HIV-1 Induced Bystander Apoptosis

Viruses

Himanshu Garg¹  Jonathon Mohl² 

[1] Center of Excellence for Infectious Disease, Department of Biomedical Science, Texas Tech University Health Sciences Center, 5001 El Paso Dr, MSB-1 Annex, El Paso, TX 79905, USA;

关键词: HIV;    AIDS;    apoptosis;    bystander;    Env;    CCR5;    immune activation;    fusion;    hemifusion;    gp41;   

DOI  :  10.3390/v4113020

来源: mdpi

【 摘 要 】

Apoptosis of uninfected bystander cells is a key element of HIV pathogenesis and believed to be the driving force behind the selective depletion of CD4+ T cells leading to immunodeficiency. While several viral proteins have been implicated in this process the complex interaction between Env glycoprotein expressed on the surface of infected cells and the receptor and co-receptor expressing bystander cells has been proposed as a major mechanism. HIV-1 utilizes CD4 as the primary receptor for entry into cells; however, it is the viral co-receptor usage that greatly influences CD4 decline and progression to AIDS. This phenomenon is relatively simple for X4 viruses, which arise later during the course of the disease, are considered to be highly fusogenic, and cause a rapid CD4+ T cell decline. However, in contrast, R5 viruses in general have a greater transmissibility, are encountered early during the disease and have a lesser pathogenic potential than the former. The above generalization gets complicated in numerous situations where R5 viruses persist throughout the disease and are capable of causing a rigorous CD4+ T cell decline. This review will discuss the multiple factors that are reported to influence HIV induced bystander apoptosis and pathogenesis including Env glycoprotein phenotype, virus tropism, disease stage, co-receptor expression on CD4+ T cells, immune activation and therapies targeting the viral envelope.

【 授权许可】

CC BY   
© 2012 by the authors; licensee MDPI, Basel, Switzerland.