HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Figures Only Full Text Full Text (PDF) Correspondence: Submit a response Correspondence: View responses Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Clifford, D. B. Articles by Evans, S. R. PubMed PubMed Citation Articles by Clifford, D. B. Articles by Evans, S. R.

Effects of active HCV replication on neurologic status in HIV RNA virally suppressed patients

From Washington University (D.B.C., L.B., M.A.), St. Louis, MO; and Harvard School of Public Health (M.S., L.S.P., T.-m.Y., Y.Z., S.R.E.), Boston, MA.

Address correspondence and reprint requests to Dr. David B. Clifford, Box 8111, Neurology, 660 South Euclid Ave, St. Louis, MO 63110 cliffordd{at}neuro.wustl.edu

Background: Hepatitis C virus (HCV) is a frequent copathogen with HIV. Both viruses appear to replicate in the brain and both are implicated in neurocognitive and peripheral neuropathy syndromes. Interaction of the viruses is likely to be complicated and better understanding of the contributions of each virus will be necessary to make evidence-based therapeutic decisions.

Methods: This study was designed to determine if active HCV infection, identified by quantitative HCV RNA determination, is associated with increased neurocognitive deficits or excess development of distal sensory peripheral neuropathy in HIV coinfected patients with stable HIV viral suppression. The AIDS Clinical Trials Group Longitudinal Linked Randomized Trials (ALLRT) study was the source of subjects with known HIV treatment status, neurocognitive and neuropathy evaluations, and HCV status. Subjects were selected based on HCV antibody status (249 positive; 310 negative).

Results: HCV RNA viral loads were detectable in 172 participants with controlled HIV infection and available neurologic evaluations in the ALLRT. These participants were compared with 345 participants with undetectable HCV viral load and the same inclusion criteria from the same cohort. Neurocognitive performance measured by Trail-Making A or B and digit symbol testing was not dissimilar between the 2 groups. In addition, there was no significant association between active HCV replication and distal sensory neuropathy.

Conclusion: Clinically significant neurocognitive dysfunction and peripheral neuropathy were not exacerbated by active hepatitis C virus infection in the setting of optimally treated HIV infection.

Abbreviations: ALLRT = AIDS Clinical Trials Group Longitudinal Linked Randomized Trials; CI = confidence interval; HAART = highly active antiretroviral therapy; HCV = hepatitis C virus; IDU = injection drug use; VL = viral load; WAIS-R = Wechsler Adult Intelligence Scale–Revised.

Supported by NIH grants including Neurologic AIDS Research Consortium Grant NS32228 from NINDS and AIDS Clinical Trials Grant AI068636 from NIAID.

Disclosure: Author disclosures are provided at the end of the article.

Received February 9, 2009. Accepted in final form April 21, 2009.

Correspondence: