DETERMINATION OF PLASMA VIRAL LOAD IN HIV-1 INFECTION BY QUANTITATIVECOMPETITIVE POLYMERASE CHAIN-REACTION

Objectives: To better characterize viral load profiles through the cou rse of HIV-1 disease and in response to treatment, and to further eval uate quantitative competitive polymerase chain reaction for measuremen t of viral load, we extended our comparative evaluation of this and ot her viral load measurements to a total of 118 patients, representing a ll stages of HIV-1 disease. Design: For cross-sectional analysis acros s the spectrum of HIV-1 disease, plasma viral load was evaluated in 11 2 HIV-1-infected patients by quantitative competitive polymerase chain reaction analysis, plasma p24 antigen assay, plasma immune complex-di ssociated p24 antigen assay and an endpoint dilution viral culture. Lo ngitudinal specimens from six additional patients were analyzed, exten ding from the time of presentation with symptomatic acute HIV-1 infect ion through up to more than 2 years of follow-up. Longitudinal specime ns were also studied for three patients over the period of initiation of zidovudine treatment, for 6 weeks of treatment and following tempor ary withdrawal of the treatment. Methods: All measurement techniques w ere assessed in replicate aliquots of plasma. Results: Quantitative co mpetitive polymerase chain reaction was the most sensitive measure of viral load, and was best correlated with CD4+ T-cell counts. In longit udinally studied patients, this technique also allowed measurement of plasma virus levels throughout the period of follow-up, even when cult ure and p24 assays became negative following resolution of acute HIV-1 infection. The quantitative competitive polymerase chain reaction was also able to detect rapid and substantial changes in viral load assoc iated with initiation and temporary withdrawal of antiviral treatment. Conclusions: The quantitative competitive polymerase chain reaction i s promising as a sensitive and accurate method for measuring plasma vi ral load in HIV-l-infected patients, and is useful for following chang es in viral load over the natural history of infection and following t reatment intervention. The technique is particularly useful for patien ts with >200 x 10(6) CD4+ T cells/l, in whom other viral markers are t ypically negative.