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Updated: Jun 3, 2026

Measurement of In Vitro Integration Activity of HIV-1 Preintegration Complexes

Measurement of In Vitro Integration Activity of HIV-1 Preintegration Complexes

Published on: February 22, 2017

Quantitation of HIV-1 Entry Cofactor Expression.

J L Riley¹, R G Carroll

¹Walter Reed Army Institute of Research, Rockville, MD.

Methods in Molecular Medicine

|March 8, 2011

Summary

This summary is machine-generated.

Human immunodeficiency virus type 1 (HIV-1) entry into CD4+ T-lymphocytes requires the CD4 receptor and an additional cofactor. The α-chemokine receptor fusin/CXCR4 and three β-chemokine receptors (CCR2b, CCR3, CCR5) have been identified as crucial HIV-1 entry cofactors.

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Area of Science:

Immunology
Virology
Cell Biology

Background:

HIV-1 infection initiates via CD4 receptor binding on T-lymphocytes.
CD4 expression alone is insufficient for HIV-1 entry, indicating a need for cofactors.
The identity of these essential entry cofactors was previously unknown.

Purpose of the Study:

To identify the cellular cofactor(s) required for HIV-1 entry.
To elucidate the mechanism of HIV-1 cell entry beyond CD4 binding.
To characterize the role of chemokine receptors in HIV-1 pathogenesis.

Main Methods:

Investigated HIV-1 entry into CD4+ T-lymphocytes.
Assessed the permissiveness of non-human cells expressing CD4 for HIV-1 entry.
Identified specific chemokine receptors functioning as HIV-1 entry cofactors.

Main Results:

The α-chemokine receptor fusin/CXCR4 was identified as the entry cofactor for T-cell line-tropic HIV-1 isolates.
Three β-chemokine receptors, CCR2b, CCR3, and CCR5, were subsequently identified as additional HIV-1 entry cofactors.
This research rapidly advanced the understanding of HIV-1 cellular tropism.

Conclusions:

HIV-1 entry into target cells is a multi-step process requiring both the CD4 receptor and specific chemokine receptors.
CXCR4, CCR2b, CCR3, and CCR5 act as critical cofactors for HIV-1 entry, influencing viral tropism.
The identification of these cofactors provides key insights into HIV-1 pathogenesis and potential therapeutic targets.