Home |
Current Issue |
Past Issues |
In the Clinic |
ACP Journal Club |
CME |
Collections |
Audio/Video |
Mobile |
Subscribe |
Tools |
Help |
ACP Online
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 February 1993 | Volume 118 Issue 3 | Pages 211-218
Purpose: To review the clinical, epidemiologic, and biological features of infection with the human immunodeficiency virus type 2 (HIV-2).
Data Identification: Studies published since 1981 identified from MEDLINE searches, articles accumulated by the author, bibliographies of identified articles, and discussions with other investigators.
Study Selection: Information for review was taken from the author's own studies, data from other investigators that have been submitted for publication, and from 131 of the more than 200 articles examined.
Data Extraction: Pertinent studies were selected and the data synthesized into a review format.
Results of Data Synthesis: Infection with HIV-2 is prevalent in West Africa and is increasingly being identified elsewhere. The human immunodeficiency virus type 2 is spread through sexual contact and via contaminated blood but, unlike HIV-1, perinatal transmission is limited. Human immunodeficiency virus type 2 is genetically much more closely related to the simian immunodeficiency virus (SIV) than to HIV-1; biological and demographic data suggest that HIV-2 may have originally been transmitted from monkeys to man. Although HIV-2 causes the acquired immunodeficiency syndrome (AIDS), the asymptomatic incubation period after infection with HIV-2 appears to be substantially longer than that following HIV-1 infection. Consistent with these clinical observations, genetic regulation of HIV-2 differs from that of HIV-1. Therapeutic studies of patients infected with HIV-2 are lacking.
Conclusions: The human immunodeficiency virus type 2 is prevalent in West Africa and is now recognized on several other continents, including North America. Its epidemiology, biology, and clinical course differ from HIV-1. Therapeutic studies are needed.
Author and Article Information
From the University of Michigan Medical Center, Ann Arbor, Michigan.
REVIEW
Infection with the Human Immunodeficiency Virus Type 2
![]()
Requests for Reprints: David M. Markovitz, MD, 5510 MSRB I, 1150 W. Medical Center Drive, Ann Arbor, MI 48109-0680.
Acknowledgments: The author thanks Phyllis Kanki, Beatrice Hahn, Ruth Markovitz, Helga Rubsamen-Waigmann, and Ron Desrosiers for helpful discussions and for providing information before publication, as well as Gary Nabel for continuing support, and Mara Van Dusen for preparation of the manuscript.
Grant Support: By grants CA01479 and AI30924 from the National Institutes of Health and a Scholar Award from the Life and Health Insurance Medical Research Fund.
This article has been cited by other articles:
![]() |
S. M. Owen, C. Yang, T. Spira, C. Y. Ou, C. P. Pau, B. S. Parekh, D. Candal, D. Kuehl, M. S. Kennedy, D. Rudolph, et al. Alternative Algorithms for Human Immunodeficiency Virus Infection Diagnosis Using Tests That Are Licensed in the United States J. Clin. Microbiol., May 1, 2008; 46(5): 1588 - 1595. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. A. Handwerger, A. W. Urban, and J. L. Gottlieb Retinopathy as the Initial Presentation of Human Immunodeficiency Virus 2 Infection Arch Ophthalmol, December 1, 2000; 118(12): 1695 - 1696. [Full Text] [PDF] |
||||
![]() |
R. E. Jeeninga, M. Hoogenkamp, M. Armand-Ugon, M. de Baar, K. Verhoef, and B. Berkhout Functional Differences between the Long Terminal Repeat Transcriptional Promoters of Human Immunodeficiency Virus Type 1 Subtypes A through G J. Virol., April 15, 2000; 74(8): 3740 - 3751. [Abstract] [Full Text] |
||||
![]() |
C. M. Browning, L. Cagnon, P. D. Good, J. Rossi, D. R. Engelke, and D. M. Markovitz Potent Inhibition of Human Immunodeficiency Virus Type 1 (HIV-1) Gene Expression and Virus Production by an HIV-2 Tat Activation-Response RNA Decoy J. Virol., June 1, 1999; 73(6): 5191 - 5195. [Abstract] [Full Text] |
||||
![]() |
S. A. Schwartz and M. P. N. Nair Current Concepts in Human Immunodeficiency Virus Infection and AIDS Clin. Vaccine Immunol., May 1, 1999; 6(3): 295 - 305. [Full Text] [PDF] |
||||
![]() |
A. S. Vallari, R. K. Hickman, J. R. Hackett Jr., C. A. Brennan, V. A. Varitek Jr., and S. G. Devare Rapid Assay for Simultaneous Detection and Differentiation of Immunoglobulin G Antibodies to Human Immunodeficiency Virus Type 1 (HIV-1) Group M, HIV-1 Group O, and HIV-2 J. Clin. Microbiol., December 1, 1998; 36(12): 3657 - 3661. [Abstract] [Full Text] |
||||
![]() |
S. M. Owen, D. Ellenberger, M. Rayfield, S. Wiktor, P. Michel, M. H. Grieco, F. Gao, B. H. Hahn, and R. B. Lal Genetically Divergent Strains of Human Immunodeficiency Virus Type 2 Use Multiple Coreceptors for Viral Entry J. Virol., July 1, 1998; 72(7): 5425 - 5432. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. K. Fu, G. Grosveld, and D. M. Markovitz DEK, an autoantigen involved in a chromosomal translocation in acute myelogenous leukemia, binds to the HIV-2 enhancer PNAS, March 4, 1997; 94(5): 1811 - 1815. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. K. Fu and D. M. Markovitz Purification of the pets Factor. A NUCLEAR PROTEIN THAT BINDS TO THE INDUCIBLE TG-RICH ELEMENT OF THE HUMAN IMMUNODEFICIENCY VIRUS TYPE 2ENHANCER J. Biol. Chem., August 9, 1996; 271(32): 19599 - 19605. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. E. Faulkner, J. M. Hilfinger, and D. M. Markovitz Protein Phosphatase 2A Activates the HIV-2 Promoter through Enhancer Elements That Include the pets Site J. Biol. Chem., July 6, 2001; 276(28): 25804 - 25812. [Abstract] [Full Text] [PDF] |
||||