Classification

Classification

HIV was classified as a member of the genus Lentivirus,[8] part of the family of Retroviridae.[9] Lentiviruses have many common morphologies and biological properties. Many species are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period.[10] Lentiviruses are transmitted as single-stranded, positive-sense, enveloped RNA viruses. Upon entry of the target cell, the viral RNA genome is converted to double-stranded DNA by a virally encoded reverse transcriptase that is present in the virus particle. This viral DNA is then integrated into the cellular DNA by a virally encoded integrase so that the genome can be transcribed. Once the virus has infected the cell, two pathways are possible: either the virus becomes latent and the infected cell continues to function, or the virus becomes active and replicates, and a large number of virus particles are liberated that can then infect other cells.

Two species of HIV infect humans: HIV-1 and HIV-2.

HIV-1 is thought to have originated in southern Cameroon after jumping from wild chimpanzees (Pan troglodytes troglodytes) to humans during the twentieth century.[11][12] HIV-1 is the virus that was initially discovered and termed LAV. It is more virulent and relatively easy transmitted and is the cause of the majority of HIV infections globally.

HIV-2 may have originated from the Sooty Mangabey (Cercocebus atys), an Old World monkey of Guinea-Bissau, Gabon, and Cameroon.[13] HIV-2 is less transmittable than HIV-1 and is largely confined to West Africa.[13]

Early history

See AIDS origin#History of known cases and spread for early cases of HIV / AIDS.

Transmission

For more details on this topic, see AIDS transmission and prevention

Estimated per act risk for acquisition
of HIV-1 by exposure route[14]
Exposure Route Estimated infections
per 10,000 exposures
to an infected source
Blood Transfusion 9,000[15]
Childbirth 2,500[16]
Needle-sharing injection drug use 67[17]
Receptive anal intercourse* 50[18][19]
Percutaneous needle stick 30[20]
Receptive penile-vaginal intercourse* 10[18][19][21]
Insertive anal intercourse* 6.5[18][19]
Insertive penile-vaginal intercourse* 5[18][19]
Receptive fellatio* 1[19]
Insertive fellatio* 0.5[19]
* assuming no condom use

Since the beginning of the pandemic, three main transmission routes for HIV have been identified:

* Sexual route. The majority of HIV infections are acquired through unprotected sexual relations. Sexual transmission can occur when infected sexual secretions of one partner come into contact with the genital, oral, or rectal mucous membranes of another.
* Blood or blood product route. This transmission route can account for infections in intravenous drug users, hemophiliacs and recipients of blood transfusions (though most transfusions are checked for HIV in the developed world) and blood products. It is also of concern for persons receiving medical care in regions where there is prevalent substandard hygiene in the use of injection equipment, such as the reuse of needles in Third World countries. HIV can also be spread through the sharing of needles. Health care workers such as nurses, laboratory workers, and doctors, have also been infected, although this occurs more rarely. People who give and receive tattoos, piercings, and scarification procedures can also be at risk of infection.
* Mother-to-child transmission (MTCT). The transmission of the virus from the mother to the child can occur in utero during the last weeks of pregnancy and at childbirth. In the absence of treatment, the transmission rate between the mother and child is 25%.[16] However, where drug treatment and Cesarian section are available, this can be reduced to 1%.[16] Breast feeding also presents a risk of infection for the baby.

HIV-2 is transmitted much less frequently by the MTCT and sexual route than HIV-1.

HIV has been found at low concentrations in the saliva, tears and urine of infected individuals, but there are no recorded cases of infection by these secretions and the potential risk of transmission is negligible.[22] The use of physical barriers such as the latex condom is widely advocated to reduce the sexual transmission of HIV. Spermicide, when used alone or with vaginal contraceptives like a diaphragm, actually increases the male to female transmission rate due to inflammation of the vagina; it should not be considered a barrier to infection.[23] Trials, in which uncircumcised men were randomly assigned to be medically circumcised in sterile conditions and given counseling and other men were not circumcised, have been conducted in South Africa,[24] Kenya[25] and Uganda[26] showing reductions in HIV transmission for heterosexual sex of 60%, 53%, and 48% respectively. As a result, a panel of experts convened by WHO and the UNAIDS Secretariat has "recommended that male circumcision now be recognized as an additional important intervention to reduce the risk of heterosexually acquired HIV infection in men [in South Africa, Kenya and Uganda] ."[27] Research is clarifying whether there is a historical relationship between rates of male circumcision and rates of HIV in differing social and cultural contexts. Critics point out that any correlation between circumcision and HIV is likely to come from cultural factors (which govern not only whether someone is circumcised, but also their sexual practices and beliefs).[28] South African medical experts are concerned that the repeated use of unsterilized blades in the ritual (not medical) circumcision of adolescent boys may be spreading HIV.[29]

Structure and genome

Main article: HIV structure and genome

Diagram of HIV
Diagram of HIV

HIV is different in structure from other retroviruses. It is about 120 nm in diameter (120 billionths of a meter; around 60 times smaller than a red blood cell) and roughly spherical.[30]
EM of HIV
EM of HIV

It is composed of two copies of positive single-stranded RNA that codes for the virus's nine genes enclosed by a conical capsid composed of 2,000 copies of the viral protein p24.[31] The single-stranded RNA is tightly bound to nucleocapsid proteins, p7 and enzymes needed for the development of the virion such as reverse transcriptase, proteases, ribonuclease and integrase. A matrix composed of the viral protein p17 surrounds the capsid ensuring the integrity of the virion particle.[31] This is, in turn, surrounded by the viral envelope which is composed of two layers of fatty molecules called phospholipids taken from the membrane of a human cell when a newly formed virus particle buds from the cell. Embedded in the viral envelope are proteins from the host cell and about 70 copies of a complex HIV protein that protrudes through the surface of the virus particle.[31] This protein, known as Env, consists of a cap made of three molecules called glycoprotein (gp) 120, and a stem consisting of three gp41 molecules that anchor the structure into the viral envelope.[32] This glycoprotein complex enables the virus to attach to and fuse with target cells to initiate the infectious cycle.[32] Both these surface proteins, especially gp120, have been considered as targets of future treatments or vaccines against HIV.[33]

Of the nine genes that are encoded within the RNA genome, three of these genes, gag, pol, and env, contain information needed to make the structural proteins for new virus particles.[31] env, for example, codes for a protein called gp160 that is broken down by a viral enzyme to form gp120 and gp41. The six remaining genes, tat, rev, nef, vif, vpr, and vpu (or vpx in the case of HIV-2), are regulatory genes for proteins that control the ability of HIV to infect cells, produce new copies of virus (replicate), or cause disease.[31] The protein encoded by nef, for instance, appears necessary for the virus to replicate efficiently, and the vpu-encoded protein influences the release of new virus particles from infected cells.[31] The ends of each strand of HIV RNA contain an RNA sequence called the long terminal repeat (LTR). Regions in the LTR act as switches to control production of new viruses and can be triggered by proteins from either HIV or the host cell.[31]