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J. Virol. doi:10.1128/JVI.02050-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Extensive Intra-subtype Recombination in South African HIV-1 Subtype C Infections

Department of Microbiology, University of Washington, Seattle, Washington 98195-8070 USA; Los Alamos National Laboratory, Los Alamos, New Mexico 87545 USA; Machine Learning and Applied Statistics Group, Microsoft Research, Redmond, Washington 98052 USA; HIV Pathogenesis Program, Doris Duke Medical Research Institute, University of KwaZulu Natal, Durban, 4015 South Africa; Partners AIDS Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02129 USA; Nuffield Department of Medicine, The Peter Medawar Building for Pathogen Research, Oxford University, Oxford, United Kingdom OX1 3SY, UK; Howard Hughes Medical Institute, Chevy Chase, Maryland 20815 USA

^* To whom correspondence should be addressed. Email: cmr{at}u.washington.edu.

	Abstract

Recombinant HIV-1 strains have been observed containing sequences from different viral genetic subtypes (inter-subtype) and different lineages from within the same subtype (intra-subtype). A consequence of recombination can be the distortion of phylogenetic signal. Several inter-subtype recombinants have been identified, however, less is known about the frequency of intra-subtype recombination. For this study, near full-length HIV-1 subtype C genomes from 270 individuals were evaluated for the presence of intra-subtype recombination. A sliding window schema (window = 2kb, step = 385bp) was used to partition the aligned sequences. The Shimodaira-Hasegawa test detected significant topological incongruence in 99.6% of the comparisons of the maximum-likelihood trees generated from each sequence partition, a result that could be explained by recombination. Using RECOMBINE, we detected significant levels of recombination using 5 random subsets of the sequences. With a set of 23 topologically-consistent sequences used as references, bootscanning followed by the interactive informative sites test defined recombination breakpoints. Using two multiple comparison correction methods, 47% of the sequences showed significant evidence for recombination in both analyses. Estimated evolutionary rates were revised from 0.51%/year (95% CI 0.39 to 0.53) with all sequences to 0.46%/year (95% CI 0.38 to 0.48) with the putative recombinants removed. The timing of the subtype C epidemic origin was revised from 1961 (95%CI 1947 to 1962) with all sequences to 1958 (95% CI 1949 to 1960) with the putative recombinants removed. Thus, intra-subtype recombinants are common within the subtype C epidemic and these impact analyses of HIV-1 evolution.

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