, are immune to the immunodeficiency virus. There are other useful mutations that can postpone the development of the disease for many years even if you are infected with HIV.
Login for the virus
It was not long after AIDS emerged that people respond differently to HIV. "Scientists have found that there is an immune pattern that makes people more or less sensitive to the immunodeficiency virus," says the head of the laboratory of molecular biology at the Institute of Immunology, head of the laboratory of immunochemistry at the Institute of Virology of the Russian Academy of Medical Sciences named after D. I. Ivanovsky, member of the coordinating council of the Global Vaccine Project Eduard Karamov: - Approximately 7-10 percent of HIV carriers belong to the group of "long-lived" - they get sick with AIDS 15-18 years after infection, while usually this period is 7-8 years. There are so-called rapid progressors, of which 15-20 percent, - such AIDS symptoms appear in a year or two. " The object of particular interest of scientists was people from another group - who were repeatedly exposed to the danger of HIV infection, but never received the infection. Trying to answer the question of why they did not get sick, the researchers decided to "dig" into their DNA.
Candidate genes encoding proteins that are on the surface of lymphocytes attacked by the virus have come under suspicion. Scientists reasoned this way: in order to invade a cell, a virus must cling to a receptor protein on the cell membrane. Malfunctions with these receptors, resulting from mutations in genes, can make it difficult for the virus to enter the cell. In 1996, while examining people who were incapable of contracting HIV, American scientists discovered that the vast majority of them had a "breakdown" in the gene for the CCR5 receptor protein. This receptor is located predominantly on the surface of immune cells and is tuned to chemokine, a low molecular weight protein that activates lymphocytes and helps recruit them to the site of infection or inflammation. However, HIV uses this receptor for another purpose - in order to enter the cells of the body. Of course, a mutation in a gene encoding a protein is most often associated with some kind of defect. But it turned out that sometimes a new variant of a gene can be useful. In the case of CCR5, the loss of 32 nucleotides from the genetic chain leads to the fact that the resulting receptor protein is greatly shortened and does not appear on the cell surface, which means that the immunodeficiency virus cannot effectively use it to attack.
“Each chromosome in a person has its own pair,” says Ilya Kofiadi. “A mutation can occur simultaneously in both paired chromosomes or only in one. If the loss of 32 nucleotide bases from the CCR5 gene occurs simultaneously in both chromosomes, then carriers of such a mutation are practically immune to HIV At least among them, not a single case of infection has yet been recorded. After all, there is simply no CCR5 receptor on the cell surface in this case. " In the second case, when the corresponding mutation occurs only in one chromosome of a pair, the possibility of HIV spreading in the body is also reduced. Proteins-receptors CCR5 are absent in exactly half of the cells, which means that it is more difficult for the immunodeficiency virus to penetrate into them.
Pomors under protection
Having discovered a useful mutation, scientists immediately wanted to determine in which peoples and how often it occurs. Comparing the results of genetic analysis of people belonging to different ethnic groups, they realized that the origins of the CCR5delta32 mutation should be sought somewhere in the north of Europe, in Scandinavia. The farther from these places, the less often it appeared, and in many countries as far as possible from the named point, such as Japan or Venezuela, it did not exist at all. The Europeans turned out to be more fortunate. Carriers of the CCR5delta32 mutation in both paired chromosomes are about one percent of the inhabitants of the Old World - in principle, not so few. After all, this means that one in every hundred of them is immune to HIV. Another 18 percent of Europeans have a mutation in only one of the paired chromosomes. Nature protects them too, although not so effectively. Infection with the immunodeficiency virus may occur, but the onset of a serious illness, AIDS, will be delayed by at least two years.
Where did the inhabitants of Europe get the beneficial mutation? Scientists were divided. Someone thinks that the plague epidemic that was raging at that time gave it to the inhabitants of the Old World about seven hundred years ago. Indeed, the causative agent of this disease, Yersinia pestis, essentially uses the same receptor proteins as HIV to attack the human body. Perhaps in Europe, which was most affected by the plague, there was a selective selection of people with this CCR5 mutation. In a plague epidemic, they had a better chance of surviving. Other researchers argue with this point of view: in their opinion, the frequency of the CCR5delta32 mutation in the Bronze Age was no different from what is observed now.
One way or another, the successful mutation gradually diverged in circles from the place of its initial origin, but did not go very far from there. Until recently, it was unclear how this mutation was spread in Russia and neighboring countries, but the staff of the Institute of Immunology painted over a white spot on the map.
