A few years ago, a human genotype resistant to HIV 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 a gene section) of CCR5-delta32 leads to the immunity of its carrier to HIV. It is assumed that this mutation arose about two and a half thousand years ago and eventually spread to 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 Black Death epidemics of 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 delays the development of AIDS.

There is a small percentage of people (about 10% of all HIV-positive people) who have the virus in their blood, but do not develop AIDS for a long time (the so-called non-progressors).

It was found that one of the main elements of the antiviral defense of humans and other primates is the TRIM5a protein, which is able to recognize the capsid of viral particles and prevent the virus from multiplying in the cell. This protein in humans and other primates has differences that cause the innate resistance of chimpanzees to HIV and related viruses, and in humans - innate resistance to the PtERV1 virus.

Another important element of antiviral protection is the 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 retaining them on the cell surface. It has been shown that CD317 directly interacts with mature progeny virions, “binding” them to the cell surface.

To explain the mechanism of such "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 herpesviruses.

CAML (calcium-modulated cyclophilin ligand) is another protein that, like CD317, inhibits the release of mature progeny virions from the cell and is suppressed by the HIV-1 Vpu protein. However, the mechanisms of action of CAML (the protein is 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 live in 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 south. Most of the HIV carriers in South Africa - about 5 million. But on a per capita basis, the figure is higher in Botswana and Swaziland. In Swaziland, one in three adults is infected.

With the exception of countries in Africa, HIV is spreading fastest today 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 plays a leading role in the transmission of HIV. It includes the sexual (most common) and contact-blood (transfusion, parenteral and contact with blood) routes of transmission of the virus. Especially intense transmission of HIV is observed during homosexual sexual intercourse, while the risk of infection of a passive homosexual is 3-4 times greater than that of an active one. There is a high probability of infection through sexual contact and through bi- and heterosexual contacts with patients (carriers), and infection of women from men occurs somewhat more often than men from women. HIV is also transmitted through infected blood. This occurs during the transfusion of blood and some of its preparations. The virus can be transmitted through the reuse of contaminated 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 mechanism of transmission of the pathogen, which is realized in the body of a pregnant woman when the fetus becomes infected in the uterus (transplacental route). 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. In this case, the most common contact infection of the child occurs during childbirth. Infection through breast milk is also possible. Cases of infection of mothers from infected infants during breastfeeding have been identified.

Transmissible 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 contact has not been established. HIV is not transmitted through air, drinking water or food.

There are occupational infections among medical workers. The risk of infection in honey. workers dealing with special manipulations associated with patient injury account for 0.5-1%. Mostly they are surgeons, obstetricians, 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 of it is in the blood and seminal fluid. The average amount of virus is in the lymph, cerebrospinal fluid, vaginal discharge (100-1000 virions per 1 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 bioliquids enter directly into the blood or lymph flow of a person, as well as onto damaged mucous membranes (which is due to the suction function of the mucous membranes). If the blood of an HIV-infected person comes into contact with an open wound of another person, from which blood flows, infection usually does not occur.

HIV is unstable - outside the body when the blood (sperm, lymph and vaginal secretions) dries up, it dies. Domestic infection does not occur. HIV almost instantly dies at temperatures above 56 degrees Celsius.

However, with intravenous injections, the probability of transmitting the virus is very high - up to 95%. Cases of transmission of HIV to medical staff through needle sticks have been reported. To reduce the likelihood of HIV transmission (to fractions of a percent) in such cases, doctors are prescribed 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 entry of the virus.

The repeated use of syringes and needles by drug users is highly likely to lead to HIV transmission. To prevent this, special charitable points are being set up where drug users can get clean syringes for free in exchange for used ones. In addition, young drug users are almost always sexually active and prone to unprotected sex, which creates additional prerequisites for the spread of the virus.

Data on HIV transmission through unprotected sexual contact vary greatly from source to source. The risk of transmission largely depends on the type of contact (vaginal, anal, oral, etc.) and the role of the partner.

HIV infection in Russia

First case HIV infection was discovered in the USSR in 1986. From this moment begins the so-called period of the emergence of the epidemic. The first cases of HIV infection among citizens of the USSR, as a rule, occurred as a result of unprotected sexual contacts with African students in the late 70s of the XX century. 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 was among 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. A 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 infecting to infected, sporadic introductions 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.

