HIV
Human immunodeficiency viruses | |
---|---|
Scanning electron micrograph of HIV-1 (in green) budding from cultured lymphocyte . Multiple round bumps on cell surface represent sites of assembly and budding of virions.
| |
Scientific classification | |
(unranked): | Virus |
Realm: | Riboviria |
Kingdom: | Pararnavirae |
Phylum: | Artverviricota |
Class: | Revtraviricetes |
Order: | Ortervirales |
Family: | Retroviridae |
Subfamily: | Orthoretrovirinae |
Genus: | Lentivirus |
Groups included | |
Other lentiviruses | |
|
The human immunodeficiency viruses (HIV) are two species of
In most cases, HIV is a sexually transmitted infection and occurs by contact with or transfer of blood, pre-ejaculate, semen, and vaginal fluids.[5][6] Non-sexual transmission can occur from an infected mother to her infant during pregnancy, during childbirth by exposure to her blood or vaginal fluid, and through breast milk.[7][8][9][10] Within these bodily fluids, HIV is present as both free virus particles and virus within infected immune cells. Research has shown (for both same-sex and opposite-sex couples) that HIV is untransmittable through condomless sexual intercourse if the HIV-positive partner has a consistently undetectable viral load.[5][6]
HIV infects vital cells in the human immune system, such as
Virology
Species | Virulence | Infectivity | Prevalence | Inferred origin |
---|---|---|---|---|
HIV-1 | High | High | Global | Common chimpanzee
|
HIV-2 | Lower | Low | West Africa | Sooty mangabey |
Classification
HIV is a member of the
Two types of HIV have been characterized: HIV-1 and HIV-2. HIV-1 is the virus that was initially discovered and termed both lymphadenopathy associated virus (LAV) and human T-lymphotropic virus 3 (HTLV-III). HIV-1 is more virulent and more infective than HIV-2,[20] and is the cause of the majority of HIV infections globally. The lower infectivity of HIV-2, compared to HIV-1, implies that fewer of those exposed to HIV-2 will be infected per exposure. Due to its relatively poor capacity for transmission, HIV-2 is largely confined to West Africa.[21]
Structure and genome
HIV is similar in structure to other retroviruses. It is roughly spherical
This is, in turn, surrounded by the
As the sole viral protein on the surface of the virus, the envelope protein is a major target for
The molecular structure of the viral spike has now been determined by
The RNA genome consists of at least seven structural landmarks (
The two
Nef also interacts with
Tropism
The term
Macrophage-tropic (M-tropic) strains of HIV-1, or non-
T-tropic strains of HIV-1, or
Dual-tropic HIV-1 strains are thought to be transitional strains of HIV-1 and thus are able to use both CCR5 and CXCR4 as co-receptors for viral entry.
The α-chemokine
that maintains infection when CD4+ T cell numbers have declined to extremely low levels.Some people are resistant to certain strains of HIV.
HIV-2 is much less pathogenic than HIV-1 and is restricted in its worldwide distribution to
Replication cycle
Entry to the cell
The HIV virion enters
Entry to the cell begins through interaction of the trimeric envelope complex (
The first step in fusion involves the high-affinity attachment of the CD4 binding domains of
After HIV has bound to the target cell, the HIV RNA and various enzymes, including reverse transcriptase, integrase, ribonuclease, and protease, are injected into the cell.[58][failed verification] During the microtubule-based transport to the nucleus, the viral single-strand RNA genome is transcribed into double-strand DNA, which is then integrated into a host chromosome.
HIV can infect
HIV-1 entry, as well as entry of many other retroviruses, has long been believed to occur exclusively at the plasma membrane. More recently, however, productive infection by
Replication and transcription
Shortly after the viral capsid enters the cell, an
The integrated viral DNA may then lie dormant, in the latent stage of HIV infection.[68] To actively produce the virus, certain cellular transcription factors need to be present, the most important of which is NF-κB (nuclear factor kappa B), which is upregulated when T cells become activated.[70] This means that those cells most likely to be targeted, entered and subsequently killed by HIV are those actively fighting infection.
