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Transcript
Proliferation of cells with HIV integrated into cancer genes
contributes to persistent infection
by Thor A. Wagner, Sherry McLaughlin, Kavita Garg, Charles Y. K. Cheung, Brendan
B. Larsen, Sheila Styrchak, Hannah C. Huang, Paul T. Edlefsen, James I. Mullins,
and Lisa M. Frenkel
Science
Volume 345(6196):570-573
August 1, 2014
Published by AAAS
Fig. 1 Representation of HIV integration sites sampled through time.(A to C) show the scaled
representation of each gene with integration sites mapped for the three participants at three
intervals (times in years given along the x axis) after initiation of suppressive ART. Integration
sites were detected in all chromosomes of all participants, except for chromosome 18 in
participant B1, and chromosome 20 and the Y chromosome in L1, the only male studied.
Thor A. Wagner et al. Science 2014;345:570-573
Published by AAAS
Fig. 2 Phylogenetic relationships between HIV-1 env (C2V5 region) genes sampled from
participant L1 through time.A neighbor-joining tree was generated using viral gene sequences
derived from PBMC DNA from participant L1 by single-genome sequencing, including from this
(with integration sites determined) and a previous study (8).
Thor A. Wagner et al. Science 2014;345:570-573
Published by AAAS
Fig. 3 HIV-1 integration sites in chromosome 6, including the BACH2 locus.(B) (bottom) shows
the integration sites mapped in the human chromosome 6 in this (SCRI, Seattle Children’s
Research Institute) and other studies of individuals sampled while on suppressive ART,
including from Han et al.
Thor A. Wagner et al. Science 2014;345:570-573
Published by AAAS