Next Article in Journal
The Enigmatic Origin of Papillomavirus Protein Domains
Next Article in Special Issue
Investigations of Pro- and Anti-Apoptotic Factors Affecting African Swine Fever Virus Replication and Pathogenesis
Previous Article in Journal
An Adenovirus-Vectored Influenza Vaccine Induces Durable Cross-Protective Hemagglutinin Stalk Antibody Responses in Mice
Previous Article in Special Issue
Interference of Apoptosis by Hepatitis B Virus
Article Menu
Issue 8 (August) cover image

Export Article

Open AccessReview
Viruses 2017, 9(8), 237;

Host and Viral Factors in HIV-Mediated Bystander Apoptosis

Center of Emphasis in Infectious Diseases, Department of Biomedical Sciences, Texas Tech University Health Sciences Center, 5001 El Paso Dr., El Paso, TX 79905, USA
Authors to whom correspondence should be addressed.
Academic Editor: Marc Kvansakul
Received: 7 July 2017 / Revised: 14 August 2017 / Accepted: 16 August 2017 / Published: 22 August 2017
(This article belongs to the Special Issue Viral Infection and Apoptosis)
Full-Text   |   PDF [648 KB, uploaded 23 August 2017]   |  


Human immunodeficiency virus (HIV) infections lead to a progressive loss of CD4 T cells primarily via the process of apoptosis. With a limited number of infected cells and vastly disproportionate apoptosis in HIV infected patients, it is believed that apoptosis of uninfected bystander cells plays a significant role in this process. Disease progression in HIV infected individuals is highly variable suggesting that both host and viral factors may influence HIV mediated apoptosis. Amongst the viral factors, the role of Envelope (Env) glycoprotein in bystander apoptosis is well documented. Recent evidence on the variability in apoptosis induction by primary patient derived Envs underscores the role of Env glycoprotein in HIV disease. Amongst the host factors, the role of C-C Chemokine Receptor type 5 (CCR5), a coreceptor for HIV Env, is also becoming increasingly evident. Polymorphisms in the CCR5 gene and promoter affect CCR5 cell surface expression and correlate with both apoptosis and CD4 loss. Finally, chronic immune activation in HIV infections induces multiple defects in the immune system and has recently been shown to accelerate HIV Env mediated CD4 apoptosis. Consequently, those factors that affect CCR5 expression and/or immune activation in turn indirectly regulate HIV mediated apoptosis making this phenomenon both complex and multifactorial. This review explores the complex role of various host and viral factors in determining HIV mediated bystander apoptosis. View Full-Text
Keywords: HIV; AIDS; apoptosis; bystander; Env; CCR5; immune activation; fusion; hemifusion; gp41 HIV; AIDS; apoptosis; bystander; Env; CCR5; immune activation; fusion; hemifusion; gp41

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
Printed Edition Available!
A printed edition of this Special Issue is available here.

Share & Cite This Article

MDPI and ACS Style

Garg, H.; Joshi, A. Host and Viral Factors in HIV-Mediated Bystander Apoptosis. Viruses 2017, 9, 237.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Viruses EISSN 1999-4915 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top