Abstract

HIV and human defense mechanisms have co-evolved to counteract each other. In the process of infection, HIV takes advantage of cellular machinery and blocks the action of the host restriction factors (RF). A small subset of HIV+ individuals control HIV infection and progression to AIDS in the absence of treatment. These individuals known as long-term non-progressors (LNTPs) exhibit genetic and immunological characteristics that confer upon them an efficient resistance to infection and/or disease progression. The identification of some of these host factors led to the development of therapeutic approaches that attempted to mimic the natural control of HIV infection. Some of these approaches are currently being tested in clinical trials. While there are many genes which carry mutations and polymorphisms associated with non-progression, this review will be specifically focused on HIV host RF including both the main chemokine receptors and chemokines as well as intracellular RF including, APOBEC, TRIM, tetherin, and SAMHD1. The understanding of molecular profiles and mechanisms present in LTNPs should provide new insights to control HIV infection and contribute to the development of novel therapies against AIDS.

Highlights

  • Both pathogens and host have an inherent variability that plays a critical role in the consequences of the infection process

  • When infected by a specific pathogen, some individuals show no sign of HIV infection or react with moderate manifestations, while others rapidly succumb to the disease

  • Subsequent studies showed the presence of fully replication-competent virus in these long-term non-progressors (LTNPs), which changed the attention to the host

Read more

Summary

Introduction

Both pathogens and host have an inherent variability that plays a critical role in the consequences of the infection process. One of the most studied genetic variations influencing HIV-1 infection and progression is the ∆32 mutation in the CCR5 gene [2], and SNPs in various chemokine receptors or HLA class I and class II alleles [3, 4].

Results
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.