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. Author manuscript; available in PMC: 2008 Sep 23.
Published in final edited form as: AIDS. 2006 Mar 21;20(5):643–651. doi: 10.1097/01.aids.0000216363.36786.2b

Fig. 2. Two examples of published inter-subtype differences in the genetic mechanisms of HIV-1 drug resistance as demonstrated by HIVseq output.

Fig. 2

(a) Association of the protease mutations V82T and V82M with protease inhibitor (PI) therapy in subtype G viruses [12]. V82I is the consensus amino acid sequence in subtype G. As a result, the mutations 82T and 82M require a change in only one nucleotide, in contrast to 82A (the most common PI-associated mutation in other subtypes), which requires changes in two nucleotides in subtype G. (b) Association of the reverse transcriptase mutation V106M in subtype C viruses with therapy with non-nucleoside reverse transcriptase inhibitors [10,11].