Subtypes of HIV

Last updated

Human immunodeficiency viruses
HIV-SIV-phylogenetic-tree straight.svg
Phylogenetic tree of the SIV and HIVs
Scientific classification OOjs UI icon edit-ltr.svg
(unranked): Virus
Realm: Riboviria
Kingdom: Pararnavirae
Phylum: Artverviricota
Class: Revtraviricetes
Order: Ortervirales
Family: Retroviridae
Subfamily: Orthoretrovirinae
Genus: Lentivirus
Groups included
Cladistically included but traditionally excluded taxa

The subtypes of HIV include two main subtypes, known as HIV type 1 (HIV-1) and HIV type 2 (HIV-2). These subtypes have distinct genetic differences and are associated with different epidemiological patterns and clinical characteristics.

Contents

HIV-1 exhibits a genetic relation to viruses indigenous to chimpanzees and gorillas that inhabit West Africa, while HIV-2 viruses are affiliated with viruses present in the sooty mangabey, a vulnerable West African primate. [2]

HIV-1 viruses can be further stratified into groups M, N, O, and P. Among these, HIV-1 group M viruses are the most prevalent, infecting nearly 90% of people living with HIV and are responsible for the global AIDS pandemic. Group M can be further subdivided into subtypes based on genetic sequence data. Certain subtypes are known for their increased virulence or drug resistance to different medications used to treat HIV.

HIV-2 viruses are generally considered to be less virulent and less transmissible than HIV-1 M group viruses, although HIV-2 is also known to still cause AIDS.

One of the prevailing challenges in the pursuit of effective management of HIV is the virus's pronounced genetic variability and rapid viral evolution. [3]

Major types

HIV-1

HIV-1 is the most common and most pathogenic strain of the virus. As of 2022, approximately 1.3 million such infections occur annually. [4] [5] Scientists divide HIV-1 into a major group (group M) and two or more minor groups, namely groups N, O and possibly a group P. Each group is believed to represent an independent transmission of simian immunodeficiency virus (SIV) into humans, excluding subtypes within a specific group. [2] The complete genome sequence of HIV-1 contains a total of 39 open reading frames (ORFs) across all six possible reading frames (RFs), but only a few of them are functional. [6]

Group M

With 'M' for "major", this is by far the most common type of HIV, with more than 90% of HIV/AIDS cases caused by infection with HIV-1 group M viruses. This major HIV, which was the source of pre-1960 pandemic viruses, originated in the 1920s in Léopoldville, the Belgian Congo, today known as Kinshasa, which is now the capital of the Democratic Republic of Congo (DRC). [7] Its zoonotic origin is the SIVcpz strain, which infects chimpanzees. The M group is subdivided further into clades, called subtypes, that are also given a letter. There are also "circulating recombinant forms" or CRFs derived from genetic recombination between viruses of different subtypes which are in addition each given a number. CRF12_BF, for example, is a recombination between subtypes B and F.[ citation needed ]

  • Subtype A is common in West and Central Africa. [8] [ failed verification ]
  • Subtype B is the dominant form in Europe, the Americas, Japan, and Australia. [9] In addition, subtype B is the most common form in the Middle East and North Africa. [10] It may have been exported from Africa when Haitian professionals visited Kinshasa in the 1960s and brought it to Haiti in 1964. [7]
  • Subtype C is the dominant form in Southern Africa, Eastern Africa, India, Nepal, and parts of China. [9]
  • Subtype D is generally only seen in Eastern and Central Africa. [9]
  • Subtype E was originally used to describe a strain that is now accounted for as the combined strain CRF01_AE. [11] This means the original, singular, E strain has disappeared, but we know it existed, as it is visible in this combined strain form.[ citation needed ]
  • Subtype F has been found in central Africa, South America, and Eastern Europe. [12]
  • Subtype G (and the CRF02_AG) have been found in Africa and central Europe. [12]
  • Subtype H is limited to central Africa. [12]
  • Subtype I was originally used to describe a strain that is now accounted for as CRF04_cpx, with the cox for "complex" recombination of several subtypes. [11]
  • Subtype J is primarily found in North, Central, and West Africa, and the Caribbean [13]
  • Subtype K is limited to the DRC and Cameroon. [12]
  • Subtype L is limited to the DRC. [14]