"Our research shows that Kazakhs, Kyrgyz, Chechens, Tuvans almost never have the CCR5delta32 mutation," says Kofiadi. We are talking about the Pomors, a small ethnic group of several thousand people living today in the Arkhangelsk region. Surprisingly, nature has perhaps the best protection on the planet against HIV for these people. According to researchers at the Institute of Immunology, as many as three percent of them are carriers of the "saving" mutation CCR5delta32 in two paired chromosomes at once, which makes them immune to the immunodeficiency virus. Another 30 percent have a mutation of this gene in one of the chromosomes and, therefore, are much less susceptible to the disease.
Russian scientists have investigated two other "good" mutations that help withstand the formidable disease. Previously, they were found in the so-called long-lived: people who became infected with the immunodeficiency virus, but for decades did not show signs of developing -AIDS. “About a dozen of such genetic mutations have already been studied in the world,” says Eduard Karamov. “However, until now it was not clear how they were widespread in Russia.” The staff of the Institute of Immunology drew attention to two of them. The first is located in the region of the SDF1 gene, which encodes the amount of production of a ligand molecule that binds to the receptors of immune cells during the body's immune response. The "work" of SDF1 is noticeable at advanced stages of infection, when a large amount of immunodeficiency virus is already circulating in the human blood. The "breakdown" of a gene, which is expressed in the increased production of a ligand molecule, in this case is able to put a natural barrier on the path of the disease. "After all, if too many SDF1 molecules appear, they bind to receptors on the surface of lymphocytes, leaving no way for HIV to enter cells," says Ilya Kofiadi. "Deprived of loopholes, the virus remains out of work." The second mutation CCR2-641, associated with the "breakdown" of another gene encoding a receptor protein on the surface of lymphocytes, remains mysterious so far. Scientists were able to find it in the "long-lived". However, how it is able to slow down the onset of AIDS, no one knows yet.
According to most researchers, both mutations are significantly older than CCR5delta32, so there are probably several starting points for them. “It is not known for certain how human migrations can be associated with their spread,” says Ilya Kofiadi. “But certain waves of these genes in the human population can still be traced. from the highest for the Central Asian region. Further its wave, gradually descending, goes to Southeast Asia. At the same time, there is an oncoming traffic - the SDF1 mutation, on the contrary, spreads from the southeast to Central Asia. " It turns out that the hordes of nomads, rushing across the expanses of Eurasia long before HIV appeared in the human population, simultaneously spread genes that could fight it ...
Happy ticket
Calculating the frequency of "useful" mutations on the territory of Russia, biologists have experienced considerable difficulties in answering the question, who are the indigenous hares. The residents of the Vologda Oblast were conventionally decided to be such. It turned out that the CCR5delta32 mutation is present in one or two paired chromosomes in about ten percent of them. It is interesting that, following the well-known phrase "scratch a Russian, you will find a Tatar", these people, in terms of the number of mutations, were exactly in the middle between the Pomors and the Tatars. "Three percent of the Pomors, thanks to the homozygous CCR5delta32 mutation, are completely protected from HIV, while the Tatars have only one percent," says Ilya Kofiadi.
Why do you need this information? First, it can be invaluable for a specific person if he undergoes an individual analysis. Nevertheless, experts do not recommend indulging in all bad news, even for those who draw a lucky ticket - they find out that they are the carrier of a successful homozygous CCR5delta32 mutation. "Until now, HIV has never been isolated from people with such a mutation in any country," says Eduard Karamov.
Without taking into account human genetics, any serious scientific research related to HIV is unlikely to be possible in the near future. For example, some experts explain the last year's failure of the Merck AIDS vaccine trials, in particular, by the fact that the cohorts of participants were not tested for genetic mutations. However, in the near future, scientists will no longer be able to make such an annoying blunder. In the United States, an ambitious scientific project is currently underway to study 300 human genes that affect the reproduction of HIV in the body. Suddenly, even genes for proteins that help muscles contract are on this list. So very soon we will all really learn about our relationship with AIDS.
This is not a beautiful fairy tale, but an amazing reality. The fact that there are people who do not become infected with this dangerous disease was proved long ago. But this is where the immunity to HIV infection comes from and why some people are not susceptible to a terrible ailment, scientists have found out quite recently.
Why don't some people get HIV?
