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Updated: May 5, 2026

A Restriction Enzyme Based Cloning Method to Assess the In vitro Replication Capacity of HIV-1 Subtype C Gag-MJ4 Chimeric Viruses
Published on: August 31, 2014
Human immunodeficiency virus type 1 Vpr polymorphisms associated with progressor and nonprogressor individuals alter
Kevin Hadi1, Leah A Walker1, Debjani Guha1
1Department of Infectious Diseases and Microbiology, University of Pittsburgh Graduate School of Public Health, Pittsburgh, PA 15261, USA.
Human immunodeficiency virus 1 (HIV-1) Vpr protein variations influence viral replication. Specific Vpr polymorphisms linked to rapid disease progression show increased replication, unlike those in long-term nonprogressors.
Area of Science:
- Virology
- Immunology
- Genetics
Background:
- Human immunodeficiency virus 1 (HIV-1) infection exhibits diverse replication rates and disease progression.
- Host and viral factors contribute to these variations in disease status.
- The viral protein R (Vpr) is a key viral factor influencing HIV-1 pathogenesis.
Purpose of the Study:
- To investigate the role of HIV-1 Vpr protein polymorphisms in disease progression.
- To compare Vpr functions between rapid progressors (RP) and long-term nonprogressors (LTNP).
Main Methods:
- Analysis of Vpr alleles from HIV-1 positive RP and LTNP subjects.
- Evaluation of Vpr polymorphism, oligomerization, and virus replication kinetics.
- Assessment of Vpr's cell cycle arrest function.
Main Results:
- Distinct Vpr phenotypes were observed between LTNP and RP subjects.
- Vpr polymorphisms at R36W and L68M, associated with RP, showed higher oligomerization and increased virus replication.
- The R77Q polymorphism exhibited poor replication kinetics.
- No correlation was found between Vpr polymorphisms and cell cycle arrest function.
Conclusions:
- HIV-1 Vpr polymorphisms contribute to altered virus replication kinetics.
- These Vpr variations may partially explain differences in disease progression observed in LTNP and RP individuals.
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