Skip Navigation LinksHome > May 2011 - Volume 6 - Issue 3 > HIV-1 replicative fitness in elite controllers
Current Opinion in HIV & AIDS:
doi: 10.1097/COH.0b013e3283454cf5
Elite controllers: Edited by Steven G. Deeks, Alexandre Harari and Joel Blankson

HIV-1 replicative fitness in elite controllers

Lobritz, Michael Aa; Lassen, Kara Gb; Arts, Eric Jc

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Abstract

Purpose of review: Differential rates of disease progression are obviously multifactorial, but the virulence of the actual infecting virus is most frequently ignored as potential source of slow or rapid disease progression. In this review, the argument will be made that nearly all elite suppressors are infected by weak HIV-1 strain (in terms of replicative capacity). Whether this poor virus replication is the cause of elite suppression or the consequence of a strong immune response remains a leading question in the field.

Recent findings: Although numerous research studies have related HIV-1 replicative capacity/fitness in tissue culture to virulence within patients, this review will focus on several recent and key discoveries on the important role of HIV-1 fitness in elite suppression. First, elite suppressors appear to harbor HIV-1 variants that encode Gag, Pol, and Env proteins that are less efficient than their counterparts of HIV-1 in typical/chronic progressors. Second, the actual HIV-1 clone(s) that establish acute infection may be less fit in patients who become elite controllers as compared with typical progressors. Finally, the fitness costs of cytotoxic T lymphocyte escape in HIV-1 may be easily compensated by secondary mutations if the infecting strain is capable of high replication kinetics and rapid evolution. A strain with weak replicative capacity might not compensate for fitness loss or even generate the initial escape mutations.

Summary: A combination of good, anti-HIV-1 host genetics (e.g. HLA-B*57) along with infection by a ‘whimpy’ HIV-1 strain may be necessary for elite suppression, whereas only one of these may lead to slow progression and viremia.

© 2011 Lippincott Williams & Wilkins, Inc.

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