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

Anila Seelamgari, Anil Maddukuri, Reem Berro, Cynthia de la Fuente, Kylene Kehn, Longwen Deng, Shabnam Dadgar, Maria Elena Bottazzi, Elodie Ghedin, Anne Pumfery, Fatah Kashanchi

Research output: Contribution to journalReview articlepeer-review


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.

Original languageEnglish (US)
Pages (from-to)2388-2413
Number of pages26
JournalFrontiers in bioscience : a journal and virtual library
StatePublished - Sep 1 2004

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology
  • General Immunology and Microbiology


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