Induction of apoptosis by protease-defective particle preparations of human immunodeficiency virus type 1 is specific to a subset of U937-derived subclones

International Immunology
M KameokaK Ikuta

Abstract

Several recent reports support the hypothesis that apoptosis occurring in leukocytes of human immunodeficiency virus type 1 (HIV-1)-infected individuals is important in progression to AIDS. Specifically, apoptosis of uninfected bystander cells appears critical in the pathogenesis of disease. Here, we present evidence that protease-defective, gp120-containing HIV-1 (L-2) particle preparations specifically induce apoptosis in cells obtained from a subset of promonocytic U937-derived subclones. The rate of apoptosis induction was inversely correlated with the susceptibility of the U937 subclones to wild-type HIV-1 infection. Three types of apoptosis experiments were performed: DNA content analysis by flow cytometry, apoptotic nuclear degradation by fluorescent microscopy and DNA fragmentation analysis by agarose gel electrophoresis. Kinetic analysis revealed that there was a slower induction of apoptosis by L-2 particle preparations than with tumor necrosis factor (TNF)-alpha or anti-Fas antibody. However, there were no significant differences in the initial binding rates of L-2 particles as well as the binding of TNF-alpha or anti-Fas antibody to the U937 subclones. The basal level of protein kinase C activity was higher in high-...Continue Reading

Related Concepts

Related Feeds

HIV/AIDS-Related Malignancies

HIV/AIDS infection increases the risk of non-communicable diseases common in the aged including HIV/AIDS-related malignancies. Discover the latest research in HIV/AIDS-related malignancies.

AIDS Malignancies (ASM)

HIV infection increases the risk of non-communicable diseases common in the aged, including cardiovascular disease, neurocognitive decline, non-aids malignancies, osteoporosis, and frailty. Discover the latest research in AIDS malignancies.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis