Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 203, Issue 10, Pages 1474-1483Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jir060
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Funding
- University of California San Francisco (UCSF)/Gladstone Center for AIDS Research [P30 AI27763, P30 MH59037]
- UCSF-San Francisco General Hospital General Clinical Research Center
- NIAID [AI065244, AI055273]
- Center for AIDS Prevention Studies [P30 MH62246]
- UCSF Clinical and Translational Science Institute [UL1 RR024131-01]
- Roche Laboratories, Inc.
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Methods. Thirty antiretroviral therapy-treated HIV-infected CMV-seropositive participants with CD4 counts < 350 cells/mm(3) were randomized to receive valganciclovir 900 mg daily or placebo for 8 weeks, followed by an additional 4-week observation period. The primary outcome was the week 8 change in percentage of activated (CD38(+) HLA-DR+) CD8(+) T cells. Results. Fourteen participants were randomized to valganciclovir and 16 to placebo. Most participants (21 [70%] of 30) had plasma HIV RNA levels < 75 copies/mL. The median CD4 count was 190 (IQR: 134-232) cells/mm(3), and 12 (40%) of 30 had detectable CMV DNA in saliva, plasma, or semen at baseline. CMV DNA continued to be detectable at weeks 4-12 in 7 (44%) of 16 placebo-treated participants, but in none of the valganciclovir-treated participants (P = .007). Valganciclovir-treated participants had significantly greater reductions in CD8 activation at weeks 8 (P = .03) and 12 (P = .02) than did placebo-treated participants. These trends were significant even among those with undetectable plasma HIV RNA levels. Conclusions. CMV (and/or other herpesvirus) replication is a significant cause of immune activation in HIV-infected individuals with incomplete antiretroviral therapy-mediated CD4(+) T cell recovery. Clinical Trials Registration. NCT00264290.
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