The spatial movement of these subtypes moved along the railways and waterways of the DRC from Kinshasa to these other areas. [15] These subtypes are sometimes further split into sub-subtypes such as A1 and A2 or F1 and F2.[ citation needed ] In 2015, the HIV strain CRF19, a recombinant of subtype A, subtype D, and subtype G, with a subtype D protease, was found to be strongly associated with rapid progression to AIDS in Cuba. [16] This is not thought to be a complete or final list, and further types are likely to be found. [17]

HIV-1 subtype prevalence in 2002 HIV-1 subtype prevalence in 2002.png
HIV-1 subtype prevalence in 2002
Geographic distribution of HIV-1 subtypes, Circulating Recombinant Forms (CRFs), and Unique Recombinant Forms (URFs) in Africa, 2015-2020 HIV-1 subtype prevalence in Africa 2015-2020.png
Geographic distribution of HIV-1 subtypes, Circulating Recombinant Forms (CRFs), and Unique Recombinant Forms (URFs) in Africa, 2015–2020

Group N

The 'N' stands for "non-M, non-O". [19] This group was discovered by a Franco-Cameroonian team in 1998, when they identified and isolated the HIV-1 variant strain, YBF380, from a Cameroonian woman who died of AIDS in 1995. When tested, the YBF380 variant reacted with an viral envelope antigen from SIVcpz rather than with those of Group M or Group O, indicating it was indeed a novel strain of HIV-1. [20] As of 2015, fewer than 20 Group N infections have been recorded. [21]

Group O

The O ("Outlier") group has infected about 100,000 individuals located in West-Central Africa and is not usually seen outside of that area. [21] It is reportedly most common in Cameroon, where a 1997 survey found that about 2% of HIV-positive samples were from Group O. [22] Its zoonotic origin is SIVgor, which infects gorillas (rather than the more common source, SIVcpz). [23] The group caused some concern because it could not be detected by early versions of the HIV-1 test kits. More advanced HIV tests have now been developed to detect both Group O and Group N. [24]

Group P

In 2009, a newly analyzed HIV sequence was reported to have greater similarity to SIVgor, than SIVcpz. The virus had been isolated from a Cameroonian woman residing in France who was diagnosed with HIV-1 infection in 2004. The scientists reporting this sequence placed it in a proposed Group P "pending the identification of further human cases". [25] [26] [27]

HIV-2

HIV-2 is mostly found in Africa, and therefore less recognized elsewhere in the world. The first identification of HIV-2 occurred in 1985 in Senegal by microbiologist Souleymane Mboup and his collaborators. [28] The first case in the United States was in 1987. [29] The first confirmed case of HIV-2 was a Portuguese man who was treated at the London Hospital for Tropical Diseases and later died in 1987. He was believed to have been exposed to the disease in Guinea-Bissau where he lived between 1956 and 1966. His pathological diagnosis at the time was cryptosporidiosis and enterovirus infection, but an analysis of his stored serum in 1987 found that he was infected with HIV-2. [30]

Many test kits for HIV-1 will also detect HIV-2. [31]

There are eight known HIV-2 groups, designated A to H. Of these, only groups A and B are pandemic. Group A is found mainly in West Africa, but has also spread to Angola, Mozambique, Brazil, India, Europe, and the US. Despite the presence of HIV-2 globally, Group B is mainly confined to West Africa. [32] [33]

HIV-2 is closely related to SIV endemic in sooty mangabeys (Cercocebus atys atys) (SIVsmm), a monkey species inhabiting the forests of Littoral West Africa. Phylogenetic analyses show that the virus most closely related to the two strains of HIV-2 which spread considerably in humans (HIV-2 groups A and B) is the SIVsmm found in the sooty mangabeys of the Tai forest, in western Ivory Coast. [32]

There are six additional known HIV-2 groups, each having been found in just one person. They all seem to derive from independent transmissions from sooty mangabeys to humans. Groups C and D have been found in two people from Liberia, groups E and F have been discovered in two people from Sierra Leone, and groups G and H have been detected in two people from the Ivory Coast. Each of these HIV-2 strains, for which humans are probably dead-end hosts, is most closely related to SIVsmm strains from sooty mangabeys living in the same country where the human infection was found. [32] [33]

