This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Clements, J. E.
Right arrow Articles by Zink, M. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Clements, J. E.
Right arrow Articles by Zink, M. C.

 Previous Article

Clinical Microbiology Reviews, 01 1996, 100-117, Vol 9, No. 1
Copyright © 1996 by the American Society for Microbiology. All rights reserved.

Molecular biology and pathogenesis of animal lentivirus infections

JE Clements and MC Zink
Division of Comparative Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

Lentiviruses are a subfamily of retroviruses that are characterized by long incubation periods between infection of the host and the manifestation of clinical disease. Human immunodeficiency virus type 1, the causative agent of AIDS, is the most widely studied lentivirus. However, the lentiviruses that infect sheep, goats, and horses were identified and studied prior to the emergence of human immunodeficiency virus type 1. These and other animal lentiviruses provide important systems in which to investigate the molecular pathogenesis of this family of viruses. This review will focus on two animal lentivirus models: the ovine lentivirus visna virus; and the simian lentivirus, simian immunodeficiency virus. These animal lentiviruses have been used to examine, in particular, the pathogenesis of lentivirus-induced central nervous system disease as models for humans with AIDS as well as other chronic diseases.


This article has been cited by other articles:

  • Duval, R., Bellet, V., Delebassee, S., Bosgiraud, C. (2002). Implication of caspases during maedi-visna virus-induced apoptosis. J. Gen. Virol. 83: 3153-3161 [Abstract] [Full Text]  
  • Patrick, M. K., Johnston, J. B., Power, C. (2002). Lentiviral Neuropathogenesis: Comparative Neuroinvasion, Neurotropism, Neurovirulence, and Host Neurosusceptibility. J. Virol. 76: 7923-7931 [Full Text]  
  • Nesbit, C. E., Schwartz, S. A. (2002). In Vitro and Animal Models of Human Immunodeficiency Virus Infection of the Central Nervous System. CVI 9: 515-524 [Full Text]  
  • Bruett, L., Clements, J. E. (2001). Functional Murine Leukemia Virus Vectors Pseudotyped with the Visna Virus Envelope Show Expanded Visna Virus Cell Tropism. J. Virol. 75: 11464-11473 [Abstract] [Full Text]  
  • Malashkevich, V. N., Singh, M., Kim, P. S. (2001). The trimer-of-hairpins motif in membrane fusion: Visna virus. Proc. Natl. Acad. Sci. USA 10.1073/pnas.151254798v1 [Abstract] [Full Text]  
  • Harrold, S. M., Cook, S. J., Cook, R. F., Rushlow, K. E., Issel, C. J., Montelaro, R. C. (2000). Tissue Sites of Persistent Infection and Active Replication of Equine Infectious Anemia Virus during Acute Disease and Asymptomatic Infection in Experimentally Infected Equids. J. Virol. 74: 3112-3121 [Abstract] [Full Text]  
  • Chen, H., He, J., Fong, S., Wilcox, G., Wood, C. (2000). Jembrana Disease Virus Tat Can Regulate Human Immunodeficiency Virus (HIV) Long Terminal Repeat-Directed Gene Expression and Can Substitute for HIV Tat in Viral Replication. J. Virol. 74: 2703-2713 [Abstract] [Full Text]  
  • Saman, E., Van Eynde, G., Lujan, L., Extramiana, B., Harkiss, G., Tolari, F., Gonzalez, L., Amorena, B., Watt, N., Badiola, J. (1999). A New Sensitive Serological Assay for Detection of Lentivirus Infections in Small Ruminants. CVI 6: 734-740 [Abstract] [Full Text]  
  • Li, F., Puffer, B. A., Montelaro, R. C. (1998). The S2 Gene of Equine Infectious Anemia Virus Is Dispensable for Viral Replication In Vitro. J. Virol. 72: 8344-8348 [Abstract] [Full Text]  
  • Oaks, J. L., McGuire, T. C., Ulibarri, C., Crawford, T. B. (1998). Equine Infectious Anemia Virus Is Found in Tissue Macrophages during Subclinical Infection. J. Virol. 72: 7263-7269 [Abstract] [Full Text]  
  • Gale, M. Jr., Blakely, C. M., Kwieciszewski, B., Tan, S.-L., Dossett, M., Tang, N. M., Korth, M. J., Polyak, S. J., Gretch, D. R., Katze, M. G. (1998). Control of PKR Protein Kinase by Hepatitis C Virus Nonstructural 5A Protein: Molecular Mechanisms of Kinase Regulation. Mol. Cell. Biol. 18: 5208-5218 [Abstract] [Full Text]  
  • Poeschla, E. M., Looney, D. J. (1998). CXCR4 Is Required by a Nonprimate Lentivirus: Heterologous Expression of Feline Immunodeficiency Virus in Human, Rodent, and Feline Cells. J. Virol. 72: 6858-6866 [Abstract] [Full Text]  
  • Edinger, A. L., Amedee, A., Miller, K., Doranz, B. J., Endres, M., Sharron, M., Samson, M., Lu, Z.-h., Clements, J. E., Murphey-Corb, M., Peiper, S. C., Parmentier, M., Broder, C. C., Doms, R. W. (1997). Differential utilization of CCR5 by macrophage and T cell tropic simian immunodeficiency virus strains. Proc. Natl. Acad. Sci. USA 94: 4005-4010 [Abstract] [Full Text]  
  • Malashkevich, V. N., Singh, M., Kim, P. S. (2001). The trimer-of-hairpins motif in membrane fusion: Visna virus. Proc. Natl. Acad. Sci. USA 98: 8502-8506 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»