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 Volsky, D. J.
Right arrow Articles by Potash, M. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Volsky, D. J.
Right arrow Articles by Potash, M. J.

 Previous Article  |  Next Article 

J. Virol., Jun 1996, 3823-3833, Vol 70, No. 6
Copyright © 1996, American Society for Microbiology

Interference to human immunodeficiency virus type 1 infection in the absence of downmodulation of the principal virus receptor, CD4

DJ Volsky, M Simm, M Shahabuddin, G Li, W Chao and MJ Potash
Molecular Virology Laboratory, St. Luke's-Roosevelt Hospital Center, New York 10019, USA. djv4@columbia.edu

It is thought that interference during human immunodeficiency virus type 1 (HIV-1) infection is established by downmodulation of the principal virus receptor, CD4. Here we present evidence to the contrary. At various times after primary infection, we superinfected T cells in vitro by exposure to a genetically distinct viral clone or to a virus carrying the chloramphenicol acetyltransferase gene. Replication of each virus strain was determined by restriction enzyme analysis of total cellular DNA, by PCR amplification of viral DNA, or by assay of cell extracts for chloramphenicol acetyltransferase activity. We found that efficient viral interference is established within 24 h of infection at a multiplicity of infection of 1. At that time, expression of viral structural proteins was low and infected cells displayed undiminished levels of surface CD4 and were fully susceptible to virus binding and fusion. Superinfection by either cell- free HIV-1 or cocultivation was blocked. Cells resistant to superinfection by HIV-1 remained susceptible to Moloney murine leukemia and vaccinia viruses. No interference was observed 4 h after primary infection or in cells infected with either UV-inactivated HIV-1 or a mutant virus defective in virus-cell fusion activity, indicating that binding of primary virus to CD4 is insufficient to prevent superinfection. The minimum viral requirements for this interference are that HIV-1 must be able to enter cells and synthesize viral DNA; Tat-mediated transcription is dispensable. Our results support the existence of a novel pathway to interference to HIV-1 infection, which we term postentry interference, which blocks superinfection during intracellular phases of the virus life cycle.


This article has been cited by other articles:

  • Levy, D. N., Aldrovandi, G. M., Kutsch, O., Shaw, G. M. (2004). From The Cover: Dynamics of HIV-1 recombination in its natural target cells. Proc. Natl. Acad. Sci. USA 101: 4204-4209 [Abstract] [Full Text]  
  • Bukovsky, A. A., Song, J.-P., Naldini, L. (1999). Interaction of Human Immunodeficiency Virus-Derived Vectors with Wild-Type Virus in Transduced Cells. J. Virol. 73: 7087-7092 [Abstract] [Full Text]  
  • Van Den Broeke, A., Bagnis, C., Ciesiolka, M., Cleuter, Y., Gelderblom, H., Kerkhofs, P., Griebel, P., Mannoni, P., Burny, A. (1999). In Vivo Rescue of a Silent tax-Deficient Bovine Leukemia Virus from a Tumor-Derived Ovine B-Cell Line by Recombination with a Retrovirally Transduced Wild-Type tax Gene. J. Virol. 73: 1054-1065 [Abstract] [Full Text]  
  • Lewis, M. G., Yalley-Ogunro, J., Greenhouse, J. J., Brennan, T. P., Jiang, J. B., VanCott, T. C., Lu, Y., Eddy, G. A., Birx, D. L. (1999). Limited Protection from a Pathogenic Chimeric Simian-Human Immunodeficiency Virus Challenge following Immunization with Attenuated Simian Immunodeficiency Virus. J. Virol. 73: 1262-1270 [Abstract] [Full Text]  
  • Pistello, M., Matteucci, D., Cammarota, G., Mazzetti, P., Giannecchini, S., Del Mauro, D., Macchi, S., Zaccaro, L., Bendinelli, M. (1999). Kinetics of Replication of a Partially Attenuated Virus and of the Challenge Virus during a Three-Year Intersubtype Feline Immunodeficiency Virus Superinfection Experiment in Cats. J. Virol. 73: 1518-1527 [Abstract] [Full Text]  
  • Gundlach, B. R., Reiprich, S., Sopper, S., Means, R. E., Dittmer, U., Matz-Rensing, K., Stahl-Hennig, C., Uberla, K. (1998). Env-Independent Protection Induced by Live, Attenuated Simian Immunodeficiency Virus Vaccines. J. Virol. 72: 7846-7851 [Abstract] [Full Text]  
  • D'Aloja, P., Olivetta, E., Bona, R., Nappi, F., Pedacchia, D., Pugliese, K., Ferrari, G., Verani, P., Federico, M. (1998). gag, vif, and nef Genes Contribute to the Homologous Viral Interference Induced by a Nonproducer Human Immunodeficiency Virus Type 1 (HIV-1) Variant: Identification of Novel HIV-1-Inhibiting Viral Protein Mutants. J. Virol. 72: 4308-4319 [Abstract] [Full Text]  
  • Saha, K., Bentsman, G., Chess, L., Volsky, D. J. (1998). Endogenous Production of beta -Chemokines by CD4+, but Not CD8+, T-Cell Clones Correlates with the Clinical State of Human Immunodeficiency Virus Type 1 (HIV-1)-Infected Individuals and May Be Responsible for Blocking Infection with NonSyncytium-Inducing HIV-1 In Vitro. J. Virol. 72: 876-881 [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»