title: Lower HIV-2 plasma viral loads may explain differences between the natural histories of HIV-1 and HIV-2 infections.
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.
authors.affiliation: 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.
authors.forename: V
authors.initials: V
authors.lastname: Shanmugam
authors.forename: W M
authors.initials: WM
authors.lastname: Switzer
authors.forename: J N
authors.initials: JN
authors.lastname: Nkengasong
authors.forename: G
authors.initials: G
authors.lastname: García-Lerma
authors.forename: T A
authors.initials: TA
authors.lastname: Green
authors.forename: E
authors.initials: E
authors.lastname: Ekpini
authors.forename: M
authors.initials: M
authors.lastname: Sassan-Morokro
authors.forename: F
authors.initials: F
authors.lastname: Antunes
authors.forename: K
authors.initials: K
authors.lastname: Manshino
authors.forename: V
authors.initials: V
authors.lastname: Soriano
authors.forename: S Z
authors.initials: SZ
authors.lastname: Wiktor
authors.forename: W
authors.initials: W
authors.lastname: Heneine
mesh_terms: D018791:CD4 Lymphocyte Count; D007560:Cote d'Ivoire; D015658:HIV Infections / Q000150:complications / Q000276:immunology / Q000821:virology*; D054303:HIV Reverse Transcriptase / Q000097:blood; D015497:HIV-1 / Q000201:enzymology; D015498:HIV-2 / Q000201:enzymology; D006801:Humans; D016133:Polymerase Chain Reaction; D011174:Portugal; D012194:RNA-Directed DNA Polymerase / Q000097:blood; D014376:Tuberculosis / Q000150:complications / Q000821:virology; D019562:Viral Load
chemical_list: C072416:reverse transcriptase, Human immunodeficiency virus 2; D054303:HIV Reverse Transcriptase; D012194:RNA-Directed DNA Polymerase