Does Acute Hepatitis C Infection Affect the Central Nervous System in HIV-1 Infected Individuals?

A. Winston; L. Garvey; E. Scotney; D. Yerrakalva; J. M. Allsop; E. C. Thomson; V. P. B. Grover; J. Main; J. I. Cox; M. Wylezinska; S. D. Taylor-Robinson


J Viral Hepat. 2010;17(6):419-426. 

In This Article

Abstract and Introduction


Central nervous system (CNS) manifestations of chronic hepatitis C virus (HCV) and chronic human immune deficiency virus-1 (HIV-1) infections have been reported, but the impact of acute HCV infection on the CNS is unknown. A total of 10 individuals with chronic stable HIV-1 with documented acute HCV (HCV-RNA polymerase chain reaction positive and HCV antibody negative, group 1) underwent cerebral proton magnetic resonance spectroscopy (MRS) using acquisition parameters to quantify myo-inositol/creatine (mI/Cr) ratio in the right basal ganglia (RBG). Two matched control groups also underwent MRS; group 2: ten with chronic HIV-1 and no evidence of HCV, and group 3: ten with no evidence of HIV or HCV. Subjects also underwent computerized neurocognitive assessments (CogState™). RBG mI/Cr ratio in group 1 (acute HCV in a background of HIV) was significantly lower than that in groups 2 and 3 [2.90 (±0.7) vs 3.34 (±0.4) and 3.43 (±0.4), mean (SD) for group 1 vs 2 and 3 respectively, P = 0.049], with 50% of subjects in group 1 having a mI/Cr ratio below the lowest observed ratio in either of the other groups. On neurocognitive testing, significant defects in the monitoring domain were observed in group-1, compared with matched controls (P = 0.021). Acute HCV in HIV-1 infected subjects is associated with CNS involvement. Clinicians should be vigilant of early CNS involvement when assessing subjects with acute HCV.


In recent years, many extrahepatic manifestations associated with chronic hepatitis C virus (HCV) infection have been described in the absence of significant chronic liver disease, such as neuropsychological symptoms[1,2] and cryoglobulinaemia.[3] The neuropsychological findings most commonly observed include reduction in processing speed and working memory ability.[4,5] In chronic human immune deficiency virus (HIV) infection, similar findings have also been reported in both the pre- and post-antiretroviral therapy (ART) eras.[6] Since the advent of ART, although the incidence of severe cognitive decline in HIV-1 infected individuals has reduced,[6] a rising incidence in minor cognitive decline has been recognized.[7,8] With the advent of therapeutic options for chronic HCV infection, improvements in neurocognitive function have also been observed after successful antiviral treatment.[9]

In both these chronic viral infections, biological mechanisms have been observed, such as pathological abnormalities in brain autopsy samples from HIV-1 infected subjects,[10,11] evidence of HIV or HCV replication in the central nervous system (CNS)[12–15] and changes in cerebral metabolites when measured by in vivo proton magnetic resonance spectroscopy (1H MRS).[5,16–19] Such changes include elevated myo-Inositol (mI) and choline (Cho) in frontal white matter (FWM) and basal ganglia respectively in chronic HCV,[2,20] and reduced levels of N-acetyl aspartate (NAA) and increased levels of mI and Cho in HIV-1 infection.[17,19]

Although viral entry into the CNS, which may cause symptomatic disease, in acute HIV-1 infection has been well described,[21] no such data exist on whether acute HCV infection affects the CNS, or if acute HCV is associated with neurocognitive decline. In many cases, HCV infection does not present to healthcare providers in the acute stage. However, recently, sexually transmitted outbreaks of acute HCV infection have been reported in HIV-1 chronically infected men-who-have-sex-with-men (MSM) in Europe, the US and Australia.[22,23] As many individuals with known chronic HIV-1 infection in resource-rich settings regularly attend for healthcare, and as this group may be susceptible to more severe neurological disease from co-morbidities, we aimed to assess if acute HCV infection was associated with changes in neurocognitive function or CNS metabolites in a cohort of HIV-1 infected subjects.


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