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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 1st, 2000

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 × 106/L (n = 26), or with tuberculosis (TB; n = 17), and 97 HIV-1-infected people with CD4+ cell counts <500 × 106/L (n = 32), CD4+ cell counts >500 × 106/L (n = 25), or TB (n = 40). Among persons with CD4+ cell counts <500 × 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 × 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 × 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 × 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 × 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.

Address correspondence and reprint requests to Walid Heneine, HIV and Retrovirology Branch, Centers for Disease Control and Prevention, 1600 Clifton Road, MS-G19, Atlanta, GA 30333, U.S.A.; email:

Use of trade names is for identification only and does not imply endorsement by the Public Health Service or the U.S. Department of Health and Human Services.

This work was presented in part at the 5th National Conference on Retroviruses and Opportunistic Infections, Chicago, Illinois, U.S.A., 1998 [abstract 578].

Manuscript received December 7, 1999; accepted April 3, 2000.

© 2000 Lippincott Williams & Wilkins, Inc.