Human immunodeficiency virus type 1 Vpr polymorphisms associated with progressor and nonprogressor individuals alter Vpr-associated functions

Following infection with Human immunodeficiency virus 1 (HIV-1) there is a remarkable variation in virus replication and disease progression. Both host and viral factors have been implicated in the observed differences in disease status. Here, we focus on understanding the contribution of HIV-1 vira...

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Published inJournal of general virology Vol. 95; no. 3; pp. 700 - 711
Main Authors Hadi, Kevin, Walker, Leah A., Guha, Debjani, Murali, Ramachandran, Watkins, Simon C., Tarwater, Patrick, Srinivasan, Alagarsamy, Ayyavoo, Velpandi
Format Journal Article
LanguageEnglish
Published England Society for General Microbiology 01.03.2014
Subjects
Animal
Disease Progression
G2 Phase Cell Cycle Checkpoints
HIV Infections - pathology
HIV Infections - physiopathology
HIV Infections - virology
HIV-1 - classification
HIV-1 - genetics
HIV-1 - isolation & purification
HIV-1 - physiology
Humans
Phylogeny
Polymorphism, Genetic
Virus Replication
vpr Gene Products, Human Immunodeficiency Virus - genetics
vpr Gene Products, Human Immunodeficiency Virus - metabolism
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Summary:Following infection with Human immunodeficiency virus 1 (HIV-1) there is a remarkable variation in virus replication and disease progression. Both host and viral factors have been implicated in the observed differences in disease status. Here, we focus on understanding the contribution of HIV-1 viral protein R (Vpr) by evaluating the disease-associated Vpr polymorphism and its biological functions from HIV-1 positive rapid progressor (RP) and long-term nonprogressor (LTNP) subjects. Results presented here show distinct variation in phenotypes of Vpr alleles from LTNP and RP subjects. Most notably, the polymorphism of Vpr at R36W and L68M associated with RP shows higher levels of oligomerization, and increased virus replication, whereas R77Q exhibits poor replication kinetics. Interestingly, we did not observe correlation with cell cycle arrest function. Together these results indicate that polymorphisms in Vpr in part may contribute to altered virus replication kinetics leading to the observed differences in disease progression in LTNP and RP groups.
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These authors contributed equally to this paper.
ISSN:0022-1317
1465-2099
1465-2099
DOI:10.1099/vir.0.059576-0