This prosperous epidemic situation led to complacency in some now independent countries of the former USSR, which was expressed, among other things, in the curtailment of some broad anti-epidemic programs, as inappropriate for the moment and extremely expensive. All this led to the fact that in 1993-95 the epidemiological service of Ukraine was unable to timely localize 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 transfer of HIV-positive prisoners from Odessa to Donetsk, where they were released, only contributed to the spread of HIV infection. The marginalization of IDUs and the unwillingness of the authorities to carry out any effective preventive measures among them greatly contributed to the spread of HIV infection. In only two years (1994-95) in Odessa and Nikolaev, several thousand HIV-infected people were identified, 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. This stage is characterized by the level of HIV infection of 5 percent or more in a certain risk group (in the case of Ukraine and Russia, this is 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 the concentrated epidemic and molecular epidemiological analysis have shown that 95% of all studied cases of HIV infection in Russia have their origin in the initial outbreaks in Nikolaev and Odessa. In general, this stage of HIV infection is characterized by the concentration of HIV infection among IDUs, the low genetic diversity of the virus, and the gradual transition of the epidemic from the risk group to other populations.

By the end of 2006 in Russian Federation about 370,000 HIV-infected people were officially registered. However, the actual number of carriers of the infection, estimated at the end of 2005, is ~940,000. Adult HIV prevalence has reached ~1.1%. Approximately 16,000 people have died from HIV and AIDS-related illnesses, including 208 children.

About 60% of cases of HIV infection 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 the Khanty-Mansi Autonomous Okrug).

Prevention of HIV infection:

Unfortunately, no effective vaccine against HIV has been developed to date, although many countries are now conducting thorough research in this area, on which great hopes are placed.

Immunization against HIV presents 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 options HIV and other viruses that are often found in the body affected by AIDS, as well as between the HIV genes and the cellular genes of the patient. So far, all attempts at immunization against the virus have used purified or cloned envelope glycoprotein. In experimental animals, it does cause 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 on several strains, but their titer is usually very low. Moreover, it is still not known exactly which component of the virus neutralizing antibodies are directed against. Nevertheless, the virus envelope 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 of the components of the virus is used for vaccination, but also in what way the vaccine is “offered” to the immune system. It has been shown that viral antigens included in “iscoms” - immunostimulating complexes can be very effective as a vaccine.

In addition, an adequate evaluation of vaccines is difficult because no species other than humans is yet known to cause HIV-like illnesses (although short-term infection is possible in some primates).

Therefore, the effectiveness of vaccines can only be tested on volunteers. Similar tests are already underway in some countries. However, how long will it take to see the results of a vaccine efficacy study if the latent period in AIDS lasts for many years? This is just one of the difficulties.

And yet, some prospects have already emerged. Genetic engineering methods for creating a vaccine against HIV are being studied: a gene for 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 allow stimulating 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 behaviors aimed at the conscious treatment of these diseases;

2. Prevention of HIV transmission through blood through the supply of safe preparations prepared from blood.

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.

ALL PHOTOS

Every tenth European can not be afraid of AIDS. These people are naturally immune to HIV. The answer to the question why the genetic mutation that gives such protection is more common in Europe than on other continents now seems to be found by biologists from the University of Liverpool: the fact is that this mutation probably also protected from the plague, writes Süddeutsche Zeitung (translation at Inopressa.ru).

Therefore, frequent plague epidemics in the Middle Ages provided a natural selection of people with a mutation. After all, the plague led to inevitable death if a person did not have this mutation, says study leader Christopher Dunken.

It has long been known that a mutation in the CCR5 protein prevents HIV from entering immune cells. British scientists conducted a simulation of the spread of a mutation on a computer and traced it back to its origins. According to their calculations, the mutation could have first appeared more than 2,500 years ago, for example, in one of the inhabitants of Mesopotamia, who thereby received immunity from the first documented plague epidemics. After that, during sporadic epidemics, his descendants had best odds survival, and thus the mutation spread until the 14th century, when it became a defense against the "black death" for one in 20,000 Europeans.

This major epidemic again gave impetus to the spread of mutation. In large cities, where the plague has always raged the most, the CCR5 mutation eventually began to occur in more than 10% of people, British researchers report. They see confirmation of their data primarily in the fact that within Europe the genetic mutation is distributed very differently: about 14% of all Russians and Finns have it, but only 4% of Sardinians.

As shown by the results of historical and computer analysis, the plague raged much longer in Northern Europe than in the Mediterranean.

Scientists have previously suggested a link between the plague and a mutation in the CCR5 protein. However, confirmation could not be found.

The work of Liverpool researchers was based on a new approach to the consideration of medieval plague epidemics. According to this approach, most of the victims of these epidemics did not die from the bubonic plague caused by the bacterium Yersinia pestis, as was often believed before. Rather, they fell victim to a virus that died out over time, the British say.

It, like the Ebola virus, caused hemorrhagic fever. This point of view is shared by other researchers, who found almost no indications of bubonic plague in the historical descriptions of the Black Death. After all, the CCR5 mutation does not protect against bacteria at all, but it does protect against viruses, the newspaper writes.

Smallpox, as a variant of the cause of the spread of the CCR5 mutation, most likely disappears. A year ago, researchers at the University of California at Berkeley suggested the possibility of such a connection. However, strong smallpox epidemics in Europe were only in the period from 1700 to 1830.

