Increased HERV-K(HML-2) Transcript Levels Correlate with Clinical Parameters of Liver Damage in Hepatitis C Patients.
Melanie WeberVidya Padmanabhan NairTanja BauerMartin Franz SprinzlUlrike ProtzerMichelle VincendeauPublished in: Cells (2021)
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.
Keyphrases
- hepatitis c virus
- end stage renal disease
- human immunodeficiency virus
- chronic kidney disease
- ejection fraction
- endothelial cells
- peritoneal dialysis
- poor prognosis
- sars cov
- multiple sclerosis
- rna seq
- oxidative stress
- patient reported outcomes
- squamous cell carcinoma
- mesenchymal stem cells
- risk assessment
- climate change
- big data
- single cell
- combination therapy
- bone marrow
- patient reported
- atomic force microscopy
- binding protein
- drug induced
- childhood cancer