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HCV infection shares pathological features with metabolic syndrome, especially liver steatosis, due to HCV's effects on lipid and glucose metabolism,[22] and thus presents an increased cardiovascular risk.[23] The magnitude of HCV-3 infection-related steatosis correlates with the level of viral replication,[24] and it disappears after successful anti-viral therapy,[25] suggesting a cause and effect relationship between the virus and the genotype

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Skagen et al., 2016)

The current hypothesis is that antibodies against specific platelet glycoproteins, such as glycoprotein IIb/IIIa (GPIIb/IIIa) complex proteins are considered to play a role in DIIT [105]