Journal of Antimicrobial Chemotherapy, Vol 40, 765-777, Copyright © 1997 by The British Society for Antimicrobial Chemotherapy
GJ Moyle
Massive viral turnover and the high error rate of reverse transcriptase
create the potential for drug-resistant viral variants to appear rapidly
under the selective pressure of antiretroviral therapy. Loss of antiviral
effect in treatment compliant persons is most commonly coincident with the
appearance of viral mutants with reduced drug sensitivity. Thus, detection
of viral resistance may represent an early marker of therapy failure.
Similarly, substantial reduction in viral replication in the plasma
compartment, to below quantification of a viral load assay, is associated
with a sustained therapeutic response and delayed development of viral
resistance. Information on patterns of resistance to and cross-resistance
between antiretroviral agents are increasingly well characterized and
represents an important consideration when deciding how to combine and/or
sequence antiretrovirals to achieve optimal antiviral effects. When
switching therapy, the change of several agents in the treatment regimen is
currently recommended. The use of novel means of evaluating resistance,
such as a genotypic probe, may guide clinicians in choosing an agent to
which the patient's dominant viral quasispecies remains sensitive,
potentially increasing the chances of achieving a therapeutic response.
However, no studies using resistance to guide clinical decision making have
yet been reported and available sequencing studies have focused largely on
switching or adding therapies to patients who have received zidovudine
monotherapy. Thus, no resistance driven treatment algorithm is currently
available.
REVIEWS
Current knowledge of HIV-1 reverse transcriptase mutations selected during nucleoside analogue therapy: the potential to use resistance data to guide clinical decisions
Kobler Clinic, Chelsea and Westminster Hospital, London, UK.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  J. Stebbing, T. Powles, M. Nelson, and M. Bower Significance of Variation Within HIV, EBV, and KSHV Subtypes J Int Assoc Physicians AIDS Care (Chic Ill), September 1, 2006; 5(3): 93 - 102. [Abstract] [PDF]
|
|
|
|
 |
|
 A. Senescau, A. Berry, F. Benoit-Vical, O. Landt, R. Fabre, J. Lelievre, S. Cassaing, and J.-F. Magnaval Use of a Locked-Nucleic-Acid Oligomer in the Clamped-Probe Assay for Detection of a Minority Pfcrt K76T Mutant Population of Plasmodium falciparum J. Clin. Microbiol., July 1, 2005; 43(7): 3304 - 3308. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Maga, U. Hübscher, M. Pregnolato, D. Ubiali, G. Gosselin, and S. Spadari Potentiation of Inhibition of Wild-Type and Mutant Human Immunodeficiency Virus Type 1 Reverse Transcriptases by Combinations of Nonnucleoside Inhibitors and D- and L-({beta})-Dideoxynucleoside Triphosphate Analogs Antimicrob. Agents Chemother., April 1, 2001; 45(4): 1192 - 1200. [Abstract] [Full Text]
|
|
|
|
 |
|
 H. Huang, R. Chopra, G. L. Verdine, and S. C. Harrison Structure of a Covalently Trapped Catalytic Complex of HIV-1 Reverse Transcriptase: Implications for Drug Resistance Science, November 27, 1998; 282(5394): 1669 - 1675. [Abstract] [Full Text]
|
|