Cited by 99HIV Research and TreatmentHIV/AIDS drug development and treatmentT-cell and Retrovirus Studies

Role of viral regulatory and accessory proteins in HIV-1 replication

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Seelamgari, Anila·2004·Frontiers in Bioscience

Abstract

Human immunodeficiency virus-1 (HIV-1) is the causative agent of acquired immune deficiency syndrome (AIDS), a disease characterized by CD4+ T lymphocyte depletion. HIV-1 replicates actively in a variety of cells by encoding several regulatory (Tat and Rev) and accessory (Vpr, Vif, Vpu, and Nef) proteins. Accessory proteins, thought initially to be dispensable for infection, have now been shown to be important for efficient infection in vivo. Recent evidence suggests that certain viral proteins, like Vif, have evolved to overcome the antiviral mechanisms of the host, while proteins like Nef, which are markers for disease pathogenesis in vivo, help to increase pathogenesis by targeting bystander cells. Thus, these proteins control many aspects of the virus life cycle as well as host cell function, namely gene regulation and apoptosis. Understanding the mechanisms by which the virus is able to successfully replicate in host cells and subsequently cause gradual destruction of the immune system may yield new approaches for therapeutic strategies. In this review, we attempt to integrate information on the role of these regulatory and accessory proteins, emphasizing their interactions with other viral and cellular components, and the subsequent effect on viral replication.

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Authors
Seelamgari, A.
Affiliations
George Washington University (US)
Corresponding author
Seelamgari, Anila
Venue
Frontiers in Bioscience
Publisher
IMR Press
Published
2004
Volume
9
Issue
1-3
Pages
2388
ISSN
  • 1093-4715 (ISSN-L)
  • 1093-9946
OpenAlex
W2107174433
Cited by
98
References
329
Citations by year
2026: 2 · 2024: 2 · 2023: 2 · 2022: 5 · 2021: 2 · 2020: 4 · 2019: 2 · 2016: 6 · 2015: 4 · 2014: 5 · 2013: 5 · 2012: 9
FWCI
0.87
Type
journal article
Language
en
Open access
Locations
  • Frontiers in bioscience (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • George Washington University
  • National Institutes of Health
  • U.S. Public Health Service (A13969)
  • National Institute of Allergy and Infectious Diseases (R29AI044357, AI 44357, R01AI043894, AI43894)
Topics
  • Life Sciences › Immunology and Microbiology › Virology › HIV Research and Treatment
  • Health Sciences › Medicine › Infectious Diseases › HIV/AIDS drug development and treatment
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and Retrovirus Studies
Keywords
HIV-1, viral regulatory proteins, viral accessory proteins, Tat, Rev, Vif, Vpr, Vpu, NEF, viral replication, host-virus interaction, apoptosis, gene expression regulation, AIDS pathogenesis, CD4 depletion
MeSH terms
Viroporin Proteins, Animals, Cell Cycle, Cell Nucleus, Chromatin, Humans, Transcription, Genetic, Virus Replication, Signal Transduction, HIV-1, Transcriptional Activation, Down-Regulation, Gene Products, nef, Gene Products, rev, Gene Products, tat, Gene Expression Regulation, Viral, Gene Products, vpr, Gene Products, vif, Apoptosis, Active Transport, Cell Nucleus, Human Immunodeficiency Virus Proteins, nef Gene Products, Human Immunodeficiency Virus, vif Gene Products, Human Immunodeficiency Virus, rev Gene Products, Human Immunodeficiency Virus, tat Gene Products, Human Immunodeficiency Virus, vpr Gene Products, Human Immunodeficiency Virus, Viral Regulatory and Accessory Proteins

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