During viral replication, the integrated DNA
RNA can also be processed to produce mature messenger RNAs (mRNAs). In most cases, this processing involves RNA splicing to produce mRNAs that are shorter than the full-length genome. Which part of the RNA is removed during RNA splicing determines which of the HIV protein-coding sequences is translated.[73]
Mature HIV mRNAs are exported from the nucleus into the
Recombination
Two RNA genomes are encapsidated in each HIV-1 particle (see Structure and genome of HIV). Upon infection and replication catalyzed by reverse transcriptase, recombination between the two genomes can occur.[80][81] Recombination occurs as the single-strand, positive-sense RNA genomes are reverse transcribed to form DNA. During reverse transcription, the nascent DNA can switch multiple times between the two copies of the viral RNA. This form of recombination is known as copy-choice. Recombination events may occur throughout the genome. Anywhere from two to 20 recombination events per genome may occur at each replication cycle, and these events can rapidly shuffle the genetic information that is transmitted from parental to progeny genomes.[81]
Viral recombination produces genetic variation that likely contributes to the evolution of resistance to anti-retroviral therapy.[82] Recombination may also contribute, in principle, to overcoming the immune defenses of the host. Yet, for the adaptive advantages of genetic variation to be realized, the two viral genomes packaged in individual infecting virus particles need to have arisen from separate progenitor parental viruses of differing genetic constitution. It is unknown how often such mixed packaging occurs under natural conditions.[83]
Bonhoeffer et al.[84] suggested that template switching by reverse transcriptase acts as a repair process to deal with breaks in the single-stranded RNA genome. In addition, Hu and Temin[80] suggested that recombination is an adaptation for repair of damage in the RNA genomes. Strand switching (copy-choice recombination) by reverse transcriptase could generate an undamaged copy of genomic DNA from two damaged single-stranded RNA genome copies. This view of the adaptive benefit of recombination in HIV could explain why each HIV particle contains two complete genomes, rather than one. Furthermore, the view that recombination is a repair process implies that the benefit of repair can occur at each replication cycle, and that this benefit can be realized whether or not the two genomes differ genetically. On the view that recombination in HIV is a repair process, the generation of recombinational variation would be a consequence, but not the cause of, the evolution of template switching.[84]
HIV-1 infection causes
Assembly and release
The final step of the viral cycle, assembly of new HIV-1 virions, begins at the
Spread within the body
The classical process of infection of a cell by a virion can be called "cell-free spread" to distinguish it from a more recently recognized process called "cell-to-cell spread".
Genetic variability
HIV differs from many viruses in that it has very high genetic variability. This diversity is a result of its fast replication cycle, with the generation of about 1010 virions every day, coupled with a high mutation rate of approximately 3 x 10−5 per nucleotide base per cycle of replication and recombinogenic properties of reverse transcriptase.[95][96][97]
This complex scenario leads to the generation of many variants of HIV in a single infected patient in the course of one day.
The closely related simian immunodeficiency virus (SIV) has evolved into many strains, classified by the natural host species. SIV strains of the African green monkey (SIVagm) and sooty mangabey (SIVsmm) are thought to have a long evolutionary history with their hosts. These hosts have adapted to the presence of the virus,[98] which is present at high levels in the host's blood, but evokes only a mild immune response,[99] does not cause the development of simian AIDS,[100] and does not undergo the extensive mutation and recombination typical of HIV infection in humans.[101]
In contrast, when these strains infect species that have not adapted to SIV ("heterologous" or similar hosts such as
Three groups of HIV-1 have been identified on the basis of differences in the envelope (env) region: M, N, and O.
HIV-2's closest relative is SIVsm, a strain of SIV found in sooty mangabees. Since HIV-1 is derived from SIVcpz, and HIV-2 from SIVsm, the genetic sequence of HIV-2 is only partially homologous to HIV-1 and more closely resembles that of SIVsm.[111][112]
Diagnosis
Many HIV-positive people are unaware that they are infected with the virus.[113] For example, in 2001 less than 1% of the sexually active urban population in Africa had been tested, and this proportion is even lower in rural populations.[113] Furthermore, in 2001 only 0.5% of pregnant women attending urban health facilities were counselled, tested or received their test results.[113] Again, this proportion is even lower in rural health facilities.[113] Since donors may therefore be unaware of their infection, donor blood and blood products used in medicine and medical research are routinely screened for HIV.[114]
HIV-1 testing is initially done using an
Although IFA can be used to confirm infection in these ambiguous cases, this assay is not widely used. In general, a second specimen should be collected more than a month later and retested for persons with indeterminate western blot results. Although much less commonly available, nucleic acid testing (e.g., viral RNA or proviral DNA amplification method) can also help diagnosis in certain situations.[115] In addition, a few tested specimens might provide inconclusive results because of a low quantity specimen. In these situations, a second specimen is collected and tested for HIV infection.
