Published online before print July 22, 2003
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
* Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland; and
Department of Pathology, George Washington University School of Medicine, Washington, D.C.
1Correspondence: Building 30, Rm. 320, 30 Convent Drive, MSC4352, NIDCR, NIH, Bethesda, MD 20892-4352. E-mail: smwahl{at}dir.nidcr.nih.gov
Human immunodeficiency virus type 1 (HIV-1) infection of CD4+ T lymphocytes leads to their progressive loss, whereas HIV-1-infected macrophages appear to resist HIV-1-mediated apoptotic death. The differential response of these two host-cell populations may be critical in the development of immunodeficiency and long-term persistence of the virus. Multiple contributing factors may favor the macrophage as a resilient host, not only supporting infection by HIV-1 but also promoting replication and persistence of this member of the lentivirus subfamily of primate retroviruses. An encounter between macrophages and R5 virus engages a signal cascade eventuating in transcriptional regulation of multiple genes including those associated with host defense, cell cycle, nuclear factor-
B regulation, and apoptosis. It is important that enhanced gene expression is transient, declining to near control levels, and during this quiescent state, the virus continues its life cycle unimpeded. However, when viral replication becomes prominent, an increase in host genes again occurs under the orchestration of viral gene products. This biphasic host response must fulfill the needs of the parasitic virus as viral replication activity occurs and leads to intracellular and cell surface-associated viral budding. Inroads into understanding how HIV-1 co-opts host factors to generate a permissive environment for viral replication and transmission to new viral hosts may provide opportunities for targeted interruption of this lethal process.
Key Words: opportunistic infections • cDNA expression array • p21 • SLPI • Vpr
This article has been cited by other articles:
 |
|
 |
|
  T. Greenwell-Wild, N. Vazquez, W. Jin, Z. Rangel, P. J. Munson, and S. M. Wahl Interleukin-27 inhibition of HIV-1 involves an intermediate induction of type I interferon Blood, August 27, 2009; 114(9): 1864 - 1874. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. P Ryan An alternative approach to medical genetics based on modern evolutionary biology. Part 2: retroviral symbiosis J R Soc Med, August 1, 2009; 102(8): 324 - 331. [Full Text] [PDF]
|
|
|
|
 |
|
 E. Cassol, L. Cassetta, C. Rizzi, M. Alfano, and G. Poli M1 and M2a Polarization of Human Monocyte-Derived Macrophages Inhibits HIV-1 Replication by Distinct Mechanisms J. Immunol., May 15, 2009; 182(10): 6237 - 6246. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Ballana, E. Pauls, J. Senserrich, B. Clotet, F. Perron-Sierra, G. C. Tucker, and J. A. Este Cell adhesion through {alpha}V-containing integrins is required for efficient HIV-1 infection in macrophages Blood, February 5, 2009; 113(6): 1278 - 1286. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J Molepo, A Pillay, B Weber, S A Morse, and A A Hoosen Molecular typing of Treponema pallidum strains from patients with neurosyphilis in Pretoria, South Africa Sex Transm Inf, June 1, 2007; 83(3): 189 - 192. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. M. Wahl, T. Greenwell-Wild, and N. Vazquez HIV accomplices and adversaries in macrophage infection J. Leukoc. Biol., November 1, 2006; 80(5): 973 - 983. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. S. Giri, M. Nebozhyn, L. Showe, and L. J. Montaner Microarray data on gene modulation by HIV-1 in immune cells: 2000-2006 J. Leukoc. Biol., November 1, 2006; 80(5): 1031 - 1043. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M.C. Herzberg, A. Weinberg, and S.M. Wahl (C3) The Oral Epithelial Cell and First Encounters with HIV-1 Advances in Dental Research, April 1, 2006; 19(1): 158 - 166. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Peng, K. J. Lei, W. Jin, T. Greenwell-Wild, and S. M. Wahl Induction of APOBEC3 family proteins, a defensive maneuver underlying interferon-induced anti-HIV-1 activity J. Exp. Med., January 23, 2006; 203(1): 41 - 46. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Vazquez, T. Greenwell-Wild, N. J. Marinos, W. D. Swaim, S. Nares, D. E. Ott, U. Schubert, P. Henklein, J. M. Orenstein, M. B. Sporn, et al. Human Immunodeficiency Virus Type 1-Induced Macrophage Gene Expression Includes the p21 Gene, a Target for Viral Regulation J. Virol., April 1, 2005; 79(7): 4479 - 4491. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Ma, T. Greenwell-Wild, K. Lei, W. Jin, J. Swisher, N. Hardegen, C. T. Wild, and S. M. Wahl Secretory Leukocyte Protease Inhibitor Binds to Annexin II, a Cofactor for Macrophage HIV-1 Infection J. Exp. Med., November 15, 2004; 200(10): 1337 - 1346. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. R. Coberley, J. J. Kohler, J. N. Brown, J. T. Oshier, H. V. Baker, M. P. Popp, J. W. Sleasman, and M. M. Goodenow Impact on Genetic Networks in Human Macrophages by a CCR5 Strain of Human Immunodeficiency Virus Type 1 J. Virol., November 1, 2004; 78(21): 11477 - 11486. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. G. Collman, C.-F. Perno, S. M. Crowe, M. Stevenson, and L. J. Montaner HIV and cells of macrophage/dendritic lineage and other non-T cell reservoirs: new answers yield new questions J. Leukoc. Biol., November 1, 2003; 74(5): 631 - 634. [Abstract] [Full Text] [PDF]
|
|
