David B Clifford1, Florin Vaida2, Yu-Ting Kao2, Donald R Franklin2, Scott L Letendre2, Ann C Collier2, Christina M Marra2, Benjamin B Gelman2, Justin C McArthur2, Susan Morgello2, David M Simpson2, Igor Grant2, Robert K Heaton2. 1. From Washington University (D.B.C.), St. Louis, MO; University of California (F.V., Y.-T.K., D.R.F., S.L.L., I.G., R.K.H.), San Diego; University of Washington (A.C.C., C.M.M.), Seattle; University of Texas at Galveston (B.B.G.); Johns Hopkins University (J.C.M.), Baltimore, MD; and The Icahn School of Medicine at Mount Sinai (S.M., D.M.S.), New York, NY. cliffordd@wustl.edu. 2. From Washington University (D.B.C.), St. Louis, MO; University of California (F.V., Y.-T.K., D.R.F., S.L.L., I.G., R.K.H.), San Diego; University of Washington (A.C.C., C.M.M.), Seattle; University of Texas at Galveston (B.B.G.); Johns Hopkins University (J.C.M.), Baltimore, MD; and The Icahn School of Medicine at Mount Sinai (S.M., D.M.S.), New York, NY.
Abstract
OBJECTIVE: To investigate the effect of hepatitis C virus (HCV) on neurocognitive performance in chronically HIV-infected patients enrolled in the CNS HIV Antiretroviral Therapy Effects Research (CHARTER) study. METHODS: A total of 1,582 participants in CHARTER who were tested for HCV antibody underwent neurocognitive testing; serum HCV RNA was available for 346 seropositive patients. Neurocognitive performance was compared in 408 HCV-seropositive and 1,174 HCV-seronegative participants and in a subset of 160 seropositive and 707 seronegative participants without serious comorbid neurologic conditions that might impair neurocognitive performance, using linear regression and taking into account HIV-associated and demographic factors (including IV drug use) and liver function. RESULTS: Neurocognitive performance characterized by global deficit scores and the proportion of individuals who were impaired were the same in the HCV-seropositive and HCV-seronegative groups. In univariable analyses in the entire sample, only verbal domain scores showed small statistically different superior performance in the HCV+ group that was not evident in multivariable analysis. In the subgroup without significant comorbidities, scores in all 7 domains of neurocognitive functioning did not differ by HCV serostatus. Among the HCV-seropositive participants, there was no association between neurocognitive performance and serum HCV RNA concentration. CONCLUSION: In HIV-infected patients, HCV coinfection does not contribute to neurocognitive impairment, at least in the absence of substantial HCV-associated liver damage, which was not evident in our cohort.
OBJECTIVE: To investigate the effect of hepatitis C virus (HCV) on neurocognitive performance in chronically HIV-infected patients enrolled in the CNS HIV Antiretroviral Therapy Effects Research (CHARTER) study. METHODS: A total of 1,582 participants in CHARTER who were tested for HCV antibody underwent neurocognitive testing; serum HCV RNA was available for 346 seropositive patients. Neurocognitive performance was compared in 408 HCV-seropositive and 1,174 HCV-seronegative participants and in a subset of 160 seropositive and 707 seronegative participants without serious comorbid neurologic conditions that might impair neurocognitive performance, using linear regression and taking into account HIV-associated and demographic factors (including IV drug use) and liver function. RESULTS: Neurocognitive performance characterized by global deficit scores and the proportion of individuals who were impaired were the same in the HCV-seropositive and HCV-seronegative groups. In univariable analyses in the entire sample, only verbal domain scores showed small statistically different superior performance in the HCV+ group that was not evident in multivariable analysis. In the subgroup without significant comorbidities, scores in all 7 domains of neurocognitive functioning did not differ by HCV serostatus. Among the HCV-seropositive participants, there was no association between neurocognitive performance and serum HCV RNA concentration. CONCLUSION: In HIV-infected patients, HCV coinfection does not contribute to neurocognitive impairment, at least in the absence of substantial HCV-associated liver damage, which was not evident in our cohort.
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