Diagnosis

HIV-2 diagnosis can be made when a patient has no symptoms but positive blood work indicating the individual has HIV. The Multispot HIV-1/HIV-2 Rapid Test is currently the only FDA approved method for such differentiation between the two viruses. Recommendations for the screening and diagnosis of HIV has always been to use enzyme immunoassays that detect HIV-1, HIV-1 group O, and HIV-2. [34] When screening the combination, if the test is positive followed by an indeterminate HIV-1 western blot, a follow-up test, such as amino acid testing, must be performed to distinguish which infection is present. [35] According to the NIH, a differential diagnosis of HIV-2 should be considered when a person is of West African descent or has had sexual contact or shared needles with such a person. West Africa is at the highest risk as it is the origin of the virus.[ citation needed ]

Treatments

HIV-2 has been found to be less pathogenic than HIV-1. [36] The mechanism of HIV-2 is not clearly defined, nor the difference from HIV-1, however the transmission rate is much lower in HIV-2 than HIV-1. Both viruses can lead to AIDS in infected individuals and both can mutate to develop drug resistance. [34] Disease monitoring in patients with HIV-2 includes clinical evaluation and CD4 cell counts, while treatment includes anti-retroviral therapy (ART), nucleoside reverse transcriptase inhibitors (NRTIs), protease inhibitors (PI), and non-nucleoside reverse transcriptase inhibitors (NNRTIs) with the addition of CCR5 co-receptor antagonists and fusion inhibitors. [37]

Choice of initial and/or second-line therapy for HIV-2 has not yet been defined. HIV-2 appears to be resistant to NNRTIs intrinsically, but may be sensitive to NRTIs, though the mechanism is poorly understood. Protease inhibitors have shown variable effect, while integrase inhibitors are also being evaluated. Combination regimens of the above listed therapies are being looked into as well, also showing variable effect depending on the types of therapies combined. While the mechanisms are not clearly understood for HIV-1 and HIV-2, it is known that they use different pathways and patterns, making the algorithms used to evaluate HIV-1 resistance-associated mutations irrelevant to HIV-2. [34]

Each virus can be contracted individually, or they can be contracted together in what is referred to as co-infection. HIV-2 seems to have lower mortality rates, less severe symptoms and slower progression to AIDS than HIV-1 alone or the co-infection. In co-infection, however, this is largely dependent on which virus was contracted first. HIV-1 tends to out compete HIV-2 for disease progression. Co-infection seems to be a growing problem globally as time progresses, with most cases being identified in West African countries, as well as some cases in the USA. [37] A study found that individuals who contract HIV-2 before HIV-1 tend to have a slower rate of disease progression, suggesting that the immune response to HIV-2 may limit the proliferation of HIV-1. [38]

Pregnancy

If a pregnant mother is exposed, screening is performed as normal. If HIV-2 is present, a number of perinatal ART drugs may be given as a prophylactic to lower the risk of mother-to-child transmission. After the child is born, a standard six-week regimen of these prophylactics should be initiated. Breast milk may also contain viral particles of HIV-2; therefore, breastfeeding is strictly advised against. [35]

Evolution

The rapid evolution of HIV can be attributed to its high mutation rate. During the early stages of mutation, evolution appears to be neutral due to the absence of an evolutionary response. However, when examining the virus in several different individuals, convergent mutations can be found appearing in these viral populations independently. [39]

HIV evolution within a host influences factors including the virus' set-point viral load. If the virus has a low set-point viral load, the host will live longer, and there is a greater probability that the virus will be transmitted to another individual. If the virus has a high set-point viral load, the host will live for a shorter amount of time and there is a lower probability that the virus will be transmitted to another individual. [40] HIV has evolved to maximize the number of infections to other hosts, and this tendency for selection to favor intermediate strains shows that HIV undergoes stabilizing selection.[ citation needed ]

The virus has also evolved to become more infectious between hosts. There are three different mechanisms that allow HIV to evolve at a population level. [40] One includes the continuous battle to evolve and overcome the immune system which slows down the evolution of HIV and shifts the virus’ focus towards a population level. Another includes the slow evolution of viral load due to viral load mutations being neutral within the host. The last mechanism focuses on the virus' preference to transmit founding viral strains stored during the early stages of infection. This preference of the virus to transmit its stored genome copies explains why HIV evolves more quickly within the host than between hosts. [40]