Research on this subject was not done out of curiosity. With their help, medical specialists and scientists in the future hope to develop a vaccine or medicine for the immunodeficiency virus, which does not exist to this day. What has become known as a result of the research? People who are immune to HIV have an extremely interesting and unusual cellular composition.
It should be noted that they also have very strong immunity. So, getting inside the CD-4 cell, the virus begins to destroy or regenerate it. Whereas in people with HIV immunity, an infected "interventionist" does not cause any changes in the enzyme composition. In other words, there is no acute reaction to a virus invasion.
Scientists believe that such a feature may be genetic. At the moment, a study is being carried out to study the genetic composition of people who do not become infected with this dangerous ailment. A genome has already been developed that resists infection. He not only is not affected by the virus, but also destroys it, as if cutting it out of the body. On its basis, it is planned to produce a vaccine against the immunodeficiency virus.
How couples do not get HIV: is it about immunity?
Many people are interested in whether people who live with infected partners and do not get infected themselves are immune to HIV. In some situations, such a combination of circumstances can be assumed. Perhaps there are indeed couples in which one of the partners is immune to HIV. But basically, the infection does not occur due to the observance of safety measures by both partners. It is about the constant use of barrier contraception. High-quality condoms purchased at the pharmacy make it possible to almost completely secure sexual intercourse. The lack of oral sex, which also poses a risk of infection, also testifies to why some people do not get HIV.
Compliance with household safety measures in this matter also plays an important role. Only in this case we are talking not only about the sexual partner, but also about everyone who surrounds the infected person.
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Reviews and comments
There is such. 10 years ago I was married, he was sick with HIV. They found out by chance, when taking blood tests before the operation. Arriving for testing at the regional hospital, a young student came up to me with glee, apparently in practice, so she told me that not everyone is predisposed to this disease, about 8-9% of women, that this disease has not been fully studied. As a result, I showed a negative test result, for 5 years I took HIV tests every year, they were not found. The husband died a year later. Like this. It is quite possible that it is, there is immunity.
Under certain conditions, the HIV virus can survive outside the body for several weeks.
Survival depends on what body fluid it is in, the volume of this fluid in the body, the concentration of the virus in it, temperature, acidity, and exposure to sunlight and humidity.
Questions regarding the survival of HIV outside the body often concern people who have had contact with body fluids. Fear of accidentally transmitting HIV also drives many people crazy because of the possibility of accidental contact with spilled blood, dried blood or other body fluids, even in microscopic quantities.
It is important to keep in mind that although HIV can live outside the body for a while, no HIV infections due to contact with spilled blood, semen, or other body fluids, although many healthcare workers come into contact with HIV-infected body fluids ( it is about spills lying on the surface, and not in a needle, for example).
Nevertheless, the awareness of the possible persistence (preservation of the virus in a functionally active state) of viable HIV in body fluids requires sanitary and epidemiological control over the safety of medical procedures.
How to determine the potential risk of HIV infection?
- At first, blood, semen, vaginal fluid, or breast milk must have the HIV virus ... This is obvious, but sometimes we are afraid of where HIV is not even present. HIV does not survive in air or acidic environments, i.e. it dies in the stomach.
- Secondly, just touching the blood with HIV is not enough, the skin protects. Those. a specific route of infection is needed: intercourse, someone else's syringe, a needle, breastfeeding.
- Thirdly, there must be a “gateway” for HIV: wounds, ulcers, damage to the skin, mucous membranes.
HIV does not pass through intact skin.
- Fourth, there must be a sufficient amount of the virus in the biological fluid, human secretions. Therefore, HIV is not transmitted through saliva, urine, tears, there is an insufficient concentration of the HIV virus necessary for infection.
Even if you just touched the syringe with the remains of HIV-infected blood, you will not get infected !!!
HIV survives
HIV dies
- from the sun and UV radiation;
- from soap, alcohol, iodine, brilliant green solution (brilliant green);
- from temperatures over 60 degrees C, boiling;
- gradually in an alkaline or acidic environment: at a pH below 7 or above 8 *.
- in Pepsi-Cola, Coca-Cola, because their pH is acidic, about 3.
- gradually in seawater.
* This is why the risk of HIV infection in a healthy woman is reduced with an appropriate degree of acidity of the vaginal fluid.
Details, nuances
In syringes
- HIV can survive in syringes for up to 7 days at temperatures ranging from 27⁰C to 37⁰C.
