Viral Hepatitis: Diagnosis, Treatment and Management—2nd Edition

A special issue of Diseases (ISSN 2079-9721).

Deadline for manuscript submissions: 30 September 2026 | Viewed by 2064

Special Issue Editors


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Guest Editor
Medilife International Hospital, Istanbul 34523, Turkey
Interests: infectious disease; liver diseases
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Guest Editor
Division of Gastroenterology and Hepatology, Department of Internal Medicine, Charleston Area Medical Center (CAMC), Northeast Ohio Medical University (NEOMED), Rootstown, OH, USA
Interests: abdominal pain; bloating; bloody stool; celiac disease; Clostridium difficile colitis (C. diff); constipation; Crohn’s disease; diarrhea; dysphagia; gastroesophageal reflux disease (GERD); hepatitis C; inflammatory bowel disease (IBD); irritable bowel syndrome (IBS); liver diseases; nausea; pancreatitis; nutrition; vomiting; colon cancer screening
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Department of Gastroenterology and Hepatology, West Virginia University, Charleston, WV, USA
Interests: colorectal cancer; colon polyps; esophageal cancer; celiac disease; Crohn's disease; inflammatory bowel disease; lactose intolerance; chronic diarrhea; constipation; gastrointestinal reflux disease
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Special Issue Information

Dear Colleagues,

This Special Issue is the second edition of the Special Issue “Viral Hepatitis: Diagnosis, Treatment and Management”, available at https://www.mdpi.com/journal/diseases/special_issues/LA151P824R.

We are pleased to invite you to contribute to our Special Issue entitled “Viral Hepatitis: Diagnosis, Treatment and Management”. Viral hepatitis is a main public health concern that can become chronic and eventually lead to end-stage liver disease. Viral hepatitis is also one of the leading indications for liver transplantation. Hepatitis can be classified into acute and chronic based on the duration of the inflammation in the liver. Depending on the etiology of hepatitis, the severity of acute hepatitis can range from mild and self-limiting to severe illness requiring liver transplantation.

Viral hepatitis is most frequently caused by the hepatitis A virus (HAV), hepatitis B virus (HBV), and hepatitis C virus (HCV). These three viruses can lead to an acute disease with signs and symptoms of nausea, abdominal pain, fatigue, malaise, and jaundice. Other viruses known to cause hepatitis include the hepatitis D virus (HDV) and hepatitis E virus (HEV). Acute infection with HBV and HCV can lead to chronic infection. For HDV infection to occur, HBV infection must have occurred previously or concurrently. Chronic hepatitis may lead to the development of liver fibrosis, cirrhosis, hepatocellular carcinoma, and portal hypertension, corresponding to significant morbidity and mortality.

This Special Issue aims to reveal the current evidence for the diagnosis, treatment and management of acute and chronic viral hepatitis. It aims to discuss the challenges associated with screening, diagnosis, and referral of viral hepatitis, current and future treatment options, and areas of potential research interests.

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following:

  • Screening and diagnosis of viral hepatitis;
  • Diagnosis and management of acute hepatitis (A, B, C, D, E);
  • Diagnosis and management of chronic hepatitis (B, C, D);
  • Prevention of reactivation of HBV infection;
  • Management of coinfections (HBV/HCV, HBV-HIV, HCV/HIV);
  • Management of chronic HBV and HCV infections in special patient groups;
  • Management of cirrhosis, hepatocellular carcinoma, and portal hypertension.

I/We look forward to receiving your contributions.

Dr. Resat Ozaras
Dr. Veysel Tahan
Dr. Ebubekir Dağlılar
Guest Editors

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Keywords

  • viral hepatitis
  • acute hepatitides (A, B, C, D, E)
  • chronic hepatitides (B, C, D)
  • HBV infection
  • HBV/HCV
  • HBV-HIV
  • HCV/HIV
  • cirrhosis
  • hepatocellular carcinoma
  • portal hypertension

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Published Papers (3 papers)

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Research

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31 pages, 13068 KB  
Article
A Unified Histopathological Framework of Liver Fibrogenesis in Chronic Viral Hepatitis B, C and Coinfection
by Alina Dumitrache (Păunescu), Nicoleta Anca Ionescu (Șuțan), Liliana Cristina Soare, Maria Cristina Ponepal, Ana Cătălina Țânțu, Monica Marilena Țânțu, Ileana Monica Baniță and Cătălina Gabriela Pisoschi
Diseases 2026, 14(5), 165; https://doi.org/10.3390/diseases14050165 - 8 May 2026
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Abstract
Background: Chronic hepatitis B and C remain major causes of progressive liver disease, while HBV–HCV coinfection is associated with accelerated fibrosis and hepatocellular injury. Methods: This study evaluated integrated biochemical, histopathological, and immunohistochemical features in patients with chronic hepatitis B (CHB, n = [...] Read more.
Background: Chronic hepatitis B and C remain major causes of progressive liver disease, while HBV–HCV coinfection is associated with accelerated fibrosis and hepatocellular injury. Methods: This study evaluated integrated biochemical, histopathological, and immunohistochemical features in patients with chronic hepatitis B (CHB, n = 29), chronic hepatitis C (CHC, n = 15), and CHB+C coinfection (CHB+C, n = 10). Liver biopsies were assessed using Ishak and METAVIR scoring systems, alongside immunohistochemical analysis of α-smooth muscle actin (α-SMA), transforming growth factor-β1 (TGF-β1), CD5L, and glial fibrillary acidic protein (GFAP), quantified by H-score. These findings were correlated with biochemical, hematological, and prognostic parameters. Results: Coinfected patients exhibited significantly higher serum ALT, AST, and GGT levels (p ≤ 0.011) and increased CD5L expression (median H-score 197.5 vs. 135 in CHB, p = 0.009), indicating enhanced macrophage-associated inflammatory activity. Although fibrosis stages were comparable across groups, median H-scores for α-SMA, TGF-β1, and GFAP showed a consistent upward trend in CHB+C, suggesting intensified profibrogenic signaling. Principal Component Analysis identified distinct biochemical clusters related to hepatocellular injury, hepatic functional impairment (synthetic and excretory axis), and lipid metabolism. Conclusions: These findings highlight a multidimensional pattern of liver injury in chronic viral hepatitis, with CHB+C coinfection amplifying profibrogenic and hepatocellular markers, both biochemically and histologically. Full article
(This article belongs to the Special Issue Viral Hepatitis: Diagnosis, Treatment and Management—2nd Edition)
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Review

