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- W1569896650 endingPage "87" @default.
- W1569896650 startingPage "75" @default.
- W1569896650 abstract "HIV appears to have diverged into several lineages upon multiple zoonotic introductions from the nonhuman primates. The HIV-2 and HIV-1 groups M, N, and O likely represent different cross-species transmission events. The radial evolution of group M in multiple clades or subtypes is likely due to adaptation and expansions in the human hosts. It is not well understood why HIV strains such as HIV-1 subtype C in particular or group M in general have spread disproportionately as compared to other subtypes, groups, or types, which often remained geographically constrained to local epidemics. Host genetic effects, transmission bottlenecks, social/behavioral and environmental limitations, founder effect and other viral factors could have contributed to variable spread through the human population. Even after transmission, viruses evolve at different rates during disease progression. Recent studies have explored phenotypic differences between HIV types, groups, and subtypes in attempts to explain or understand this radial evolution and expansion. This review explores some of the important aspects relating to fitness during disease progression, during global distribution of different HIV subtypes, and related to circulation of recombinant forms in the epidemic." @default.
- W1569896650 created "2016-06-24" @default.
- W1569896650 creator A5003924565 @default.
- W1569896650 creator A5018319496 @default.
- W1569896650 creator A5020162929 @default.
- W1569896650 creator A5046062050 @default.
- W1569896650 date "2007-08-19" @default.
- W1569896650 modified "2023-09-29" @default.
- W1569896650 title "HIV diversity, recombination and disease progression: how does fitness fit into the puzzle?" @default.
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- W1569896650 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17694675" @default.
- W1569896650 hasPublicationYear "2007" @default.
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