Antiretroviral therapy for HIV-2 infected patients.
OBJECTIVE
To evaluate clinical and RNA load response to antiretroviral therapy amongst patients infected with HIV-2 and to study the development of drug resistance.


METHODS
Seven HIV-2 seropositive patients were monitored with clinical examination, CD4 cell count and HIV-2 viral RNA load. Viruses from four subjects were genotyped and in vitro recovery of virus by co-cultivation with PBMCs and HVS T-cells was attempted. Viruses isolated from two subjects were assayed for phenotypic antiviral resistance. The main outcome measures were the relationship between disease stage, viral load, CD4 cell count, viral subtype and the clinical course of HIV-2 infection and the effect of combination antiretroviral therapy on disease progression, CD4 cell count, HIV-2 RNA 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 genotyped, three were infected with HIV-2 subtype B and one with subtype A. Viraemia 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 reverse 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 clearly capable of causing CD4 cell depletion resulting in symptomatic disease. The 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.
Smith
N A
NA
Chelsea Hospital, London, UK.
Shaw
T
T
Berry
N
N
Vella
C
C
Okorafor
L
L
Taylor
D
D
Ainsworth
J
J
Choudhury
A
A
Daniels
R S
RS
El-Gadi
S
S
Fakoya
A
A
Moyle
G
G
Oxford
J
J
Tedder
R
R
O'Shea
S
S
de Ruiter
A
A
Breuer
J
J
D000163:Acquired Immunodeficiency Syndrome / Q000188:drug therapy*; D000354:Africa, Western / Q000208:ethnology; D019380:Anti-HIV Agents / Q000494:pharmacology / Q000627:therapeutic use*; D018791:CD4 Lymphocyte Count; D004352:Drug Resistance, Microbial; D004359:Drug Therapy, Combination; D005260:Female; D005500:Follow-Up Studies; D015658:HIV Infections / Q000188:drug therapy* / Q000276:immunology / Q000821:virology; D006679:HIV Seropositivity / Q000188:drug therapy* / Q000276:immunology / Q000821:virology; D015498:HIV-2 / Q000187:drug effects / Q000235:genetics / Q000472:pathogenicity; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000821:virology; D008297:Male; D010802:Phylogeny; D012367:RNA, Viral / Q000032:analysis; D006113:United Kingdom; D019562:Viral Load; D014766:Viremia
D019380:Anti-HIV Agents; D012367:RNA, Viral