J Acquir Immune Defic Syndr. 2000 Jul 1;24(3):257-63. Unique Identifier : AIDSLINE MED/20429904
Shanmugam V; Switzer WM; Nkengasong JN; Garcia-Lerma G; Green TA; Ekpini E; Sassan-Morokro M; Antunes F; Manshino K; Soriano V; Wiktor SZ; Heneine W; HIV and Retrovirology Branch, Division of HIV/AIDS, STDs, and TB; Laboratory Research, National Center for Infectious Diseases,; Centers for Disease Control and Prevention, Atlanta, Georgia; 30333, USA.
Abstract: 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-infected-people 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.
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