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Previous Volume 344:472-480 February 15, 2001 Number 7 Next

	Full Text PDF Editorial by Frenkel, L. M. Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited PubMed Citation

ABSTRACT

Background In many patients with human immunodeficiency virus (HIV) infection, therapy with potent antiretroviral drugs does not result in complete suppression of HIV replication. The effect of cessation of therapy in these patients is unknown.

Methods Sixteen patients who had a plasma HIV RNA level of more than 2500 copies per milliliter during combination antiretroviral-drug therapy were randomly assigned, in a 2:1 ratio, to discontinue or continue therapy. Plasma HIV RNA levels, CD4 cell counts, and drug susceptibility were measured weekly. Viral replicative capacity was measured at base line and at week 12.

Results Discontinuation of therapy for 12 weeks was associated with a median decrease in the CD4 cell count of 128 cells per cubic millimeter and an increase in the plasma HIV RNA level of 0.84 log copies per milliliter. Virus from all patients with detectable resistance at entry became susceptible to HIV-protease inhibitors within 16 weeks after the discontinuation of therapy. Drug susceptibility began to increase a median of six weeks after the discontinuation of therapy and was temporally associated with increases in plasma HIV RNA levels and decreases in CD4 cell counts. Viral replicative capacity, measured by means of a recombinant-virus assay, was low at entry into the study and increased after therapy was discontinued. Despite the loss of detectable resistance in plasma, resistant virus was cultured from peripheral-blood mononuclear cells in five of nine patients who could be evaluated. Plasma HIV RNA levels, CD4 cell counts, and drug susceptibility remained stable in the patients who continued therapy.

Conclusions Despite the presence of reduced drug susceptibility, antiretroviral-drug therapy can provide immunologic and virologic benefit. This benefit reflects continued antiviral-drug activity and the maintenance of a viral population with a reduced replicative capacity.

Source Information

From the University of California, San Francisco, and San Francisco General Hospital, San Francisco (S.G.D., R.H.); ViroLogic, South San Francisco, Calif. (T.W., N.S.H., C.J.P.); Gladstone Institute of Virology and Immunology, San Francisco (T.L., M.H., J.D.B., J.M.M., R.M.G.); and the Department of Nutritional Sciences, University of California, Berkeley, Berkeley (M.K.H.). Presented in part at the Seventh Conference on Retroviruses and Opportunistic Infections, San Francisco, January 31–February 2, 2000, and at the Eighth Conference on Retroviruses and Opportunistic Infections, Chicago, February 4–8, 2001.

Address reprint requests to Dr. Deeks at 995 Potrero Ave., San Francisco General Hospital, San Francisco, CA 94110, or at sdeeks{at}php.ucsf.edu.

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