Human Immunodeficiency Virus (HIV) is the causal agent of acquired immunodeficiency syndrome (AIDS), a disease characterized by the depletion of CD4+ T cells which impairs immune response. Analysis of HIV-1 infected patients has identified two distinctive phenotypes that differ in length of time towards the development of AIDS, Rapid Progressor (RP) and Long-Term Non-Progressor (LTNP) patients. The cause of the differences between these two groups is a process that is still under investigation. Hints about a possible cause have been attributed to the discovery of mutations in the viral protein R (Vpr) that have been associated with these phenotypes: mutations producing the isoforms R36W to RP patients and R77Q to LTNP patients. It has been suggested that these mutations play an important role in the depletion of CD4+ T cells, however more studies are needed to clarify and support this idea. This study examines the effect of the two isoforms in the infection of human primary CD4+ T cells and a model cell line, using the viral strain HIV-1 JR-CSF and derived strains to which the aforementioned mutations have been induced. Our results show that after infection, isoform R77Q has the capacity to significantly induce more apoptosis (identified by Annexin V staining) than Vpr wild type (WT) and the viral strain expressing the isoform R36W. Moreover, R36W significantly induces more cell death by necrosis than R77Q. Notably, the differences found in the way these isoforms of Vpr induce necrosis and apoptosis support the idea of the correlation between strains harboring these mutations and the phenotypes of RP and LTNP patients.



College and Department

Life Sciences; Microbiology and Molecular Biology



Date Submitted


Document Type





HIV-1, AIDS, viral protein R (Vpr), apoptosis.



Included in

Life Sciences Commons