Objectives: To evaluate clinical and RNA load response to antiretroviral th
erapy amongst patients infected with HIV-2 and to study the development of
drug resistance.
Methods: Seven HIV-2 seropositive patients were monitored with clinical exa
mination, CD4 cell count and HIV-2 viral RNA load. Viruses From four subjec
ts were genotyped and in vitro recovery of virus by co-cultivation with PBM
Cs and HVS T-cells was attempted, Viruses isolated from two subjects were a
ssayed for phenotypic antiviral resistance. The main outcome measures were
the relationship between disease stage, viral load, CD4 cell count, viral s
ubtype and the clinical course of HIV-2 infection and the effect of combina
tion antiretroviral therapy on disease progression, CD4 cell count. HIV-2 R
NA viral load and drug resistance.
Results: The median time of follow-up was 3 years (range 0-8 years). Three
patients had AIDS, and one had symptomatic disease, Of the four patients ge
notyped, three were infected with HIV-2 subtype B and one with subtype A. V
iraemia was detectable only at CD4 counts of less than 300 x 10(6)/ml, Two
patients with high viral loads failed to respond to antiretroviral therapy
although their treatment may not have been optimal, One developed in vitro
phenotypic antiviral resistance, The genotype of this patient's viral rever
se transcriptase is being analysed,
Conclusions: In contrast to HIV-1,HIV-2 RNA levels were often undetectable
despite advanced disease and low CD4 cell counts. However, HIV-2 was dearly
capable of causing CD4 cell depletion resulting in symptomatic disease. Th
e principles of highly active antiretroviral therapy seem to apply to HIV-2
and suboptimal therapy may lead to drug resistance. The timing of therapy
initiation, monitoring of response and the measurement of resistance remain
unresolved issues and conclusions cannot be extrapolated from HIV-1. (C) 2
001 The British Infection Society.