Hepatitis C virus (HCV), a common blood-borne infection with an estimated 180 million people infected worldwide, causes neurocognitive impairment (NCI) in up to one-third of those with chronic infection. Multiple factors contribute to brain injury and include indirect mechanisms (chronic immune activation and liver damage) and direct mechanisms (infection of glial cells, CNS inflammation, and HCV protein-related neurotoxicity). Identification of factors that include laboratory assays conducted as part of routine clinical care (e.g. alanine aminotransferase (ALT), aspartate aminotransferase (AST), AST to platelet ratio index (APRI), and HCV RNA levels) may predict NCI in HCV+ individuals who can then be targeted for early HCV treatment. The objective of our study was to determine whether host factors and HCV RNA predict NCI in HCV+ individuals.
A cross-sectional study of 275 HCV+ individuals enrolled from 1995-2015 in the HIV Neurobehavioral Research Program who had undergone comprehensive neuropsychological (NP) testing using a test battery that covers 7 neurocognitive ability domains (verbal fluency, information processing speed, learning, memory, executive functions, attention and working memory, fine motor skills). Impairment was defined as global deficit score (GDS) ≥ 0.5. Laboratory assays included routine tests (complete blood count and comprehensive metabolic panel), APRI and MELD scores, and HCV RNA. Analyses were done to correlate host and viral factors to overall NCI and individual neurocognitive domain impairment.
Eighty-six out of 275 (31%) participants had NCI (GDS ≥ 0.5). Analyses showed that host and viral factors did not predict overall NCI or individual domain impairment in HCV+ participants (p values > 0.05).
NCI, measured using comprehensive NP battery, prevalence in HCV+ individuals in our cohort was similar to published studies. Host and HCV factors tested in routine clinical care do not predict NCI. Future studies should measure biomarkers indicative of direct effect on the brain, such as host and viral factors in cerebrospinal fluid and neuroimaging changes, to better delineate predictors of NCI in individuals with chronic HCV infections.
S. Letendre, None
A. Mccutchan, None
R. Ellis, None
I. Grant, None
A. Bharti, None