基因1、2型丙肝患者血脂情况对HCV RNA的影响

Chen-Hua Liu*. Department of Internal Medicine， National Taiwan University Hospital， Taipei， Taiwan

Chronic hepatitis C virus (HCV) infection， a leading cause of cirrhosis， hepatocellular carcinoma (HCC) and liver failure， affects more than 170 million people worldwide. Despite the improving sustained virologic response (SVR) rates with the currently approved interferon-based therapies， these therapies are limited by the on-treatment side effects and by the relatively inferior response in patients with HCV genotype 1 infection. Several host and viral factors have been implicated to influence the disease progression and the treatment response in chronic hepatitis C (CHC) patients， and efforts to modify these factors to the optimize the therapeutic response are ungently needed.

Recently， host metabolic factors， such as diabetes mellitus (DM)， insulin resistance (IR)， hepatic steatosis， and impaired lipid metabolism have been found to closely associated with HCV infection. Ample clinical evidence indicate that deranged lipid profiles and hepatic steatosis correlate with HCV infection， suggesting their potential roles of predicting therapeutic responses.

Furthermore， it has been demonstrated in vitro that the lipid rafts， mainly composed of cholesterol and sphingolipid， and the lipid droplet， an organelle for storing neutral lipids， play the crutial roles of producing infectious viruses. While HCV genotypes 3 virus may directly cause hepati steatosis， the association of viral loads in HCV genotype 1 or 2 virues， the mainly types in infected individuals in the world， with the lipid profiles still remains elusive. The search of the association between lipid profiles and the HCV genotypic differences is therefore important.

A recent study recruting 531 patients with either HCV genotype 1 or 2 infection showed that high serum triglyceride， totoal cholesterol and low-density lipoprotein (LDL) correlated with high HCV RNA levels. In patients with low body mass index (BMI)， high modeal assessment of insulin resistance index (HOMA-IR) and total cholesterol levels were associated with high HCV viral load. After stratification by HCV genotypes， lipid profiles were highly associated with HCV viral load in genotype 2， rather than genotype 1 patients. The study indicated that differed mechanisms of deranged lipid profiles between HCV genotype 1 and 2 viruses. Because the casual relationship of the viral load and the lipid profiles are still to be determined， manipulation of the lipid profiles aiming in improving the anti-HCV therapy deserves further studies.