Low peripheral blood viral HIV-2 RNA in individuals with high CD4 percentage differentiates HIV-2 from HIV-1 infection.
OBJECTIVE
To elucidate why the virulence of HIV-1 and HIV-2 infections differ in West African populations.


METHODS
Peripheral blood plasma virion RNA and cellular proviral DNA levels were measured in a cross-section of 59 HIV-1 and 49 HIV-2 singly infected individuals representing all stages of infection in The Gambia, West Africa. Novel reverse transcriptase polymerase chain reaction (RT-PCR) assays specific and sensitive for virus quantification of non-clade B HIV-1 and HIV-2 infections were used.


RESULTS
HIV-1 and HIV-2 proviral and plasma RNA levels were inversely correlated with CD4+ count for both infections with cellular proviral load similar at each stage of infection. Critically, up to three-fourths of HIV-2-infected individuals with high CD4 percentages (> 28%) had undetectable (< 500 copies/mL) levels of peripheral blood HIV-2 RNA in contrast to HIV-1-infected individuals who had readily detectable plasma virus at all stages of infection (P < .0001). Plasma RNA levels were similar in the intermediate and end stages of infection, indicating similar replication potential for both viruses. In the cross-section of HIV-1- and HIV-2-infected patients studied, the data indicate a wider dynamic range of HIV-2 RNA in vivo compared with HIV-1.


CONCLUSIONS
Low levels of HIV-2 replication and virion expression characterize individuals with high CD4+ lymphocyte counts, suggesting that a very different dynamic equilibrium exists between virus and host for HIV-2 compared with HIV-1. By analogy with HIV-1, our data implicate a considerably lower turnover of HIV-2 virion RNA in vivo with a markedly reduced production of infectious genomes in individuals during the subclinical phase of infection.


CONCLUSIONS
The lower levels of virion expression of HIV-2 infections in vivo are compatible with observed differences in the natural history of HIV-1 and HIV-2 infections, relating to overall differences in the pathogenesis and disease progression of the two infections.
Berry
N
N
Department of Virology, Windeyer Institute of Medical Sciences, University College London Medical School, U.K.
Ariyoshi
K
K
Jaffar
S
S
Sabally
S
S
Corrah
T
T
Tedder
R
R
Whittle
H
H
D000163:Acquired Immunodeficiency Syndrome / Q000175:diagnosis* / Q000276:immunology / Q000821:virology; D015704:CD4 Antigens / Q000097:blood*; D018791:CD4 Lymphocyte Count; D003430:Cross-Sectional Studies; D003937:Diagnosis, Differential; D018450:Disease Progression; D005714:Gambia / Q000453:epidemiology; D015497:HIV-1 / Q000235:genetics / Q000302:isolation & purification*; D015498:HIV-2 / Q000235:genetics / Q000302:isolation & purification*; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000821:virology; D016133:Polymerase Chain Reaction; D011533:Proviruses / Q000302:isolation & purification; D012367:RNA, Viral / Q000097:blood*; D019562:Viral Load; D014774:Virulence
D015704:CD4 Antigens; D012367:RNA, Viral