HIV is evolving toward a milder form, but it is still "an awfully long way" from no longer being deadly, [41] [42] with severe variants still appearing. [43] [44]

Drug resistance mutations

Isolates of HIV-1 and HIV-2 with resistance to antiretroviral drugs arise through natural selection and genetic mutations, which have been tracked and analyzed. The Stanford HIV Drug Resistance Database and the International AIDS Society publish lists of the most important of these; first year listing 80 common mutations, and the latest year 93 common mutations, and made available through the Stanford HIV RT and Protease Sequence Database.[ citation needed ]

See also

Related Research Articles

<span class="mw-page-title-main">HIV</span> Human retrovirus, cause of AIDS

The human immunodeficiency viruses (HIV) are two species of Lentivirus that infect humans. Over time, they cause acquired immunodeficiency syndrome (AIDS), a condition in which progressive failure of the immune system allows life-threatening opportunistic infections and cancers to thrive. Without treatment, the average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype.

<span class="mw-page-title-main">HIV vaccine development</span> In-progress vaccinations that may prevent or treat HIV infections

An HIV vaccine is a potential vaccine that could be either a preventive vaccine or a therapeutic vaccine, which means it would either protect individuals from being infected with HIV or treat HIV-infected individuals. It is thought that an HIV vaccine could either induce an immune response against HIV or consist of preformed antibodies against HIV.

The spread of HIV/AIDS has affected millions of people worldwide; AIDS is considered a pandemic. The World Health Organization (WHO) estimated that in 2016 there were 36.7 million people worldwide living with HIV/AIDS, with 1.8 million new HIV infections per year and 1 million deaths due to AIDS. Misconceptions about HIV and AIDS arise from several different sources, from simple ignorance and misunderstandings about scientific knowledge regarding HIV infections and the cause of AIDS to misinformation propagated by individuals and groups with ideological stances that deny a causative relationship between HIV infection and the development of AIDS. Below is a list and explanations of some common misconceptions and their rebuttals.

<i>Simian immunodeficiency virus</i> Species of retrovirus

Simian immunodeficiency virus (SIV) is a species of retrovirus that cause persistent infections in at least 45 species of non-human primates. Based on analysis of strains found in four species of monkeys from Bioko Island, which was isolated from the mainland by rising sea levels about 11,000 years ago, it has been concluded that SIV has been present in monkeys and apes for at least 32,000 years, and probably much longer.

<span class="mw-page-title-main">Feline immunodeficiency virus</span> Species of virus

Feline immunodeficiency virus (FIV) is a Lentivirus that affects cats worldwide, with 2.5% to 4.4% of felines being infected.

<i>Human polyomavirus 2</i> Species of virus

Human polyomavirus 2, commonly referred to as the JC virus or John Cunningham virus, is a type of human polyomavirus. It was identified by electron microscopy in 1965 by ZuRhein and Chou, and by Silverman and Rubinstein. It was later isolated in culture and named using the initials of a patient by the name of John Cunningham from whom it was isolated and had developed progressive multifocal leukoencephalopathy (PML). The virus causes leukoencephalopathy and other diseases only in cases of immunodeficiency, as in AIDS or during treatment with immunosuppressive drugs.

The oral polio vaccine (OPV) AIDS hypothesis is a now-discredited hypothesis that the AIDS pandemic originated from live polio vaccines prepared in chimpanzee tissue cultures, accidentally contaminated with simian immunodeficiency virus and then administered to up to one million Africans between 1957 and 1960 in experimental mass vaccination campaigns.

<span class="mw-page-title-main">CCR5</span> Immune system protein

C-C chemokine receptor type 5, also known as CCR5 or CD195, is a protein on the surface of white blood cells that is involved in the immune system as it acts as a receptor for chemokines.

<span class="mw-page-title-main">Sooty mangabey</span> Species of mammal

The sooty mangabey is an Old World monkey found in forests from Senegal in a margin along the coast down to the Ivory Coast.