- HIV can survive up to a month in syringes after they have collected and released HIV-infected blood.
"Survival of HIV-1 in syringes". Abdala N, Stevens P.S., Griffith B.P., Haymer R. Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, CT, 06520-8034, USA.
A study of blood collected from more than 800 syringes with blood residues and stored for different periods of time showed that HIV can be isolated from 10% of syringes after 11 days from a quantity of blood less than 2 microliters, but 53% of syringes contained 20 microliters of blood. Longer HIV survival was associated with storage at lower temperatures (less than 4 degrees C), at higher temperatures (from 27 to 37 degrees) the AIDS virus died 100% after 7 days.
"Survival of HIV-1 in syringes: effects of storage temperature." Abdala N, Reyes R., Carney JM, Haymer R. Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, CT, 06520-8034, USA:
“This study was conducted to determine the effect of storage temperature on the survival of HIV-1 inside syringes. At 40 gr. 50% of all syringes contained viable HIV-1 at 42 days storage, which is the longest proven shelf life.
At room temperature (20 degrees C), the last day the syringes with 2 μL of contaminated blood tested positive was day 21 and viable HIV-1 was removed from 8% of the syringes.
The last day the 20 μL syringes tested positive was Day 42 and viable HIV-1 was removed from 8% of the syringes.
Above room temperature (27, 32 and 37 degrees C), the likelihood of exposure to viable HIV-1 syringes when stored for more than 1 week dropped to less than 1%.
The temperature at which injecting drug users can store their used syringes will vary depending on the climate, time of year and the circumstances the drug user faces. The survival rate of HIV-1 in contaminated syringes varied across temperature ranges, and this may be a factor influencing HIV-1 transmission through syringes. ”
In blood
- At room temperature in a drop of blood, HIV feels stable and can live a week in dried blood at 4 grams. WITH.
In semen
- There have been no studies of HIV survival in semen outside the body, but in laboratory studies, very low concentration of HIV virus was detected in semen outside the body.
In corpses
- HIV can survive in organs and corpses for up to 2 weeks.
- The infectious AIDS virus was isolated from human corpses between 11 and 16 days after death, the corpses were stored at a temperature of 2 degrees. C. It is not yet clear how long HIV can survive in decaying corpses at room temperature, but HIV was isolated from organs stored at 20 ° C up to 14 days of storage after death... HIV was not found in sufficient quantities to become contaminated after 16 days of storage, indicating that such corpses are less dangerous to gravediggers and pathologists.
PH
- HIV can only survive at a pH of 7 to 8, the optimum for it is 7.1. That is why it does not survive well in snot, urine, vomit, and vomit.
In the cold
- HIV does not die from cold, the lower the temperature, the higher the probability of HIV survival.
- HIV persists at very low temperatures, when deep frozen, it is perfectly preserved, for example NS freezing the AIDS virus(HIV, HIV virus are one and the same) at minus 70 gr. the virus survived perfectly and did not lose its infectious properties.
In water
Water itself destroys HIV and rapidly reduces the infectiousness of the virus. Moore's research shows that tap water is not conducive to HIV survival and that chlorinated water deactivates the virus completely.
Survival of Human Immunodeficiency Virus (HIV), HIV-infected Lymphocytes and Poliovirus in Water. Moore B.E. Journal of Applied and Environmental Microbiology (AEM) 1993, May; 59 (5): 1437-43. Department of Microbiology, University of Texas Medical Branch, Galveston 77555-1019.
HIV loses its infectiousness within hours of being immersed in tap water.
The osmotic pressure of water disrupts the protein-lipid membrane that HIV needs to infect target cells. Chlorine and ammonia, which are present in tap water and wastewater, can act as virucides to kill HIV.
None of the studies have provided a viable, routine scenario for HIV transmission through wastewater or biowaste from wastewater treatment.
Scientists have studied the survival of HIV in faeces, sewage and biological waste by inoculating samples of the HIV virus directly into these media.
It is important to note that the collected wastewater samples contained a much higher amount of the virus than the city's wastewater collection and treatment system.
Casson et. et al. inoculated HIV in non-chlorinated secondary wastewater samples from conventional wastewater treatment plants. The seeded virus lost most of its infectivity within 48 hours. The results were similar in primary effluent samples contaminated with HIV. In one experimental set, free and cell-bound HIV, seeded in dechlorinated tap water, lost 90 percent
infectivity within two hours and 99.9 percent infectivity within eight hours.
