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Pairwise Growth Competition Assay for Determining the Replication Fitness of Human Immunodeficiency Viruses
Published on: May 4, 2015
HIV-1 replicative fitness in elite controllers
Michael A Lobritz1, Kara G Lassen, Eric J Arts
1Department of Medicine, Stanford University Hospital and Clinics, Palo Alto, USA.
Current Opinion in HIV and AIDS
|March 25, 2011
Summary
Elite HIV-1 controllers often harbor weaker virus strains, suggesting viral fitness impacts disease progression. This viral weakness, combined with host genetics, may be key to elite suppression.
Area of Science:
- Virology
- Immunology
- Infectious Diseases
Background:
- Disease progression in Human Immunodeficiency Virus type 1 (HIV-1) infection varies significantly among individuals.
- While host genetics are known to influence disease course, the role of the infecting HIV-1 strain's virulence is often overlooked.
Purpose of the Study:
- To review the evidence supporting the hypothesis that Human Immunodeficiency Virus type 1 (HIV-1) strain fitness is a critical factor in elite suppression.
- To explore the relationship between viral replicative capacity and the ability of certain individuals to control HIV-1 without antiretroviral therapy.
Main Methods:
- Review of recent research on HIV-1 replicative capacity and its association with elite suppression.
- Analysis of studies comparing viral fitness markers (Gag, Pol, Env proteins) in elite controllers versus typical progressors.
- Examination of the impact of cytotoxic T lymphocyte escape mutations on viral fitness.
Main Results:
- Elite suppressors tend to harbor HIV-1 variants with reduced efficiency in Gag, Pol, and Env protein function compared to typical progressors.
- The initial HIV-1 clone in elite controllers may possess lower fitness than strains in individuals with chronic progression.
- Weak HIV-1 strains may struggle to compensate for fitness losses from immune escape mutations, unlike highly replicative strains.
Conclusions:
- Elite suppression likely results from a synergistic effect of favorable host genetics (e.g., HLA-B*57) and infection with a low-replicating HIV-1 strain.
- Either strong host immunity or a weak viral strain alone may contribute to slower disease progression but are less likely to achieve complete viral control.
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