HIV and related viruses

HIV was discovered by Barré-Sinoussi, Montagnier, and colleagues at the Institut Pasteur, Paris, in 1983 and given the name lymphadenopathy associated virus (LAV). In 1984 Popovic, Gallo, and co-workers described the development of cell lines permanently and productively infected with the virus.

In line with two previously described retroviruses, HTLV-I and HTLV-II, they designated this virus HTLV-III. Other virus isolates from patients with AIDS and AIDS-related disease in America, Europe and Central Africa have proved to be all the same virus, now referred to as HIV-1. Eight subtypes of HIV-1, alphabetically designated, have so far been described.

Around 1985 another human retrovirus, different from HIV- 1, was recognised in patients from West Africa. This virus, referred to by the Paris investigators as LAV-2 and more recently as HIV-2, is also associated with human AIDS and AIDS-related disease. It is closely related to the simian retrovirus, SIV, carried by healthy African green monkeys, and the cause of an AIDS-like disease in captive rhesus monkeys.

Though potentially important worldwide, HIV-2 infections remain uncommon outside West Africa and they have proved far less virulent than HIV-1 infections.

The virus and the tests

Although it is clear that HIV is the underlying cause of AIDS and AIDS-related disease, its origin remains obscure. There is firm serological evidence of infection on the east and west coasts of the USA from the mid 1970s, and HIV infection in central Africa may have antedated infection in North America.
Phylogenetic analysis of the HIV-1 genome has suggested an origin in chimpanzees while, in the case of HIV-2, similarity to the simian immunodeficiency virus (SIV) genome may point to an origin in sooty mangabey monkeys. In both cases the butchery and consumption of these “bush meats” has been incriminated in transmissions to the human host. Like some other RNA viruses, HIV appears to have mutated and shifted its
host range and virulence, explaining how a new pathogenic retrovirus could arise in man. Its virulence may since have been amplified as a result of travel, population dislocation and promiscuous sexual contact, with rapid passage of the virus.

Retroviruses are so named because their genomes encode an unusual enzyme, reverse transcriptase, which allows DNA to be transcribed from RNA. Thus, HIV can make copies of its own
genome, as DNA, in host cells such as the human CD4 “helper” lymphocyte. The viral DNA becomes integrated in the lymphocyte genome, and this is the basis for chronic HIV infection. Integration of the HIV genome into host cells is a formidable obstacle to any antiviral treatment that would not
just suppress but also eradicate the infection. Nevertheless, modern treatment with combinations of nucleoside analogues and protease inhibitors has transformed the prognosis for carriers of HIV, usually achieving a sustained fall in virus concentration in blood and restoration of the main target cell (CD4 lymphocyte) to near normal levels.