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Epidemiology

Human retroviral infection was first documented in 1980, with the discovery of what is now termed HTLV-1. This virus is recognized as the cause of certain T-cell leukemias and lymphomas, as well as tropical spastic paraparesis, characterized by advancing spasticity and weakness with sensory disturbances. Another retrovirus, HTLV-II, appears closely associated with intravenous drug use, but its role in human disease remains unclear. It is most common in West Africa, but has been seen in Europe, North America, and recently in India. It is closely related to the simian immunodeficiency virus (SIV) and also causes a similar immunodeficiency syndrome. There are five subtypes. Recent studies have suggested that the clinical course of HIV-2 may be more indolent than that of HIV-1 (Markovitz) and that the complications may differ from those of HIV-1, with increased rates of cytomegalovirus, HIV encephalitis, and cholangitis (Lucas et al). Furthermore, a study of prostitutes in Dakaar, Senegal, indicates that HIV-2 is less easily transmitted sexually than HIV-1 (Kanki et al). Perinatal transmission appears to be rare (Markovitz). Some patients are co-infected with HIV-1 and HIV-2, or with HIV-1 and HTLV-1. HTLV-III, redesignated HIV-1, the cause of AIDS, has spread worldwide in epidemic proportions. There are two major groups, M (containing ten subtypes, subtype B being the most common worldwide) and (containing various heterogeneous viruses). There is some evidence that when an individual is co-infected with multiple subtypes, in vivo genetic recombination may occur, creating hybrid genomes, resulting in further antigenic diversity (and thus a potential threat to vaccine development).

No one can be sure when the AIDS mutation occurred. The HIV has now been identified in blood samples from Zaire as far back as 1959. Because an early poliomyelitis vaccine is known to have been contaminated with at least one monkey virus, SV40, some have speculated that HIV represents a mutation of SIV, introduced into the human population by a contaminated poliomyelitis vaccine used in Africa in the 1950s. Genetic analysis suggests that mutation occurred in the late 1940s or 1950s. Regardless of its origins, there is no clinical evidence that AIDS developed as a significant clinical disease before the mid 1970s. Blood samples from central and southern Africa from 1970 to 1974 are negative for HIV. The autopsy services at major medical centers in Africa were active, taking part in extensive and careful 5-year cancer surveys. There was no evidence of an AIDS-like syndrome or "slim disease". Significant numbers of AIDS cases did not develop until the mid 1970s. It can only be concluded that since the first edition of this book, a new disease has come to the fore, replacing a disease (smallpox) which has been eradicated.

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Copyright: Palmer and Reeder