Modern HIV testing is extremely accurate, when the window period is taken into consideration. A single screening test is correct more than 99% of the time.[118] The chance of a false-positive result in a standard two-step testing protocol is estimated to be about 1 in 250,000 in a low risk population.[119] Testing post-exposure is recommended immediately and then at six weeks, three months, and six months.[120]
The latest recommendations of the US
- 1. HIV-1 (+) & HIV-2 (−): HIV-1 antibodies detected
- 2. HIV-1 (−) & HIV-2 (+): HIV-2 antibodies detected
- 3. HIV-1 (+) & HIV-2 (+): both HIV-1 and HIV-2 antibodies detected
- 4. HIV-1 (−) or indeterminate & HIV-2 (−): Nucleic acid test must be carried out to detect the acute infection of HIV-1 or its absence.[121]
Research
HIV/AIDS research includes all medical research that attempts to prevent, treat, or cure HIV/AIDS, as well as fundamental research about the nature of HIV as an infectious agent and AIDS as the disease caused by HIV.
Many governments and research institutions participate in HIV/AIDS research. This research includes behavioral
Treatment and transmission
The management of HIV/AIDS normally includes the use of multiple
HIV latency, and the consequent viral reservoir in CD4+ T cells, dendritic cells, as well as macrophages, is the main barrier to eradication of the virus.[19][123]
Although HIV is highly virulent, transmission does not occur through sex when an HIV-positive person has a consistently undetectable viral load (<50 copies/ml) due to anti-retroviral treatment. This was first argued by the Swiss Federal Commission for AIDS/HIV in 2008 in the Swiss Statement, though the statement was controversial at the time.[124][125] However, following multiple studies, it became clear that the chance of passing on HIV through sex is effectively zero where the HIV-positive person has a consistently undetectable viral load; this is known as U=U, "Undetectable=Untransmittable", also phrased as "can't pass it on".[126][127] The studies demonstrating U=U are: Opposites Attract,[128] PARTNER 1,[129] PARTNER 2,[5][130] (for male-male couples)[131] and HPTN052[132] (for heterosexual couples) when "the partner living with HIV had a durably suppressed viral load."[131] In these studies, couples where one partner was HIV positive and one partner was HIV negative were enrolled and regular HIV testing completed. In total from the four studies, 4097 couples were enrolled over four continents and 151,880 acts of condomless sex were reported; there were zero phylogenetically linked transmissions of HIV where the positive partner had an undetectable viral load.[133] Following this, the U=U consensus statement advocating the use of "zero risk" was signed by hundreds of individuals and organisations, including the US CDC, British HIV Association and The Lancet medical journal.[134] The importance of the final results of the PARTNER 2 study were described by the medical director of the Terrence Higgins Trust as "impossible to overstate", while lead author Alison Rodger declared that the message that "undetectable viral load makes HIV untransmittable ... can help end the HIV pandemic by preventing HIV transmission.[135] The authors summarised their findings in The Lancet as follows:[5]
Our results provide a similar level of evidence on viral suppression and HIV transmission risk for gay men to that previously generated for heterosexual couples and suggest that the risk of HIV transmission in gay couples through condomless sex when HIV viral load is suppressed is effectively zero. Our findings support the message of the U=U (undetectable equals untransmittable) campaign, and the benefits of early testing and treatment for HIV.[5]
This result is consistent with the conclusion presented by
Genital herpes (HSV-2) reactivation in those infected with the virus have an associated increase in CCR-5 enriched CD4+ T cells as well as inflammatory dendritic cells in the submucosa of the genital skin. Tropism of HIV for CCR-5 positive cells explains the two to threefold increase in HIV acquisition among persons with genital herpes. Daily antiviral (e.g. acyclovir) medication does not reduce the sub-clinical post reactivation inflammation and therefore does not confer reduced risk of HIV acquisition.[136][137]
History
Discovery
The first news story on "an exotic new disease" appeared May 18, 1981, in the gay newspaper New York Native.[138]
AIDS was first clinically observed in 1981 in the United States.
