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The Body Covers: The 6th Conference on Retroviruses and Opportunistic Infections
Late Breaker No. LB12: Viral Rebound in the Presence of Indinavir Without Protease Inhibitor Resistance

February 4, 1999

A note from TheBody.com: Since this article was written, the HIV pandemic has changed, as has our understanding of HIV/AIDS and its treatment. As a result, parts of this article may be outdated. Please keep this in mind, and be sure to visit other parts of our site for more recent information!

The observed phenomenon of viral rebound in the absence of resistance to all components of the antiviral regimen was discussed at ICAAC in September, and further described here in Havlir et al's report of 26 patients from ACTG 343. In this study, some patients were randomized to receive indinavir monotherapy folllowing a six month induction course of AZT/3TC/indinavir. Nine of these patients achieved undetectable level of virus in blood (<400 copies) at six months of therapy but then rebounded above 400 (range varied between 1000 and 100,000 copies). Upon phenotypic analysis of isolates from these patients, all were sensitive to indinavir and demonstrated no indinavir resistance mutations. An additional 17 patients were studied who were randomized to continue triple therapy (AZT/3TC/indinavir) but who also experienced viral rebound after achieving undetectable levels of virus in their blood. Again, all were found to be sensitive to indinavir on phenotypic testing, and only one out of the 17 demonstrated any genotypic resistance mutation. By contrast, 82% exhibited 3TC resistance.

Discussion continues around the reasons behind this observation. One thought -- that patients were simply not taking their drug on study -- was refuted when random indinavir levels were measured and compared between the rebounders and the non-rebounders, revealing no discernable difference. Clearly, the data cannot be explained on the basis of inadherence. One other thought is that wild-type virus (that is virus still sensitive to indinavir) emerges first after a period of immune reconstitution has occurred as a consequence of antiretroviral therapy: because there are more CD4 cells circulating during therapy, and because wild-type virus is more fit than mutant virus (though with the passage of time indinavir-resistant virus would be most certain to emerge). When performed in a similar clinical setting where viral rebound has developed after a achieving levels of undetectability, viral resistance testing may help with clinical decision-making.

A note from TheBody.com: Since this article was written, the HIV pandemic has changed, as has our understanding of HIV/AIDS and its treatment. As a result, parts of this article may be outdated. Please keep this in mind, and be sure to visit other parts of our site for more recent information!

Abstract: Viral Rebound in the Presence of Indinavir Without Protease Inhibitor Resistance
Authored by: D. Havlir, N. Hellmann, C. Petropoulos, J. Whitcomb, A. Collier, M. Hirsch, P. Tebas, and D. Richman

See Also
More on HIV Medications
More Indinavir (Crixivan) Research



  
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Please note: Knowledge about HIV changes rapidly. Note the date of this summary's publication, and before treating patients or employing any therapies described in these materials, verify all information independently. If you are a patient, please consult a doctor or other medical professional before acting on any of the information presented in this summary. For a complete listing of our most recent conference coverage, click here.

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