Survival and Recovery of Selected HIV in Water and Wastewater Casson, Leonard W., Michael O. D. Ritter, Lisa M. Cossentino, and Phalguni Gupta. "Survival and Recovery of Seeded HIV in Water and Wastewater." Water Environment Research 69, no. 2 (1997): 174-79.
In another experiment, during which blood with HIV got into tap water, HIV was found to be incapable of infection. Thus, water itself is an unfavorable environment for HIV infection.
HIV has not been detected in actual untreated wastewater samples collected from the city sewage treatment plant. Palmer et al. no detectable levels of HIV were found despite studies of streams into which effluent was discharged from at least one major medical research facility. Even a large amount of contaminated blood discharged into the sewer is diluted with a much larger flow of water in the sewer system.
Also, many medical institutions disinfect
material before disposal. In any case, the fragility and dependence of HIV on the host precludes the survival of the virus in the sewer system and wastewater treatment.
However, researcher Tamez Water proved that HIV can survive in wastewater for days in LABORATORY conditions.
Survival of Human Immunodeficiency Virus in Water, Wastewater and Sea Water. Slade, J.S. & Pike, E.B. & Eglin, R.P. & Colbourne, J.S. & Kurtz, J.B .. (1989). Water Science & Technology. 21.55-59. 10.2166 / wst.1989.0078:
“Drinking water treatment serves as an effective barrier against waterborne transmission of intestinal viruses. In modern practice, a standard of less than 1 cultured enterovirus per 1000 liters of purified water is achieved. The likely susceptibility of HIV to water treatment processes was determined in the laboratory by comparing its environmental resistance to poliovirus 2, for which quantitative information already exists. HIV cultured in a human T cell line was added to samples of dechlorinated drinking water, precipitated crude wastewater, and seawater. They were incubated at 16 ° C and samples were taken for 11 days. HIV was determined by serial dilution and subculture followed by analysis of fluorescent antibodies to infected cells and by enzyme-linked immunosorbent assay for p24 antigen. Survival rates of herpes simplex virus and poliovirus type 2 were analyzed in parallel. The median time to a tenfold decrease in HIV concentration was calculated as 1.8 days in tap water, 2.9 days in wastewater, 1.6 days in seawater, and 1.3 days in tissue culture fluid controls. The 10-fold degradation of poliovirus 2 occurred after 23-30 days in wastewater, seawater, and tissue culture fluid, but there was no significant decrease in tap water after 30 days. Herpes simplex was the most sensitive virus, taking only 1.4 days to remove from wastewater. Controls in tissue culture fluid showed no significant change at 7 days. These tests show that while HIV was more resistant than herpes simplex virus when associated with organic matter found in wastewater, it was more susceptible than poliovirus, an enterovirus widely used as an indicator of the effectiveness of water treatment processes. This sensitivity makes it highly unlikely that HIV poses any threat to the disinfected water supply. "
The immune system of some patients is able to effectively resist the human immunodeficiency virus without the help of drugs, American scientists believe. According to the staff of Johns Hopkins University, the existence of this phenomenon is proved by the case history of HIV-infected spouses from the United States described by them.
It is known that in some cases, HIV infection does not lead to the destruction of the patient's immune system. Scientists disagree on the explanation of this rare phenomenon: according to one version, the ability to resist infection in such patients is due to the characteristics of their immune system, according to the other, the slow development of the disease is explained by genetic defects of the immunodeficiency virus itself.
To clarify the mechanisms behind the extraordinary resistance to HIV infection, the researchers looked to the medical history of a black couple who had been married for more than twenty years. Ten years ago, a man contracted HIV through intravenous drug injection, and soon the infection was also found in a woman.
The infected man is now at an advanced stage of the disease: he is forced to take large doses of antiretroviral drugs every day. At the same time, his wife's HIV infection is still asymptomatic: she does not need antiretroviral therapy, and the content of viral particles in her blood remains at a minimum.
Laboratory tests of samples of the virus from the spouses' blood have unequivocally confirmed that both of them were infected with the same strain of the virus. The next series of experiments showed that the immune system of patients copes with a viral infection in different ways. The woman's killer cells detected and destroyed the virus in the infected cells three times faster than the analogous cells of the man.