In the beginning, the CDC did not have an official name for the disease, often referring to it by way of the diseases that were associated with it, for example,
In 1983, two separate research groups led by American
Another group working contemporaneously with the Montagnier and Gallo groups was that of Jay A. Levy at the University of California, San Francisco. He independently discovered the AIDS virus in 1983 and named it the AIDS associated retrovirus (ARV).[157] This virus was very different from the virus reported by the Montagnier and Gallo groups. The ARV strains indicated, for the first time, the heterogeneity of HIV isolates and several of these remain classic examples of the AIDS virus found in the United States.[158]
Origins
Both HIV-1 and HIV-2 are believed to have originated in non-human primates in West-central Africa, and are believed to have transferred to humans (a process known as zoonosis) in the early 20th century.[159][160]
HIV-1 appears to have originated in southern
HIV-1 is thought to have jumped the species barrier on at least three separate occasions, giving rise to the three groups of the virus, M, N, and O.[164]
There is evidence that humans who participate in bushmeat activities, either as hunters or as bushmeat vendors, commonly acquire SIV.[165] However, SIV is a weak virus, and it is typically suppressed by the human immune system within weeks of infection. It is thought that several transmissions of the virus from individual to individual in quick succession are necessary to allow it enough time to mutate into HIV.[166] Furthermore, due to its relatively low person-to-person transmission rate, it can only spread throughout the population in the presence of one or more high-risk transmission channels, which are thought to have been absent in Africa prior to the 20th century.
Specific proposed high-risk transmission channels, allowing the virus to adapt to humans and spread throughout the society, depend on the proposed timing of the animal-to-human crossing. Genetic studies of the virus suggest that the most recent common ancestor of the HIV-1 M group dates back to c. 1910.
The earliest, well-documented case of HIV in a human dates back to 1959 in the Belgian Congo.[169] The virus may have been present in the United States as early as the mid- to late 1960s, as a sixteen-year-old male named Robert Rayford presented with symptoms in 1966 and died in 1969.[170]
An alternative and likely complementary hypothesis points to the widespread use of unsafe medical practices in Africa during years following World War II, such as unsterile reuse of single-use syringes during mass vaccination, antibiotic, and anti-malaria treatment campaigns.[166][171][172] Research on the timing of most recent common ancestor for HIV-1 groups M and O, as well as on HIV-2 groups A and B, indicates that SIV has given rise to transmissible HIV lineages throughout the twentieth century.[173] The dispersed timing of these transmissions to humans implies that no single external factor is needed to explain the cross-species transmission of HIV. This observation is consistent with both of the two prevailing views of the origin of the HIV epidemics, namely SIV transmission to humans during the slaughter or butchering of infected primates, and the colonial expansion of sub-Saharan African cities.[173]
See also
- Antiviral drug
- Discovery and development of HIV-protease inhibitors
- HIV/AIDS denialism
- World AIDS Day
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Further reading
- Berlier W, Bourlet T, Lawrence P, Hamzeh H, Lambert C, Genin C, Verrier B, Dieu-Nosjean MC, Pozzetto B, Delézay O (2005). "Selective sequestration of X4 isolates by human genital epithelial cells: Implication for virus tropism selection process during sexual transmission of HIV". Journal of Medical Virology. 77 (4): 465–74. S2CID 25762969.
- Joint United Nations Programme on HIV/AIDS (UNAIDS) (2011). Global HIV/AIDS Response, Epidemic update and health sector progress towards universal access (PDF). Joint United Nations Programme on HIV/AIDS.
- Muciaccia B, Padula F, Vicini E, Gandini L, Lenzi A, Stefanini M (2005). "Beta-chemokine receptors 5 and 3 are expressed on the head region of human spermatozoon". The FASEB Journal. 19 (14): 2048–50. S2CID 7928126.
External links
- HIV/AIDS at Curlie