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Updated: Jun 17, 2026

Prediction of HIV-1 Coreceptor Usage (Tropism) by Sequence Analysis using a Genotypic Approach
Published on: December 1, 2011
Chemokine coreceptor signaling in HIV-1 infection and pathogenesis
1Department of Molecular and Microbiology, George Mason University, Manassas, Virginia, USA. ywu8@gmu.edu
Insights
Human immunodeficiency virus type 1 (HIV-1) exploits chemokine coreceptor signaling to infect resting CD4 T cells. This hijacked signaling pathway is crucial for viral entry and may contribute to HIV pathogenesis.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Chemokine coreceptors are critical for HIV-1 entry into host cells.
- While HIV-1 fusion is understood, the role of coreceptor signaling in infection remains unclear.
- Recent findings highlight signaling's necessity for latent HIV-1 infection in CD4 T cells.
Purpose of the Study:
- To revisit the role of chemokine coreceptor signaling in HIV-1 infection.
- To explore how HIV-1 may exploit host cell signaling pathways.
- To discuss the implications of coreceptor signaling in viral pathogenesis.
Main Methods:
- Review of existing literature on HIV-1 coreceptor signaling.
- Analysis of studies demonstrating signaling requirements for infection.
- Discussion of proposed mechanisms of viral exploitation of signaling networks.
Main Results:
- HIV-1 envelope binding to coreceptors triggers both fusion and signaling.
- Chemokine coreceptor signaling is essential for latent HIV-1 infection of resting CD4 T cells.
- Virus-hijacked signaling may facilitate HIV-1 entry and pathogenesis.
Conclusions:
- Chemokine coreceptor signaling is a key, yet underappreciated, factor in HIV-1 infection.
- HIV-1 likely exploits host chemokine signaling pathways to enhance infectivity.
- Understanding this aberrant signaling is vital for developing new therapeutic strategies against HIV-1.
Abstract:
Binding of the HIV-1 envelope to its chemokine coreceptors mediates two major biological events: membrane fusion and signaling transduction. The fusion process has been well studied, yet the role of chemokine coreceptor signaling in viral infection has remained elusive through the past decade. With the recent demonstration of the signaling requirement for HIV latent infection of resting CD4 T cells, the issue of coreceptor signaling needs to be thoroughly revisited. It is likely that virus-mediated signaling events may facilitate infection in various immunologic settings in vivo where cellular conditions need to be primed; in other words, HIV may exploit the chemokine signaling network shared among immune cells to gain access to downstream cellular components, which can then serve as effective tools to break cellular barriers. This virus-hijacked aberrant signaling process may in turn facilitate pathogenesis. In this review, we summarize past and present studies on HIV coreceptor signaling. We also discuss possible roles of coreceptor signaling in facilitating viral infection and pathogenesis.
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