Viral liver disease is an umbrella term for liver damage caused by a viral infection. Hepatitis B and C (HBV and HCV) are the most common viral infections leading to liver damage. Despite the different underlying viral infections, the pathogenesis of fibrosis can be divided in two stages. The acute inflammatory stage is followed by a chronic inflammatory stage with simultaneously occurring inflammation, tissue destruction, and repair processes.

How many have viral liver disease?
The prevalence of HBV and HCV varies throughout the world. In 2015, an estimated 2 billion people globally were infected with HBV leading lto 650,000 deaths a year. HCV was estimated to infect 71 million people in 2015.

How is viral liver disease treated?
Treating the underlying viral infection is most optimal. Currently, several antiviral drugs (lamivudine, adefovir, entecavir, telbivudine, tenofovir, emtricitabine, standard, and PEG-IFN) have shown to delay the progression of cirrhosis but rarely cure the viral infection. Lifelong treatment is therefore necessary in most cases. 

How is viral liver disease diagnosed?
The diagnosis of viral liver disease relies primarily on symptoms. Currently, diagnosis is based on the presence of a viral agent and on blood tests to assess the liver function. If blood tests suggest decreased liver function and advanced liver damage, further tests including imaging and liver biopsies might be necessary.

The medical need for biomarkers in viral liver disease today is two-fold. Firstly, the prediction of progression to especially cirrhosis has proven difficult. Patients react differently to viral infections and prediction of which patients progress and when is not currently possible. Secondly, there is a need for new treatments that can better manage or cure viral liver disease. To achieve this, there is a need for biomarkers to improve the screening process and evaluation of treatment efficacy.

Prognostic, predictive and efficacy biomarkers have the potential to greatly benefit patients, by aiding in more accurate clinical trials and directing the most appropriate treatment at the right time, preventing the end stage liver disease death process. Nordic Bioscience offers an accurate liver fibrosis biomarker panel that gives insight into disease progression.

Viral liver disease is characterized by both inflammation and scar formation in tissue (fibrosis).
The liver is rich in different collagens, proteoglycans and matricellular proteins. These proteins are remodeled as part of liver homeostasis and regeneration. During remodeling, proteins are broken down and rebuild as part of normal repair and maintenance of the tissue. In viral liver disease, the balance between degradation and formation of tissue is interrupted resulting in net formation (build-up and scar formation) of the tissue. Protein fingerprint serum biomarkers for liver fibrosis can quantify this tissue turnover directly in serum plasma samples.

While there are several diagnostic and disease activity measures in the liver field, some are invasive whereas others have limited predictive capacity. Therefore, there is still a medical and drug development need for biomarkers that can characterize and quantify structural tissue change and predict disease progression. The tissue-derived Protein Fingerprint biomarkers of liver function can be measured in serum and plasma and can accurately quantify changes in tissue turnover in the different layers of liver tissues in the individual patient.

Biomarkers for liver disease and tissue characterization:
Pericellular fibrosis by type IV collagen fragments: C4M, PRO-C4.

Bridging fibrosis by type III collagen fragments: PRO-C3, PC3X, C3M.

Protein Fingerprint biomarkers measured in serum are differently expressed in hepatitis B and C (HBV and HCV). HBV is generally a higher tissue turnover disease with increased collagen formation and degradation.

Collagen formation (type III collagen; PRO-C3, type IV collagen; PRO-C4) and degradation (type I collagen; C3M, type III collagen; C3M, type IV collagen; C4M, type VI collagen; C6M) are differently remodeled in the same fibrosis stages in HCV and HBV.

Reference: Nielsen MJ et al. APT 2016

Type III collagen formation (PRO-C3) measured in serum is related to outcome in hepatitis C (HCV). PRO-C3 is higher in patients with an outcome compared to none and patients with high PRO-C3 are more likely to have a sooner outcome than patients with low PRO-C3.

Protein Fingerprint biomarkers allow pharmacodynamic profiling of novel treatments by measuring protein degradation fragments directly in a serum sample. Baseline levels of PRO-C3 predict changes in fibrogenesis in response to treatment in hepatitis C (HCV) patients.

Percentage changes of PRO-C3 in response to Farglitazar treatment is dependent on baseline PRO-C3 levels.

Reference: Karsdal MA et al. Am J Physiol Gastrointest Liver Physiol, 2016

Baseline PRO-C3 is predictive of changes in ISHAK score in response to Farglitazar treatment in hepatitis C patients (HCV).

Percentage changes of ISHAK in response to Farglitazar treatment is dependent on baseline PRO-C3 levels.

Reference: Karsdal MA et al. Am J Physiol Gastrointest Liver Physiol, 2016

Please don't hesitate to contact us if you have any questions or other inquiries.

Please don't hesitate to contact us if you have any questions or other inquiries.

Are you interested in learning more about Nordic Bioscience?
Enter your information in the form and a representative will contact you shortly.

By submitting this form you agree to our terms and conditions.

We use cookies on our site to enable essential services and functionalities, and collect data in regards to visitor information to provide the best possible experience. By using our website, you agree to our Privacy Policy and our cookies usage. Cookie Policy Privacy Statement