Lower HIV-2 plasma viral loads may explain differences between the natural histories of HIV-1 and HIV-2 infections.

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.

[1]  S. Popper,et al.  Lower human immunodeficiency virus (HIV) type 2 viral load reflects the difference in pathogenicity of HIV-1 and HIV-2. , 1999, The Journal of infectious diseases.

[2]  W. Heneine,et al.  Rapid screening of phenotypic resistance to nevirapine by direct analysis of HIV type 1 reverse transcriptase activity in plasma. , 1999, AIDS research and human retroviruses.

[3]  H. Agut,et al.  Status of long‐term asymptomatic HIV‐1 infection correlates with viral load but not with virus replication properties and cell tropism , 1999, Journal of medical virology.

[4]  D. Pieniążek,et al.  Predominance of human immunodeficiency virus type 2 subtype B in Abidjan, Ivory Coast. , 1999, AIDS research and human retroviruses.

[5]  C. Macken,et al.  The Ariel Project: A prospective cohort study of maternal-child transmission of human immunodeficiency virus type 1 in the era of maternal antiretroviral therapy. , 1999, The Journal of infectious diseases.

[6]  I. Thior,et al.  Human immunodeficiency virus type 1 subtypes differ in disease progression. , 1999, The Journal of infectious diseases.

[7]  D. Levy,et al.  Surveillance for waterborne-disease outbreaks--United States, 1995-1996. , 1998, MMWR. CDC surveillance summaries : Morbidity and mortality weekly report. CDC surveillance summaries.

[8]  H. Whittle,et al.  Low peripheral blood viral HIV-2 RNA in individuals with high CD4 percentage differentiates HIV-2 from HIV-1 infection. , 1998, Journal of human virology.

[9]  W. Heneine,et al.  Measurement of human immunodeficiency virus type 1 plasma virus load based on reverse transcriptase (RT) activity: evidence of variabilities in levels of virion-associated RT. , 1998, The Journal of infectious diseases.

[10]  K. D. de Cock,et al.  The Côte d'Ivoire national HIV counseling and testing program for tuberculosis patients: implementation and analysis of epidemiologic data , 1998, AIDS.

[11]  P. Vernazza,et al.  Association of CD4 cell depletion and elevated blood and seminal plasma human immunodeficiency virus type 1 (HIV-1) RNA concentrations with genital ulcer disease in HIV-1-infected men in Malawi. , 1998, The Journal of infectious diseases.

[12]  S. Hammer,et al.  Use of changes in plasma levels of human immunodeficiency virus type 1 RNA to assess the clinical benefit of antiretroviral therapy. , 1998, The Journal of infectious diseases.

[13]  W. Heneine,et al.  Evidence of Nef truncation in human immunodeficiency virus type 2 infection. , 1998, The Journal of infectious diseases.

[14]  S. Hammer,et al.  Antiretroviral therapy for HIV infection in 1997. Updated recommendations of the International AIDS Society-USA panel. , 1998, JAMA.

[15]  R. Royce,et al.  Sexual transmission of HIV. , 1997, The New England journal of medicine.

[16]  W. Heneine,et al.  Highly sensitive qualitative and quantitative detection of reverse transcriptase activity: optimization, validation, and comparative analysis with other detection systems. , 1996, Journal of virological methods.

[17]  John W. Mellors,et al.  Prognosis in HIV-1 Infection Predicted by the Quantity of Virus in Plasma , 1996, Science.

[18]  H. Whittle,et al.  A community-based study of human immunodeficiency virus type 2 provirus load in rural village in West Africa. , 1996, The Journal of infectious diseases.

[19]  H. Whittle,et al.  HIV‐2-specific cytotoxic T‐lymphocyte activity is inversely related to proviral load , 1995, AIDS.

[20]  W. Heneine,et al.  Detection of reverse transcriptase by a highly sensitive assay in sera from persons infected with human immunodeficiency virus type 1. , 1995, The Journal of infectious diseases.

[21]  J. Mellors,et al.  Quantitation of HIV-1 RNA in Plasma Predicts Outcome after Seroconversion , 1995, Annals of Internal Medicine.

[22]  F. Brun-Vézinet,et al.  Autologous neutralizing antibodies and viral load in HIV-2-infected individuals. , 1995, AIDS.

[23]  D. van Strijp,et al.  A one-tube quantitative HIV-1 RNA NASBA nucleic acid amplification assay using electrochemiluminescent (ECL) labelled probes. , 1994, Journal of virological methods.

[24]  H. Gayle,et al.  Prospective comparison of mother-to-child transmission of HIV-1 and HIV-2 in Abidjan, Ivory Coast. , 1994, JAMA.

[25]  C. Elbim,et al.  Comparison of plasma cytokine levels in African patients with HIV‐1 and HIV‐2 infection , 1994, AIDS.

[26]  H. Gayle,et al.  Epidemiology and transmission of HIV-2. Why there is no HIV-2 pandemic. , 1993, JAMA.

[27]  M. Urdea,et al.  Direct and quantitative detection of HIV‐1 RNA in human plasma with a branched DNA signal amplification assay , 1993, AIDS.

[28]  F. Brun-Vézinet,et al.  Cellular and plasma viral load in patients infected with HIV‐2 , 1993, AIDS.

[29]  S. J. Clark,et al.  High levels of HIV-1 in plasma during all stages of infection determined by competitive PCR. , 1993, Science.

[30]  J. Albert,et al.  Autologous neutralizing antibodies prevail in HIV-2 but not in HIV-1 infection. , 1993, Virology.

[31]  K. D. de Cock,et al.  Tuberculosis and HIV infection in sub-Saharan Africa. , 1992, JAMA.

[32]  R. Desrosiers,et al.  Importance of the nef gene for maintenance of high virus loads and for development of AIDS , 1991, Cell.

[33]  M. Lafontaine,et al.  Rapid and specific diagnosis of HIV-1 and HIV-2 infections: an evaluation of testing strategies. , 1990, AIDS.

[34]  F. Brun-Vézinet,et al.  Isolation of a new human retrovirus from West African patients with AIDS. , 1986, Science.

[35]  S. Mboup,et al.  New human T-lymphotropic retrovirus related to simian T-lymphotropic virus type III (STLV-IIIAGM). , 1986, Science.

[36]  J. Allan,et al.  SEROLOGICAL EVIDENCE FOR VIRUS RELATED TO SIMIAN T-LYMPHOTROPIC RETROVIRUS III IN RESIDENTS OF WEST AFRICA , 1985, The Lancet.

[37]  M. Dixon,et al.  Letter: Treatment of acute paracetamol hepatotoxicity. , 1973, Lancet.