<span class="mw-page-title-main">History of HIV/AIDS</span>

AIDS is caused by a human immunodeficiency virus (HIV), which originated in non-human primates in Central and West Africa. While various sub-groups of the virus acquired human infectivity at different times, the present pandemic had its origins in the emergence of one specific strain – HIV-1 subgroup M – in Léopoldville in the Belgian Congo in the 1920s.

Following infection with HIV-1, the rate of clinical disease progression varies between individuals. Factors such as host susceptibility, genetics and immune function, health care and co-infections as well as viral genetic variability may affect the rate of progression to the point of needing to take medication in order not to develop AIDS.

<span class="mw-page-title-main">Envelope glycoprotein GP120</span> Glycoprotein exposed on the surface of the HIV virus

Envelope glycoprotein GP120 is a glycoprotein exposed on the surface of the HIV envelope. It was discovered by Professors Tun-Hou Lee and Myron "Max" Essex of the Harvard School of Public Health in 1984. The 120 in its name comes from its molecular weight of 120 kDa. Gp120 is essential for virus entry into cells as it plays a vital role in attachment to specific cell surface receptors. These receptors are DC-SIGN, Heparan Sulfate Proteoglycan and a specific interaction with the CD4 receptor, particularly on helper T-cells. Binding to CD4 induces the start of a cascade of conformational changes in gp120 and gp41 that lead to the fusion of the viral membrane with the host cell membrane. Binding to CD4 is mainly electrostatic although there are van der Waals interactions and hydrogen bonds.

HIV superinfection is a condition in which a person with an established human immunodeficiency virus infection acquires a second strain of HIV, often of a different subtype. These can form a recombinant strain that co-exists with the strain from the initial infection, as well from reinfection with a new virus strain, and may cause more rapid disease progression or carry multiple resistances to certain HIV medications.

<span class="mw-page-title-main">CXCR6</span> Mammalian protein found in Homo sapiens

C-X-C chemokine receptor type 6 is a protein that in humans is encoded by the CXCR6 gene. CXCR6 has also recently been designated CD186.

Stuart C. Ray is an American physician. He is Vice Chair of Medicine for Data Integrity and Analytics, Associate Director of the Infectious Diseases Fellowship Training Program at the Johns Hopkins School of Medicine, and a Professor in the Department of Medicine, Division of Infectious Diseases. Ray also holds appointments in Viral Oncology and the Division of Health Sciences Informatics. He is affiliated with the Institute for Computational Medicine at Johns Hopkins and is licensed to practice medicine in Maryland.

Viral phylodynamics is the study of how epidemiological, immunological, and evolutionary processes act and potentially interact to shape viral phylogenies. Since the term was coined in 2004, research on viral phylodynamics has focused on transmission dynamics in an effort to shed light on how these dynamics impact viral genetic variation. Transmission dynamics can be considered at the level of cells within an infected host, individual hosts within a population, or entire populations of hosts.

Anna-Lise WilliamsonMASSAf is a Professor of Virology at the University of Cape Town. Williamson obtained her PhD from the University of the Witwatersrand in 1985. Her area of expertise is human papillomavirus, but is also known on an international level for her work in developing vaccines for HIV. These vaccines have been introduce in phase 1 of clinical trial. Williamson has published more than 120 papers.

Beatrice H. Hahn is an American virologist and biomedical researcher best known for work which established that HIV, the virus causing AIDS, began as a virus passed from apes to humans. She is a professor of Medicine and Microbiology in the Perelman School of Medicine at the University of Pennsylvania. In November 2002, Discover magazine listed Hahn as one of the 50 most important women scientists.

<span class="mw-page-title-main">Host switch</span> Evolutionary change of the host specificity of a parasite or pathogen

In parasitology and epidemiology, a host switch is an evolutionary change of the host specificity of a parasite or pathogen. For example, the human immunodeficiency virus used to infect and circulate in non-human primates in West-central Africa, but switched to humans in the early 20th century.

<span class="mw-page-title-main">Bette Korber</span> American computational biologist

Bette Korber is an American computational biologist focusing on the molecular biology and population genetics of the HIV virus that causes infection and eventually AIDS. She has contributed heavily to efforts to obtain an effective HIV vaccine. She created a database at Los Alamos National Laboratory that has enabled her to design novel mosaic HIV vaccines, one of which is currently in human testing in Africa. The database contains thousands of HIV genome sequences and related data.