“But it takes at least 600 years of epidemics for the mutation to be in more than 10% of people,” Dunken said.

So, it is possible that the "black death", which rampaged for so many years, still left something good behind, the publication concludes.

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 they described.

It is known that in some cases HIV infection does not lead to destruction immune system patient. Scientists differ in explaining 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 another, the slow development of the disease is explained by genetic defects of the immunodeficiency virus itself.

To elucidate the mechanisms of extraordinary resistance to HIV infection, the scientists turned 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 use, and soon the infection was discovered in a woman.

Now the infected man is at a late stage of the disease: every day he is forced to take large doses of antiretroviral drugs. At the same time, his wife's HIV infection is still asymptomatic: she does not require antiretroviral therapy, and the content of viral particles in her blood remains at a minimum level.

Laboratory studies of virus samples from the blood of the spouses 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 infected cells three times faster than those 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, attenuated samples of the virus prevailed in the woman, while they were significantly less in the man. According to scientists, the selection of weakened variants of the virus that was 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 opens up new opportunities for developers of vaccines and drugs for the treatment of HIV infection. It is possible, they believe, that the mechanism of immune defense of individual patients resistant to the virus in the future can be artificially modeled with the help of drugs. Research report published in

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 has been proven long ago. But this is where immunity to HIV infection comes from and why some people are not susceptible to a terrible disease, 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 professionals and scientists in the future hope to develop a vaccine or cure for the immunodeficiency virus, which still does not exist. What became known as a result of research? People with immunity to HIV have an extremely interesting and unusual cellular composition.

It is worth noting 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 immunity against HIV, the infected "intervention" does not cause any changes in the enzyme composition. In other words, there is no acute reaction to the invasion of the virus.

Scientists believe that this 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 disease. A genome has already been bred that resists infection. It is not only not affected by the virus, but also destroys it, as if cutting it out of the body. Based on it, they plan to produce a vaccine against the immunodeficiency virus.

How not to become infected with HIV in couples: is it immunity?

Many people wonder if there is immunity to HIV in people who live with infected partners and do not become infected themselves. In some situations, such a combination of circumstances can be assumed. Perhaps there really are couples in which one of the partners is immune to HIV. But basically, infection does not occur due to the observance of security measures by both partners. We are talking about the constant use of barrier contraception. High-quality condoms purchased at a pharmacy can almost completely secure sexual contact. Another reason why some people don't get HIV is the lack of oral sex, which also poses a risk for infection.

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.

Chances of HIV transmission in different settings
It is possible to transmit a dangerous infection that can cause destruction of the body's immune system from a virus carrier to a healthy person through blood, semen and vaginal lubrication. However, the probability is not ... Effective remedies for the treatment of papillomas.
The papillomavirus causes uncontrolled single or multiple growths of the upper layer of the epidermis, which do not differ in color from the skin and are attached to it with a leg....

Reviews and comments

There is such a thing. She was married 10 years ago, he was sick with HIV. We found out by chance, during the delivery of blood tests before the operation. Arriving at the regional hospital for tests, a young student came up to me crying, apparently she was 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 studied to the end. As a result, I showed a negative result of the analysis, for 5 years I tested for HIV every year, they were not found. The husband died a year later. Like this. It is quite possible that it is, there is immunity.

HIV resistant

Any infection at different people proceeds differently. The course of a disease in a particular person is determined by a number of factors: the general condition of the body and previous diseases, the type of microorganism that entered the body, the characteristics of the patient's genotype, the presence of concomitant infections, etc. For most diseases, the statistics of typical symptoms and the timing of their course does not include cases when the disease has passed "mildly" or is generally asymptomatic. And although such situations usually fall out of the medical field, they are of particular interest, because they can point to unknown mechanisms of protection against infections. In this sense, the infamous AIDS, which today is considered an incurable disease, is no exception.

Almost from the very beginning of the HIV epidemic, rare cases have been noted when a person turned out to be completely resistant to the virus or the carriage of the virus did not pass into the stage of AIDS. Studies have shown that the surface lymphocytic protein CCR5 is “to blame” for this, or rather, its absence in some people.

The fact is that when the HIV virus enters the body, it seeks to penetrate into lymphocytes - the most important immune blood cells involved in protecting the body from infections. To be able to enter a lymphocyte, the envelope protein on the surface of the virus must bind to two cellular protein receptors on the surface of lymphocytes, one of which is the CCR5 protein (Deng et al., 1996). It turned out that some people are carriers of a mutation that prevents the synthesis of CCR5 and, accordingly, their lymphocytes are resistant to infection by most HIV variants.