Mutations that reduce the ability of the immunodeficiency virus to reproduce have been found in HIV samples taken from both partners. At the same time, the weakened samples of the virus prevailed in the woman, while in the man there were significantly fewer of them. According to scientists, the selection of attenuated variants of the virus, favorable for the patient, did not play a decisive role in the development of the disease and, on the contrary, became possible due to the initially increased activity of her immune system.
According to the authors of the study, the data they obtained open up new opportunities for the developers of vaccines and drugs for the treatment of HIV infection. It is quite possible, they believe, that the mechanism of immune defense of individual virus-resistant patients in the future can be artificially simulated with the help of drugs. Research report published in
Several years ago, the HIV-resistant human genotype was described. The penetration of the virus into the immune cell is associated with its interaction with the surface receptor: the CCR5 protein. But the deletion (loss of the gene region) of CCR5-delta32 leads to the immunity of its carrier to HIV. It is believed that this mutation originated about two and a half thousand years ago and has spread over time in Europe.
Now on average 1% of Europeans are actually resistant to HIV, 10-15% of Europeans have partial resistance to HIV.
Scientists at the University of Liverpool explain this unevenness by the fact that the CCR5 mutation increases resistance to bubonic plague. Therefore, after the epidemics of the "black death" in 1347 (and in Scandinavia also in 1711), the proportion of this genotype increased.
A mutation in the CCR2 gene also reduces the chance of HIV entering the cell and leads to a delay in the development of AIDS.
There is a small percentage of people (about 10% of all HIV-positive) who have the virus in their blood, but they do not develop AIDS for a long time (so-called nonprogressors).
It was found that one of the main elements of antiviral defense in humans and other primates is the TRIM5a protein, which is capable of recognizing the capsid of viral particles and preventing the virus from multiplying in the cell. This protein in humans and other primates has differences that determine the innate resistance of chimpanzees to HIV and related viruses, and in humans - innate resistance to the PtERV1 virus.
Another important element of antiviral defense is interferon-induced transmembrane protein CD317 / BST-2 (bone marrow stromal antigen 2), also called "tetherin" for its ability to suppress the release of newly formed daughter virions by keeping them on the cell surface. It has been shown that CD317 directly interacts with mature daughter virions, "binding" them to the cell surface.
To explain the mechanism of this “binding”, models have been proposed according to which two CD317 molecules form a parallel homodimer;
one or two homodimers bind simultaneously to one virion and the cell membrane. In this case, either both membrane “anchors” (transmembrane domain and GPI) of one of the CD317 molecules, or one of them, interact with the virion membrane. The spectrum of activity of CD317 includes at least four families of viruses: retroviruses, filoviruses, arenaviruses, and herpes viruses.
CAML (calcium-modulated cyclophilin ligand) is another protein that, like CD317, inhibits the release of mature daughter virions from the cell and whose activity is inhibited by the HIV-1 Vpu protein. However, the mechanisms of action of CAML (protein localized in the endoplasmic reticulum) and Vpu antagonism are unknown.
Epidemiology
In total, about 40 million people in the world are living with HIV infection. More than two thirds of them inhabit sub-Saharan Africa. The epidemic began here in the late 1970s and early 1980s. The center is considered to be a strip stretching from West Africa to the Indian Ocean. Then HIV spread to the south. South Africa has the largest number of HIV carriers - about 5 million. But in per capita terms, this figure is higher in Botswana and Swaziland. In Swaziland, one in three adults is infected.
With the exception of countries in Africa, HIV is now spreading fastest in Central Asia and Eastern Europe. From 1999 to 2002, the number of people infected here almost tripled. These regions contained the epidemic until the late 1990s, and then the number of infected people began to increase sharply - mainly due to drug addicts.
Mechanism, ways of transmission of the virus.
The contact mechanism of transmission of the pathogen is of leading importance in the transmission of HIV. It includes the sexual (most common) and contact-blood (transfusion, parenteral and in contact with blood) transmission of the virus. Especially intensive transmission of HIV is observed during homosexual sexual intercourse, while the risk of infecting a passive homosexual is 3-4 times higher than that of an active one. There is a high probability of infection through sexual contact and through bi- and heterosexual contacts with sick (carriers), and women are infected from men more often than men from women. HIV is also transmitted through infected blood. This happens during transfusion of blood and some of its products. The virus can be transmitted by reusing infected medical equipment, including syringes and needles. Most often this occurs in drug addicts with intravenous administration of narcotic drugs with the same syringes and needles.
