Viral liver disease is a generic term for liver damage caused by viral infection. Hepatitis B and C (HBV and HCV) are the most common viral infections that cause liver damage. Despite the different underlying viral infections, the pathogenesis of fibrosis can be divided into two phases. The acute inflammatory stage is followed by a chronic inflammatory stage with concurrent inflammatory, tissue destruction and repair processes.

How many people have viral liver disease?
The prevalence of HBV and HCV varies worldwide. In 2015, an estimated 2 billion people worldwide were infected with HBV, resulting in 650,000 deaths per year. An estimated 71 million people were infected with HCV in 2015.

How is viral liver disease treated?
Treatment of the underlying viral infection is best. 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. In most cases, therefore, lifelong treatment is required.

How is viral liver disease diagnosed?
Diagnosis of viral liver disease is based primarily on symptoms. Currently, diagnosis is based on the presence of a viral pathogen and blood tests to assess liver function. If blood tests indicate decreased liver function and advanced liver damage, further testing including imaging and liver biopsies may be required.

The medical need for viral liver disease biomarkers today is twofold. First, predicting disease progression, especially cirrhosis, has proven difficult. Patients respond differently to viral infections, and predicting which patients will progress and when is currently impossible. Second, there is a need for new treatments that can better control or cure viral liver disease. To achieve this, biomarkers are needed to improve the screening process and the evaluation of treatment efficacy.

Prognostic, predictive, and efficacious biomarkers have the potential to greatly benefit patients by contributing to more accurate clinical trials and by deploying the most appropriate treatment at the right time to prevent end-stage liver disease death.

Nordic Bioscience offers an accurate liver fibrosis biomarker panel that gives insight into disease progression.

Viral liver disease is characterized by both inflammation and tissue scarring (fibrosis). The liver is rich in various collagens, proteoglycans, and matricellular proteins. These proteins are remodeled as part of liver homeostasis and regeneration. During remodeling, proteins are broken down and rebuilt as part of normal tissue repair and maintenance.

In viral liver disease, the balance between tissue breakdown and rebuilding is disturbed, resulting in net tissue formation (buildup and scarring). Protein Fingerprint serum biomarkers for liver fibrosis can quantify this tissue turnover directly in serum plasma samples.

Visit our liver biomarker portfolio and choose a panel that fits your clinical research or drug development targets!

Although there are several diagnostic measures and measures of disease activity in the liver, some are invasive while others have limited predictive power. Therefore, there is still a need in medicine and drug development for biomarkers that can characterize and quantify structural tissue changes and predict disease progression. 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 tissue in individual patients.

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 differ in hepatitis B and C (HBV and HCV). HBV is usually a disease with higher tissue turnover and 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 remodeled differently 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 in PRO-C3 in response to treatment with farglitazar depend on baseline PRO-C3.

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 treatment with farglitazar in hepatitis C (HCV) patients.


Percentage changes in ISHAK in response to treatment with farglitazar depend on baseline levels PRO-C3.

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

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