The human immunodeficiency virus, HIV, is among the quickest known evolving entities. It multiplies sloppily, piling up lots of mutations during the process of copying its genetic material. It also multiplies at a high speed where one virus can breed billions of copies in only a single day. Acquired Immune Deficiency Syndrome, AIDS, was first acknowledged as a new disease in the year 1981 during which rising numbers of youthful homosexual men died of strange opportunistic infections, as well as unusual malignancies (Greene). A retrovirus, now referred to as human immunodeficiency virus type 1, HIV-1, was later on keyed out as the causative agent of what has turned out to be the most annihilating infectious diseases to have emerged in history. This virus spreads through percutaneous, sexual, as well as perinatal routes. Since it was first keyed out, the HIV-1pandemic, also referred to as the main (M) group, has left at least 60 million persons infected and over 25 million dead. Developing nations have gone through the greatest mortality, as well as morbidity of HIV/AIDS, with the highest prevalence rates registered in young adults in sub-Saharan Africa. Even though antiretroviral intervention has lowered the AIDS- related deaths toll, there is no universal access to therapy. Therefore, the prospects of an effective vaccine, as well as curative treatments are uncertain. Hence, AIDS will keep on being a significant threat to the public health. An important step in fighting HIV, however, is to understand its evolution and then finally find a way to manage its evolution.
For a long time, HIV-1 has been surmised to have originated from chimpanzee. Nevertheless, until lately, the perceived absence of a chimpanzee reservoir made the HIV-1 source open to question. These doubts have since been answered through noninvasive essaying of populations of wild-living ape. It is now well demonstrated that every naturally occurring strain of SIVcpz falls into two subspecies-specific lineages, known as SIVcpzPts and SIVcpzPtt, which are limited to the home ranges of their various hosts. Viruses in these two lineages are divergent and differ in their Pol, Gag, as well as Env sequences of protein. Studies of population genetic have demonstrated that eastern and central chimpanzees are hardly differentiated, raising question about their status as separate subspecies. Nevertheless, the fact that they hold distinct lineages of SIVcpz proposes that eastern and central chimpanzees have been efficaciously isolated for some time. Additionally, studies on molecular epidemiology in south of Cameroon have demonstrated that SIVcpzPtt strains portray phylogeographic clustering, with viruses from certain regions to form monophyletic lineages. The SIVgor discovery has keyed out a second species of ape as a possible human infection reservoir (Van Heuverswyn, Li and Neel). These results have collectively allowed unravel of the origins of HIV-1.
HIV-1 is not only a single virus, but is also composed of four distinct lineages, namely M, N, O, and P. Each of this was a result of an independent transmission event between species. Group M, which was the first to be keyed out represents the HIV-1pandemic form. HIV-1 evolves about one million times more than the DNA of mammals, since the HIV-1 reverse transcriptase is prone to error and the virus has a short generation time. This leaning for rapid genetic alteration has offered a unique chance to acquire perceptivity into the time and the place where is the origin of the AIDS pandemic. Statistical, as well as phylogenetic analyses, have dated the last common HIV-1 group M ancestor to between 1910 and 1930 with constrict confidence intervals. This demonstrates that following pandemic HIV-1 initial emergence in West Africa, it extended for 50 to 70 years prior to its recognition. The likely location of the first epidemic has as well been keyed out. Studies of molecular epidemiology have demonstrated that most of the first HIV-1 group M diversification probably took place in the region around Kinshasa, which was that time referred to as Leopoldville. All the subtypes of HIV-1 group M were keyed out in this area, and extra lineages that have continued being confined to this region (Vidal, Peeters and Mulanga-Kabeya).
The earliest HIV-1 group M strains were also discovered in Leopoldville. From the infected tissue and blood samples’ genetic analysis collected from Kinshasa residents in 1959 and 1960, it was evident that HIV-1 had already radiated into various subtypes. Eventually, demographic data demonstrate that pandemic HIV-1 came out at a time when west central African urban populations were increasing. The largest city in the region at that time was and, therefore, a probable destination for a freshly rising infection. Furthermore, rivers that served as key commerce and travel routes at the time would have offered a connection between the HIV-1 group M chimpanzee reservoir in southeastern Cameroon and Leopoldville on the Congo banks. Hence, all present prove points to Kinshasa/Leopoldville as the AIDS pandemic cradle.
As the group M of HIV-1 spread worldwide, its dispersion entailed several population challenges, which resulted in the prepotency of various lineages of group M, currently referred to as subtypes, in various geographic regions. Currently, the HIV-1 group M is grouped into nine subtypes, and over 40 different circulating recombinant forms that were generated when the same population was infected by numerous subtypes (Taylor, Sobieszczyk and McCutchan). It has been possible to retrace the pathways of migration of a number of these CRFs and subtypes. For instance, subtypes A and D origin is central Africa, though finally established epidemics in East Africa, while subtype C was brought in, and prevails in, south of Africa from where it extended to India, as well as other Asian nations. Subtype B, which is the greatest majority of infections of HIV-1 in the Americas and Europe, originated from one African strain, which seems to have initially extended to Haiti in the 1960s and later onward to the US, as well as other western nations. The recombination occurrence that formed CRF01 most likely took place in Central Africa, but this viral lineage was initially observed in the late 1980s leading to a heterosexual Thailand epidemic, contemporary with viruses of the subtype B extending among endovenous drug users (Taylor, Sobieszczyk and McCutchan). CRF01 has continued to dominate the Southeast Asian AIDS epidemic. Even though the first distribution of these CRFs, as well as subtypes, may have been mainly as a result of chance occurrences, current studies have proposed that different subtype’s viruses differ in their biological traits that may determine their epidemiology. For example, subtype D has been linked to greater pathogenicity and a raised occurrence of cognitive impairment, as well as AIDS dementia. It, therefore, seems that not only the genetic but also the HIV-1 group M CRF and subtypes biological diversity is rising.
HIV is an unambiguously persistent syndrome that evolves to invariably avoid the human immune system. During the early periods of this pandemic, many positively declared that a vaccine would be created within a short time-frame, which has not been achieved. The success of finding a vaccine or a cure for this virus lies in the understanding of its evolution, and subsequent management of the evolution.
Works Cited
Greene, W. C. "A history of AIDS: Looking back to see ahead." Eur J Immunol 37.Suppl. 1 (2007): S94–S102. http://onlinelibrary.wiley.com/doi/10.1002/eji.200737441/full
Taylor, B. S., et al. "The challenge of HIV-1 subtype diversity." N Engl J Med 358 (2008): 1590–1602. http://www.nejm.org/doi/full/10.1056/NEJMra0706737
Van Heuverswyn, F., et al. "Human immunodeficiency viruses: SIV infection in wild gorillas." Nature 444 (2006): 164. http://www.nature.com/nature/journal/v444/n7116/abs/444164a.html
Vidal, N., et al. "Unprecedented degree of human immunodeficiency virus type 1 (HIV-1) group M genetic diversity in the Democratic Republic of Congo suggests that the HIV-1 pandemic originated in Central Africa." J Virol 74 (2000): 10498–10507. http://jvi.asm.org/content/74/22/10498.full
