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HCV/HIV Co-infection Affects Neurocognitive Performance But Not Diffusion Tensor Imaging Measures
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Reported by Jules Levin
CROI 2010 SF Feb 16-19
Huiling Peng1, Jewell Thomas1, Neva Parker1 , Tammie Benzinger1 , David Clifford1 ,Robert Paul2 , Beau Ances1
1Washington University in St Louis, Saint Louis, MO, USA and 2University of Missouri-St Louis, US, St. Louis, MO, USA
ABSTRACT
Background: Hepatitis C virus (HCV) is a frequent co-infection with HIV. Both affect brain function raising the possibility of synergistic interactions. We utilized a brief neuropsychometric screen and diffusion tensor imaging to investigate the relationship between neurological function and white matter integrity in mono (n=15) and co-infected (n=13) participants. We hypothesized that co-infected subjects would have more white matter abnormalities and neurocognitive impairment.
Methods: Neuropsychometric assessment included Trailmaking A/B and the digit symbol test (DST). Raw scores were standardized into Z scores, and a composite neuropsychological (NPZ3) score constructed from the average of standardized values. Diffusion tensor imaging measures of fractional anisotropy, mean diffusivity, and axial and radial diffusivity were obtained. Subjects taking ART were subdivided into either mono or co-infected based on serum HCV antibody status. HIV status was characterized by CD4 count and viral load. Diffusion tensor imaging indices were mapped to a common whole brain white matter skeleton for between-subject voxel-wise analysis. Regions-of-interest corresponding to the cingulum and genu of the corpus callosum were selected based on previous studies. Independent t-tests were utilized to assess possible differences in neuropsychometric and neuroimaging measures between mono and co-infected subjects.
Results: HIV+ subjects within the 2 groups did not differ in regards to sex (P =0.94) or education (P =0.77), but were dissimilar for age with co-infected subjects being older (P =0.001). Co-infected participants were more impaired than mono-infected HIV+ subjects on each neuropsychological test with Trailmaking B (P =0.01) and DST (P =0.04) significantly different. Diffusion tensor imaging values for mean diffusivity (P =0.15) and axial diffusivity (P =0.07) were lower for co-infected HIV+ subjects, but no significant differences occurred for regions-of-interest diffusion tensor imaging measures. No correlation between CD4 or HIV viral load and diffusion tensor imaging measures or NPZ3 score.
Conclusions: The combination of HIV/HCV co-infection affected brief neurocognitive screening, but not neuroimaging measures. Neither neuropsychological nor neuroimaging measures correlated with existing HIV serum markers. This lack of association may reflect relatively good virologic control by ART. Clinically significant neurocognitive dysfunction but not neuroimaging abnormalities are exacerbated by HCV infection in the setting of optimally treated HIV infection.
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