References

  1. ↑ Although ICTV lists HIV-1 and HIV-2 as distinct species from SIV, they do cladistically fall into the group of SIV.
  2. 1 2 Sharp PM, Hahn BH (September 2011). "Origins of HIV and the AIDS pandemic". Cold Spring Harbor Perspectives in Medicine. 1 (1): a006841. doi:10.1101/cshperspect.a006841. PMC   3234451 . PMID   22229120.
  3. ↑ Robertson DL, Hahn BH, Sharp PM (March 1995). "Recombination in AIDS viruses". Journal of Molecular Evolution. 40 (3): 249–259. Bibcode:1995JMolE..40..249R. doi: 10.1007/BF00163230 . PMID   7723052. S2CID   19728830.
  4. ↑ Gary EN, Weiner DB (August 2020). "DNA vaccines: prime time is now". Current Opinion in Immunology. Vaccines • Special Section on Evolutionary and systems immunology. 65: 21–27. doi:10.1016/j.coi.2020.01.006. PMC   7195337 . PMID   32259744.
  5. ↑ "UNAIDS Global HIV statistics fact sheet 2023" (PDF). UNAIDS 2023 epidemiological estimates. UNAIDS. 2023. Retrieved 2023-09-19.
  6. ↑ Dhar DV, Amit P, Kumar MS (November 2012). "In-Silico Identification of New Genes in HIV-1 by ORF Prediction Method" (PDF). International Research Journal of Biological Sciences. 1 (7): 52–54.
  7. 1 2 Faria NR, Rambaut A, Suchard MA, Baele G, Bedford T, Ward MJ, et al. (October 2014). "HIV epidemiology. The early spread and epidemic ignition of HIV-1 in human populations". Science. 346 (6205): 56–61. Bibcode:2014Sci...346...56F. doi:10.1126/science.1256739. PMC   4254776 . PMID   25278604.
  8. ↑ Bobkov AF, Kazennova EV, Selimova LM, Khanina TA, Ryabov GS, Bobkova MR, et al. (October 2004). "Temporal trends in the HIV-1 epidemic in Russia: predominance of subtype A". Journal of Medical Virology. 74 (2): 191–196. doi:10.1002/jmv.20177. PMID   15332265. S2CID   33267610.
  9. 1 2 3 Goudsmit J (1997). Viral Sex; The Nature of AIDS . New York: Oxford University Press. pp.  51–58. ISBN   978-0-19-509728-3.
  10. ↑ Sallam M, Şahin GÖ, Ingman M, Widell A, Esbjörnsson J, Medstrand P (July 2017). "Genetic characterization of human immunodeficiency virus type 1 transmission in the Middle East and North Africa". Heliyon. 3 (7): e00352. Bibcode:2017Heliy...300352S. doi: 10.1016/j.heliyon.2017.e00352 . PMC   5506879 . PMID   28725873.
  11. 1 2 "Human Immunodeficiency Virus (HIV)". Transfusion Medicine and Hemotherapy. 43 (3): 203–222. May 2016. doi:10.1159/000445852. PMC   4924471 . PMID   27403093.
  12. 1 2 3 4 "Introduction to HIV types, groups and subtypes". 3 March 2008. Archived from the original on 13 September 2008. Retrieved 25 May 2008.
  13. ↑ Hemelaar J, Gouws E, Ghys PD, Osmanov S (October 2006). "Global and regional distribution of HIV-1 genetic subtypes and recombinants in 2004". AIDS. 20 (16): W13–W23. doi: 10.1097/01.aids.0000247564.73009.bc . PMID   17053344. S2CID   7354033.
  14. ↑ Weintraub K (6 November 2019). "First New HIV Strain in 19 Years Identified". Scientific American .
  15. ↑ Cohen J (October 2014). "Virology. Early AIDS virus may have ridden Africa's rails". Science. 346 (6205): 21–22. doi: 10.1126/science.346.6205.21 . PMID   25278591.
  16. ↑ Kouri V, Khouri R, Alemán Y, Abrahantes Y, Vercauteren J, Pineda-Peña AC, et al. (March 2015). "CRF19_cpx is an Evolutionary fit HIV-1 Variant Strongly Associated With Rapid Progression to AIDS in Cuba". eBioMedicine. 2 (3): 244–254. doi:10.1016/j.ebiom.2015.01.015. PMC   4484819 . PMID   26137563.
