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Lower HIV-2 Plasma Viral Loads May Explain Differences Between the Natural Histories of HIV-1 and HIV-2 Infections.

Shanmugam, Vedapuri; Switzer, William M.; Nkengasong, John N.; García-Lerma, Gerardo; Green, Timothy A.; Ekpini, Ehounou; Sassan-Morokro, Madeleine; Antunes, Francisco; Manshino, Kamal; Soriano, Vincent; Wiktor, Stefan Z.; Heneine, Walid
JAIDS Journal of Acquired Immune Deficiency Syndromes: July 1, 2000
EPIDEMIOLOGY: PDF Only

: To explain the low transmissibility and pathogenicity of HIV-2 infection's plasma viral loads in both HIV-1- and HIV-2-infected persons were compared by using the polymerase chain reaction (PCR)-based Amp-RT assay to measure levels of reverse transcriptase (RT) activity. The study comprised a total of 155 HIV-infectedpeople including 58 who were infected with HIV-2 with CD4+ cell counts <500 x 106/L (n = 15), CD4+ cell counts >500 x 106/L (n = 26), or with tuberculosis (TB; n = 17), and 97 HIV-1-infected people with CD4+ cell counts <500 x 106/L (n = 32), CD4+ cell counts >500 x 106/L (n = 25), or TB (n = 40). Among persons with CD4+ cell counts <500 x 106/L, 11 (73.3%) of 15 HIV-2-infected persons had detectable plasma RT activity compared with 25 (78.1%) of 32 HIV-1-infected persons (p = .725). However, the median HIV-2 plasma RT activity in this group was significantly lower (2561 x 10-10 U/ml; p = .036; detectable range, 1712-644,868 x 10"-10 U/ml) than the RT activity of HIV-1-infected persons with similar CD4+ cell counts (13,241 x 10-10 U/ml; detectable range, 8482-1,478,880 x 10-10 U/ml). Among TB patients, 10 (58.8%) of 17 HIV-2-infected persons had detectable plasma RT activity compared with 30 (75%) of 40 HIV-1-infected persons (p = .342). In contrast, among patients with CD4+ cell counts >500 x 106/L, none of 26 HIV-2-infected persons had detectable RT activity compared with 13 (52%) of 25 HIV-1-infected persons (p < .001). Our data suggest that unlike HIV-1 infection, HIV-2 infections with CD4+ cell counts >500 x 106/L are associated with a low level of viral replication, which may explain the longer clinical latency and lower transmissibility seen in HIV-2 infection.

(C) 2000 Lippincott Williams & Wilkins, Inc.