There may be other mechanisms of resistance to HIV that we simply do not know about. For example, a team of French scientists working with a group of 1700 HIV-infected people recently published the results of a study of two unusual cases of resistance to infection that were not associated with the absence of the CCR5 protein (Colson et al., 2014). In the first case, the patient was diagnosed as early as 1985, but although he did not take any antiviral drugs, standard tests indicated complete elimination of the virus. Neither in the blood nor in the blood cell culture of this person were traces of the presence of a "live" virus.

Of course, the first question that arose was – was the patient really infected, or did the researchers encounter a rare diagnostic error? However, additional tests showed that the fact of infection had taken place: antibodies to HIV and individual fragments of viral proteins were found in his blood, as well as negligible amounts of viral DNA, which could only be determined using highly sensitive methods.

The researchers tried to infect lymphocytes taken from this patient with a "laboratory" variant of HIV. However, this attempt failed, unlike control lymphocytes taken from other patients. This time, the researchers accurately established that the CCR5 protein is present on the lymphocytes of an unusual patient, and realized that they are dealing with a new mechanism for blocking the replication of the HIV genome.

* Codon - a unit of the genetic code, which is a triple of nucleotide residues in DNA or RNA that codes for one amino acid

A possible clue to the explanation of this phenomenon was found in the small amounts of viral DNA that were still able to be isolated from the patient's blood. An analysis of their nucleotide sequence showed that this viral genome is simply crammed with mutations. About a quarter of the codons * encoding the amino acid tryptophan turned out to be mutated, which as a result turned into stop codons that stop protein synthesis.

In fact, the immune defense mechanisms that could inactivate the virus in this way are already known. HIV refers to viruses with an RNA genome, and in order to multiply, it must go through the reverse transcription stage, i.e. RNA must turn into DNA. A group of cellular proteins from the APOBEC3G family can “intercept” the viral genome at this stage. They “tear off” the amino group (–NH 2) from cytosine nucleotides, turning them into uracil ones. As a result, instead of complementary pairs of nucleotides "cytosine-guanine", pairs "uracil-adenine" appear in the genome. And since two guanines enter the tryptophan codon, replacing them with adenine turns the tryptophan codon into a stop codon (Sheehy et al., 2002).

Usually HIV manages to bypass this level of protection: it has a special protein that attacks and destroys APOBEC3G. But for some reason this did not happen this time, and the entire viable virus was mutated to a state of complete loss of functionality.

Assuming that this case may not be isolated, the researchers began to search among their 1500 patients with a similar history. And found! This person also failed to detect DNA or RNA viruses using standard methods. The tiny fragments of viral DNA that were found in his blood also contained a large number of mutations similar to those found in the first case. However, the lymphocytes of the second patient turned out to be unstable to infection with the “laboratory” version of HIV, so it is possible that he has a different mechanism of resistance to the virus.

A promising direction of this work is the further study of the mechanisms of resistance of lymphocytes of the first patient in experiments on infection with a "laboratory" strain of the virus. This person is thought to have a rare variant of the APOBEC3G gene that HIV cannot bypass. But although this would be an interesting find, such a discovery, most likely, will not be widely practical application, since only its carriers can benefit from such a mutation. However, the hope remains that the study will uncover some hitherto unknown immune defense mechanisms, which will give impetus to the development of new drugs or methods to prevent HIV infection.

The authors of this work also put forward a hypothesis that virus "fragments" in the form of short proteins, formed as a result of early stoppage, may play a role in protecting cells from re-infection with HIV. protein synthesis on new stop codons. These proteins can perform a protective function either, for example, by competing with some proteins necessary for the virus, or by stimulating the immune system in some special way. It has even been suggested that the observed phenomenon of the formation of viral resistance is a natural process of HIV endogenization, i.e., an evolutionary process, as a result of which the viral nucleic acid becomes part of the genome of another species (in this case, a human).

This assumption is not so fantastic: our genomes are full of "traces" of ancient infections - infections with retroviruses that can integrate their hereditary material into our DNA. After all, if not a pathogenic, but an inactivated virus is inserted into the carrier's genome, which also provides protection against re-infection, then it has a much greater chance of spreading in the population. And if we start a large-scale search for people who carry a virus with a large number of inactivating mutations, then we will have a chance to observe HIV endogenization in real time.

Literature.
Colson P., Ravaux I., Tamalet C., et al. HIV infection enroute to endogenization: two cases. // Clin. Microbiol Infect. 2014. V. 20. N. 12. P. 1280-1288.
Sheehy A. M, Gaddis N. C., Choi J. D., and Malim M. H. Isolation of a human gene that inhibits HIV-1 infection and is suppressed by the viral Vif protein. // Nature. 2002. V. 418. P. 646-650. DOI: 10.1038/nature00939.
Deng H., Liu R., Ellmeier W., et al. Identification of a major co-receptor for primary isolates of HIV-1. Nature. 1996. V. 381. P. 661-666.