  17. ↑ "What are HIV and AIDS?". Be in the KNOW.
  18. ↑ Giovanetti M, Ciccozzi M, Parolin C, Borsetti A (December 2020). "Molecular Epidemiology of HIV-1 in African Countries: A Comprehensive Overview". Pathogens. 9 (12): 1072. doi: 10.3390/pathogens9121072 . PMC   7766877 . PMID   33371264.
  19. ↑ Tebit, Denis M.; Patel, Hamish; Ratcliff, Annette; Alessandri, Elodie; Liu, Joseph; Carpenter, Crystal; Plantier, Jean-Christophe; Arts, Eric J. (2016-07-01). "HIV-1 Group O Genotypes and Phenotypes: Relationship to Fitness and Susceptibility to Antiretroviral Drugs". AIDS Research and Human Retroviruses. 32 (7): 676–688. doi:10.1089/aid.2015.0318. ISSN   0889-2229. PMC   4931737 . PMID   26861573.
  20. ↑ Mourez T, Simon F, Plantier JC (July 2013). "Non-M variants of human immunodeficiency virus type 1". Clinical Microbiology Reviews. 26 (3): 448–461. doi:10.1128/cmr.00012-13. PMC   3719493 . PMID   23824367.
  21. 1 2 D'arc M, Ayouba A, Esteban A, Learn GH, Boué V, Liegeois F, et al. (March 2015). "Origin of the HIV-1 group O epidemic in western lowland gorillas". Proceedings of the National Academy of Sciences of the United States of America. 112 (11): E1343–E1352. Bibcode:2015PNAS..112E1343D. doi: 10.1073/pnas.1502022112 . PMC   4371950 . PMID   25733890.
  22. ↑ Peeters M, Gueye A, Mboup S, Bibollet-Ruche F, Ekaza E, Mulanga C, et al. (March 1997). "Geographical distribution of HIV-1 group O viruses in Africa". AIDS. 11 (4): 493–498. doi: 10.1097/00002030-199704000-00013 . PMID   9084797. S2CID   24238394.
  23. ↑ Van Heuverswyn F, Li Y, Neel C, Bailes E, Keele BF, Liu W, et al. (November 2006). "Human immunodeficiency viruses: SIV infection in wild gorillas". Nature. 444 (7116): 164. Bibcode:2006Natur.444..164V. doi: 10.1038/444164a . PMID   17093443. S2CID   27475571.
  24. ↑ "Abbott RealTime HIV-1 assay" (PDF). Abbott Molecular. Archived from the original (PDF) on 2007-09-21. Retrieved 2008-05-18.
  25. ↑ Plantier JC, Leoz M, Dickerson JE, De Oliveira F, Cordonnier F, Lemée V, et al. (August 2009). "A new human immunodeficiency virus derived from gorillas". Nature Medicine. 15 (8): 871–872. doi:10.1038/nm.2016. PMID   19648927. S2CID   76837833.
  26. ↑ "New HIV strain discovered". CBC News. Associated Press. 2009-08-03. Retrieved 2009-08-03.
  27. ↑ McNeil DG (September 16, 2010). "Precursor to H.I.V. Was in Monkeys for Millennia". New York Times . Retrieved 2010-09-17. But P appears to have crossed over from a gorilla; it was discovered only last year, and in only one woman, who was from Cameroon, where lowland gorillas are hunted for meat.
  28. ↑ "The Senegal Sex Workers Study". Harvard AIDS Initiative. Boston, MA: Harvard University. 2018-06-29. Retrieved 2020-06-18.
  29. ↑ "Human Immunodeficiency Virus Type 2". HIV/AIDS Workshop. Archived from the original on 18 February 2009.
  30. ↑ Bryceson A, Tomkins A, Ridley D, Warhurst D, Goldstone A, Bayliss G, et al. (July 1988). "HIV-2-associated AIDS in the 1970s". Lancet. 2 (8604): 221. doi:10.1016/s0140-6736(88)92325-2. PMID   2899693. S2CID   32378074.
  31. ↑ "Donor Screening Assays for Infectious Agents and HIV Diagnostic Assays". Center for Biologics Evaluation and Research. U.S. Food and Drug Administration. Archived from the original on 11 May 2009.
