Abstract
Chronic hepatitis C virus (HCV) infection is closely associated with a plethora of diseases, including cancers and autoimmune disorders. However, the distinct triggers and cellular networks leading to such HCV-derived diseases are poorly understood. Around 8% of the human genome consists of human endogenous retroviruses. They are usually silenced but can be reactivated by environmental conditions, including viral infections. Our current understanding indicates that the activation of one specific family—namely, HERV-K(HML-2)—is linked to distinct pathologies, including cancer and autoimmunity. In this study, we analyzed the transcription levels of HERV-K(HML-2) in 42 HCV-infected patients receiving direct-acting antiviral therapies. Samples from the start of treatment until 12 weeks post-treatment were investigated. Our results show increased HERV-K(HML-2) transcript levels in patients with HCV-derived liver cirrhosis throughout the observation period. Several clinical parameters specifying poor liver function are positively correlated with HERV-K(HML-2) expression. Of note, patients without a sustained viral clearance showed a drastic increase in HERV-K(HML-2) transcript levels. Together, our data suggest that increased HERV-K(HML-2) expression is correlated with reduced liver function as well as therapy success in HCV-infected patients.
Highlights
Liver cirrhosis was present in 31 patients with direct-acting antivirals (DAAs)
In two patients the hepatitis C virus (HCV) RNA levels could again be detected after 12 weeks, suggesting a lack of viral clearance upon DAA
The alanine amino transferase (ALAT) (p < 0.001) (Figure 2C), aspartate amino transferase (ASAT) (p < 0.001) (Figure 2D), and Gamma-Glutamyl-Transferase (GGT) (p < 0.001) (Figure 2E) activities significantly decreased in our cohort between the start and end of treatment (EOT) and remained low until SVR12
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Around 71 million people worldwide are chronically infected with hepatitis C. With the development of direct-acting antivirals (DAAs), sustained viral response rates of >90%. Could be achieved [1,2]. Hepatitis C virus (HCV) infection remains a risk factor for the development of liver cirrhosis and hepatocellular carcinoma (HCC). Several other diseases such as neurocognitive disorders or mixed cryoglobulinemia [3] are associated with the infection of persistent, exogenous viruses such as HCV. The exact mechanisms driving these related diseases are still not completely understood
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