We describe the fate of viral DNA forms during HIV-1 infection. Our study reveals the interplay between various forms of the viral DNA genome, the distribution of which can be affected by mutations and by inhibitors of HIV-1 viral proteins. In the latter case, the quantification of 3'-processed DNA in infected cells can be informative about the mechanisms of future integrase inhibitors directly in the cell context.
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Munir et al. (2013) studied this question.
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