Another, less significant, is the vertical transmission mechanism of the pathogen, which is realized in the body of a pregnant woman when the fetus becomes infected in the uterus (transplacental pathway). It should be noted that the risk of HIV transmission to children from seropositive mothers is 15-30% (according to some sources, up to 50%), depends on the stage of the disease and increases with breastfeeding. Moreover, most often, contact infection of a child occurs during childbirth. Infection through breast milk is also possible. Cases of infection of mothers from infected infants during breastfeeding have been identified.
Transmission of HIV is practically impossible, since the pathogen does not multiply in the body of bloodsuckers. Household transmission of the virus during normal human communication has not been established. HIV is not spread through the air, drinking water and food.
There are occupational infections among healthcare workers. The risk of infection in honey. workers dealing with special manipulations associated with patient injury are 0.5-1%. These are mainly surgeons, obstetricians, and dentists.
HIV can be found in almost all body fluids. In an infected person, the virus is excreted with all biological fluids: the maximum amount is in the blood and semen. The average amount of the virus is in the lymph, cerebrospinal fluid, vaginal discharge (100-1000 virions per ml). There is even less virus in the milk of a nursing mother, in saliva, tears, sweat. The content of the virus in them is such that it is not enough to cause an infection.
Infection can occur when hazardous biofluids enter the blood or lymph flow of a person, as well as damaged mucous membranes (which is due to the absorption function of the mucous membranes). If the blood of an HIV-infected person gets into an open wound of another person from which blood flows, infection usually does not occur.
HIV is unstable - outside the body, when blood (sperm, lymph and vaginal secretions) dries up, it dies. Infection does not occur through the household route. HIV almost instantly dies at temperatures above 56 degrees Celsius.
However, with intravenous injections, the probability of transmission of the virus is very high - up to 95%. Cases of HIV transmission to medical personnel through needlesticks have been reported. To reduce the likelihood of HIV transmission (up to a fraction of a percent) in such cases, doctors prescribe a four-week course of highly active antiretroviral therapy. Chemoprophylaxis may also be given to other individuals at risk of infection. Chemotherapy is prescribed no later than 72 hours after the probable penetration of the virus.
The repeated use of syringes and needles by drug users is highly likely to lead to the transmission of HIV. To prevent this, special charity points are being set up where drug users can get clean syringes free of charge in exchange for used ones. In addition, young drug users are almost always sexually active and prone to unprotected sex, which creates additional preconditions for the spread of the virus.
Data on HIV transmission through unprotected sex vary widely from one source to another. The risk of transmission is highly dependent on the type of contact (vaginal, anal, oral, etc.) and the role of the partner.
HIV infection in Russia
The first case of HIV infection in the USSR was discovered in 1986. From this moment, the so-called period of the inception of the epidemic begins. The first cases of HIV infection among citizens of the USSR, as a rule, occurred as a result of unprotected sex with African students in the late 1970s. Further epidemiological measures to study the prevalence of HIV infection in various groups living on the territory of the USSR showed that the highest percentage of infection at that time fell on students from African countries, in particular from Ethiopia. The collapse of the USSR led to the collapse of the unified epidemiological service of the USSR, but not the unified epidemiological space. The brief outbreak of HIV infection in the early 1990s among men who have sex with men did not spread further. In general, this period of the epidemic was distinguished by an extremely low level of infection (for the entire USSR, less than 1000 detected cases) of the population, short epidemic chains from infectious to infected, sporadic transmission of HIV infection and, as a result, a wide genetic diversity of detected viruses. At that time, in Western countries, the epidemic was already a significant cause of death in the age group from 20 to 40 years old.
