- Steven G Deeks, associate professor of medicine (email@example.com)1
- 1 University of California, San Francisco and San Francisco General Hospital, San Francisco, CA 94110, USA
- Correspondence to: S G Deeks
- Accepted 18 May 2006
It has been about 10 years since the first report that three drug combination antiretroviral therapy can durably suppress HIV replication.1 Subsequent studies have confirmed that when used appropriately highly active antiretroviral therapy (see box 1) can suppress viral replication to such low levels that the virus is unable to generate drug resistance mutations. Theoretically, once this level of viral suppression is achieved, treatment should work indefinitely, and the long term risk of morbidity and morality related to HIV associated immunodeficiency becomes negligible. Experience to date suggests that lifelong suppression of HIV is feasible.
This review is aimed at informing clinicians about the current management of HIV infection. Authoritative and continuously updated reviews are available on the web (for example, the US Department of Health and Human Services treatment guidelines at www.hivatis.org); this review does not attempt to exhaustively summarise the literature or to provide guidance to clinicians with expertise in HIV. Rather, I summarise those issues that are likely to confront clinicians, including clinicians who do not routinely treat people infected with HIV.
Sources and selection criteria
I searched PubMed databases for studies pertaining to antiretroviral therapy and its complications, lipodystrophy and lipoatrophy, and immune reconstitution. I also consulted recently published national and international treatment guidelines and considered unpublished data presented at international meetings.
What is the goal of therapy?
HIV seems to be designed to mutate and evolve as rapidly as possible. This evolutionary capacity is the result of at least three properties: an extremely high rate of virus turnover (at least 1010 new virions are produced per day), a high mutation rate (about one mutation per new virion), and an impressive capacity of many HIV proteins to function in the face of multiple amino acid changes (for example, at least 33 of the 99 amino acids in HIV protease can mutate and cause drug resistance …