  32. 1 2 3 Santiago ML, Range F, Keele BF, Li Y, Bailes E, Bibollet-Ruche F, et al. (October 2005). "Simian immunodeficiency virus infection in free-ranging sooty mangabeys (Cercocebus atys atys) from the Taï Forest, Côte d'Ivoire: implications for the origin of epidemic human immunodeficiency virus type 2". Journal of Virology. 79 (19): 12515–12527. doi:10.1128/JVI.79.19.12515-12527.2005. PMC   1211554 . PMID   16160179.
  33. 1 2 Marx PA, Alcabes PG, Drucker E (June 2001). "Serial human passage of simian immunodeficiency virus by unsterile injections and the emergence of epidemic human immunodeficiency virus in Africa". Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences. 356 (1410): 911–920. doi:10.1098/rstb.2001.0867. PMC   1088484 . PMID   11405938.
  34. 1 2 3 "Clinical Guidelines". AidInfo. U.S. National Library of Medicine. Archived from the original on 2016-11-07. Retrieved 2014-10-24.
  35. 1 2 "Human Immunodeficiency Virus Type 2 (HIV-2)". New York State Department of Health AIDS Institute.
  36. ↑ Baltic S (11 December 2018). "HIV-2 is Deadlier Than Thought, Despite Slower Progression to AIDS". Medscape. Archived from the original on 2019-04-19. Retrieved 2018-12-28.
  37. 1 2 R Kannangai, S David, G Sridharan. "Human immunodeficiency virus type 2-A milder, kinder virus: An update". Indian Journal of Medical Micobiology, (2012) 30(1): 6–15.
  38. ↑ Nyamweya S, Hegedus A, Jaye A, Rowland-Jones S, Flanagan KL, Macallan DC (July 2013). "Comparing HIV-1 and HIV-2 infection: Lessons for viral immunopathogenesis". Reviews in Medical Virology. 23 (4): 221–40. doi:10.1002/rmv.1739. PMID   23444290. S2CID   206448956.
  39. ↑ Bons E, Bertels F, Regoes RR (July 2018). "Estimating the mutational fitness effects distribution during early HIV infection". Virus Evolution. 4 (2): vey029. doi:10.1093/ve/vey029. PMC   6172364 . PMID   30310682.
  40. 1 2 3 Fraser C, Hollingsworth TD, Chapman R, de Wolf F, Hanage WP (October 2007). "Variation in HIV-1 set-point viral load: epidemiological analysis and an evolutionary hypothesis". Proceedings of the National Academy of Sciences of the United States of America. 104 (44): 17441–17446. Bibcode:2007PNAS..10417441F. doi: 10.1073/pnas.0708559104 . PMC   2077275 . PMID   17954909.
  41. ↑ Payne R, Muenchhoff M, Mann J, Roberts HE, Matthews P, Adland E, et al. (December 2014). "Impact of HLA-driven HIV adaptation on virulence in populations of high HIV seroprevalence". Proceedings of the National Academy of Sciences of the United States of America. 111 (50): E5393–E5400. Bibcode:2014PNAS..111E5393P. doi: 10.1073/pnas.1413339111 . PMC   4273423 . PMID   25453107.
  42. ↑ Gallagher J (December 2014). "HIV evolving 'into milder form'". BBC News. Retrieved 20 July 2017.
  43. ↑ Guglielmi G (February 2022). "Highly virulent HIV variant found circulating in Europe". Nature. doi:10.1038/d41586-022-00317-x. PMID   35115695. S2CID   246530234.
  44. ↑ Wymant C, Bezemer D, Blanquart F, Ferretti L, Gall A, Hall M, et al. (February 2022). "A highly virulent variant of HIV-1 circulating in the Netherlands". Science. 375 (6580): 540–545. Bibcode:2022Sci...375..540T. doi: 10.1126/science.abk1688 . hdl: 1887/3502598 . PMID   35113714. S2CID   246530612.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.