This favorable epidemic situation led to complacency in some of the now independent countries of the former USSR, which was expressed, among other things, in the curtailment of some broad anti-epidemic programs, as inappropriate and extremely expensive. All this led to the fact that in 1993-1995 the epidemiological service of Ukraine was unable to localize in time two outbreaks of HIV infection that occurred among injecting drug users (IDUs) in Nikolaev and Odessa. As it turned out later, these outbreaks were independently caused by different viruses belonging to different subtypes of HIV-1. Moreover, the movement of HIV-infected prisoners from Odessa to Donetsk, where they were released, only contributed to the spread of HIV infection. The marginalization of IDUs and the reluctance of the authorities to carry out any effective preventive measures among them greatly contributed to the spread of HIV infection. In just two years (1994-95), several thousand HIV-infected were identified in Odessa and Nikolaev, in 90% of cases - IDUs. From this moment on the territory of the former USSR, the next stage of the HIV epidemic begins, the so-called concentrated stage, which continues to the present day. This stage is characterized by a level of HIV infection of 5 percent or more in a certain risk group (in the case of Ukraine and Russia, these are IDUs). In 1995, there was an outbreak of HIV infection among IDUs in Kaliningrad, then successively in Moscow and St. Petersburg, then outbreaks among IDUs followed one after another throughout Russia in the direction from west to east. The direction of movement of the concentrated epidemic and molecular epidemiological analysis showed that 95% of all studied HIV cases in Russia originate from the initial outbreaks in Nikolaev and Odessa. In general, this stage of HIV infection is characterized by the concentration of HIV infection among IDUs, low genetic diversity of the virus, and a gradual transition of the epidemic from the risk group to other populations.
By the end of 2006, about 370,000 HIV-positive people were officially registered in the Russian Federation. However, the real number of carriers of the infection, according to estimates at the end of 2005, is ~ 940,000. The prevalence of HIV infection among adults has reached a value of ~ 1.1%. Approximately 16,000 people have died from diseases related to HIV and AIDS, including 208 children.
About 60% of HIV cases among Russians occur in 11 out of 86 Russian regions (Irkutsk, Saratov regions, Kaliningrad, Leningrad, Moscow, Orenburg, Samara, Sverdlovsk and Ulyanovsk regions, St. Petersburg and Khanty-Mansiysk Autonomous Okrug).
Prevention of HIV infection:
Unfortunately, to date, no effective vaccine against HIV has been developed, although in many countries there is now extensive research in this area, which has high hopes.
Immunization against HIV poses particular challenges. In addition, the strong variability of the virus interferes. It is mainly due to the accumulation of mutations. It is impossible to exclude the role of genetic recombinations - the exchange of genes between different variants of HIV and other viruses, which are often found in the body affected by AIDS, as well as between HIV genes and the patient's cellular genes. So far, all attempts at immunization against the virus have used a purified or cloned envelope glycoprotein. In experimental animals, it actually causes the formation of neutralizing antibodies to the virus, but only to the strain that was used for immunization. Sometimes neutralizing antibodies are produced that act against several strains, but their titers are usually very low. Moreover, it is still not known exactly which component of the virus the neutralizing antibodies are directed against. Nevertheless, the envelope of the virus retains its attractiveness as an antigen for immunization, since the process of binding to the CD4 molecule turned out to be common for all strains studied to date, and this indicates the possibility of the presence of common epitopes in their envelopes. Probably, neutralizing antibodies to these conserved regions can be obtained using antibodies to CD4 as antigen (anti-idiotypic method).
The results of experiments with animals suggest that it is important not only which component of the virus is used for vaccination, but also how the vaccine is “offered” to the immune system. It has been shown that viral antigens included in “iskoms” - immunostimulating complexes, can be very effective as a vaccine.
In addition, adequate evaluation of vaccines is difficult, since no species other than humans is known yet in whom HIV causes AIDS-like diseases (although short-term infection is possible in some primates).
Therefore, the effectiveness of vaccines can only be tested in volunteers. Similar tests are already underway in some countries. However, how long will it take to get the results of vaccine efficacy studies if the latency period in AIDS lasts for many years? This is only one of the difficulties.
And yet, some prospects have already emerged. Genetic engineering methods of creating a vaccine against HIV are being studied: the gene of one of the HIV proteins is inserted into the genetic apparatus of the vaccinia virus. Of interest is the work carried out at the Institute of Immunology of the Ministry of Health of Russia. The method is based on the use of synthetic immunogens that stimulate B-lymphocytes, bypassing T-cell control.
WHO identifies 4 main areas of activity aimed at combating the HIV epidemic and its consequences:
1. Prevention of sexual transmission of HIV, including such elements as teaching safe sexual behavior, distributing condoms, treating other STDs, teaching behavior aimed at deliberately treating these diseases;
2. Prevention of bloodborne transmission of HIV through the provision of safe blood-derived drugs.
3. Prevention of perinatal transmission of HIV by disseminating information on the prevention of HIV transmission through the provision of medical care, including counseling for women infected with HIV and chemoprophylaxis;
4. Organization of medical care and social support for HIV-infected patients, their families and others.
