Nucleoside resistance pathways may differ between HIV-1 and HIV-2

Simon Collins and Polly Clayden, HIV i-Base

Only two classes of ARVs, protease inhibitors and nucleoside reverse transcriptase inhibitors, have activity against HIV-2, and optimising treatment in this population is therefore particularly important. The assumption, in the absence of detailed studies of HIV-2 that resistance would develop in a comparable pattern to HIV-1, was questioned in one study at the meeting. [1]

Genotypic and phenotypic responses to treatment in five HIV-2 infected subjects were followed over a median duration of 15 months therapy (IQR 11-20). Median baseline CD4 count was 69 cells/mm3 (IQR, 49-233) and viral load 4 log (IQR, 4-5 log).

That despite the relatively low baseline viral load, none of these patients achieved undetectable viral load after treatment, is a concern itself. Additionally two of the five patients were found to have the relatively rare multi-nucleoside resistant Q151M mutation after treatment for 10 and 11 months with ZDV and ddI respectively. Full details of treatment regimens were not clear in the study abstract although other mutation associated with NRTIs and PIs were also detected in the study.

In contrast to HIV-1, the Q151M mutation, which allows resistance to ZDV, d4T, ddI and ddC, might represent a frequent pathway for HIV-2 nucleoside resistance in HIV-2. Although there are only limited numbers of patients with HIV-2 in the UK, further study in the population is clearly warranted.


  1. Kagan RM et al – Response to antiretroviral therapy in HIV-2 infected persons: increased selection of Q151M mutations. Abstract 58. Antiviral Therapy 2001; 6 (Supplement1):45

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