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Abstract
Methods We used both Jurkat and primary cell latency models. In Jurkat cells, wt and drug-resistant latent populations were superinfected with wt or drug-resistant viruses, including nef or tat mutants, and treated with various inhibitors. Viral reporter gene expression was measured by FACS. Sequence tags on each resistant virus permitted identification of recombinants. We also performed superinfection experiments in primary cells.
Highlights
Latent HIV-1 can be reactivated by superinfection in a Tat-dependent manner, which can lead to the emergence of recombinant viruses
The HIV-1 latent reservoir represents an important source of genetic diversity that could contribute to viral evolution and drug resistance
Latent virus reactivation required gene expression of the superinfecting virus, since latent viruses were reactivated in the presence of a protease inhibitor, but not a reverse transcriptase (RT) or integrase inhibitor
Summary
Latent HIV-1 can be reactivated by superinfection in a Tat-dependent manner, which can lead to the emergence of recombinant viruses. Daniel Aaron Donahue1*, Sophie M Bastarache, Richard D Sloan, Mark A Wainberg. From Frontiers of Retrovirology: Complex retroviruses, retroelements and their hosts Cambridge, UK. From Frontiers of Retrovirology: Complex retroviruses, retroelements and their hosts Cambridge, UK. 16-18 September 2013
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