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Cognitive function associated with increased microglia activation in patients with HCV

Preserved cognitive function was associated with increased microglia activation with predominance in the basal ganglia in patients with HCV, according to recent findings published in Journal of Viral Hepatitis.

“This study evaluates microglia activation in HCV-infected patients with only mild liver disease in context of absence or presence of chronic fatigue, mood disturbances, history of interferon therapy and cognitive dysfunction, using the binding of [¹¹C]-PK11195 to the TSPO receptor,” the researchers wrote. “The TSPO receptor is located on the outer mitochondrial membrane of microglia, astrocytes and endothelial cells.”

About 50% of patients with HCV also develop chronic fatigue and deficits in concentration, attention and memory. These symptoms are independent of liver disease grade and virus replication rate. Because HCV can infect monocytes and macrophages, it could use the immune system to migrate over the blood brain barrier to infect the brain. In fact, HCV replication was found in the microglia, which contains the immune competent cells of the brain. The researchers aimed to determine whether neuropsychiatric symptoms or cognitive dysfunction in HCV-infected patients are related to microglia activation and whether microglia activation differs between HCV polymerase chain reaction positive and negative as well as patients with and without a history of an interferon therapy.

The researchers assessed microglia activation in vivo in 22 patients with chronic HCV and compared them with six healthy controls. The researchers assessed microglia activation using [¹¹C]-PK11195 positron emission tomography combined with magnetic resonance tomography for anatomical localization. The researchers divided the patients by their PCR status, Fatigue Impact Scale (FIS) score and attention test sum (ATS) score.

They found that 12 patients were HCV PCR positive, of which seven had an abnormal FIS and seven had an abnormal ATS. They found that 10 patients were HCV PCR negative, of which five had an abnormal FIS and five had an abnormal ATS. Compared with controls, patients without attention deficits showed a significantly higher accumulation of [¹¹C]-PK11195 in the putamen (P = .05), caudate nucleus (P = .03) and thalamus (P = .04). Patients with and without fatigue did not differ significantly regarding their specific tracer binding in PET.

“In conclusion, [¹¹C]-PK11195 BPnd measurement showed a significant negative correlation between ATS and [¹¹C]-PK11195 binding suggesting a protective role of microglia activation in HCV infection associated with encephalopathy,” the researchers wrote. “Further studies looking at the long term pathophysiological effect of microglia activation in HCV infection with higher patient numbers and different HCV genotypes are needed to verify our conclusion.”– by Will Offit

Disclosure: The researchers report no relevant financial disclosures.