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15 pages, 685 KB  
Review
Ocular Clues to Liver Disease: A Strategic Diagnostic Lens
by Muhammad Dahshan, Hassan Dahshan, Ayhan Basoglu and Huseyin Kadikoy
Diseases 2026, 14(5), 152; https://doi.org/10.3390/diseases14050152 - 24 Apr 2026
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Abstract
Background/Objectives: Hepatic diseases frequently present with ocular manifestations that aid diagnosis, provide prognostic data, and guide therapy. Despite the clear utility of the liver–eye axis, the literature lacks reviews that categorize these manifestations by etiology. This review evaluates current evidence to identify ocular [...] Read more.
Background/Objectives: Hepatic diseases frequently present with ocular manifestations that aid diagnosis, provide prognostic data, and guide therapy. Despite the clear utility of the liver–eye axis, the literature lacks reviews that categorize these manifestations by etiology. This review evaluates current evidence to identify ocular findings that serve as clinical tools for diagnosis, prognosis, and therapeutic monitoring of hepatic pathologies. Methods: A narrative review was conducted using PubMed and Google Scholar to identify English-language articles addressing ocular manifestations associated with liver disease. The primary search encompassed publications from 2000 to 2025, with inclusion of select foundational works published prior to 2000 when they represented seminal studies establishing diagnostic criteria, pathophysiological mechanisms, or natural history data not superseded by subsequent research. Search terms included combinations of liver, hepatic, hepatitis, cirrhosis, cholestasis, eye, ocular, retina, cornea, sclera, conjunctiva, ophthalmic manifestations, and specific disease names. All study designs were eligible. Society guidelines, systematic reviews, and studies from high-impact journals were prioritized. The final selection comprised 59 references representing the most authoritative sources across the spectrum of hepatic conditions. Results: A spectrum of ocular findings linked to distinct hepatic conditions was identified. Manifestations with established clinicopathologic associations were categorized into congenital and acquired etiologies. Congenital liver pathologies included metabolic disorders (Wilson disease, galactosemia, lysosomal storage disorders) and syndromic/genetic causes (Alagille syndrome, hereditary hemochromatosis). Acquired liver diseases encompassed infectious (hepatitis B/C), drug-induced and iatrogenic (interferon, immune checkpoint inhibitors), nutritional (vitamin A deficiency), neoplastic (metastatic hepatocellular carcinoma), and cirrhotic causes. Conclusions: Specific ocular signs raise clinical suspicion for underlying liver disease and warrant targeted hepatic evaluation. Recognizing these associations facilitates earlier diagnosis and improves outcomes. Systematic screening for these signs is supported in at-risk populations, and prospective validation studies should establish their sensitivity and specificity. Full article
(This article belongs to the Special Issue Viral Hepatitis: Diagnosis, Treatment and Management—2nd Edition)
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22 pages, 1489 KB  
Review
Chronic Hepatitis C in the Direct-Acting Antivirals Era: Carcinogenesis and Clinical Implications
by Yucel Aydin, Ramazan Kurt, Veysel Tahan and Ebubekir Daglilar
Diseases 2025, 13(12), 393; https://doi.org/10.3390/diseases13120393 - 5 Dec 2025
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Abstract
Chronic hepatitis C virus (HCV) infection remains a major global health burden, responsible for substantial morbidity and mortality despite the advent of curative antiviral therapy. HCV induces hepatic injury and carcinogenesis through direct viral effects, persistent inflammation, oxidative stress, and metabolic disturbance. The [...] Read more.
Chronic hepatitis C virus (HCV) infection remains a major global health burden, responsible for substantial morbidity and mortality despite the advent of curative antiviral therapy. HCV induces hepatic injury and carcinogenesis through direct viral effects, persistent inflammation, oxidative stress, and metabolic disturbance. The introduction of direct-acting antivirals (DAAs) has revolutionized therapy, achieving sustained virologic response rates exceeding 95% and transforming HCV from a chronic, progressive disease into a curable infection. Nevertheless, viral eradication does not fully normalize hepatic or systemic risk. Patients with advanced fibrosis or cirrhosis continue to face an elevated incidence of hepatocellular carcinoma (HCC) and other complications, reinforcing the need for long-term monitoring. This review summarizes current knowledge of the molecular mechanisms underlying HCV-mediated carcinogenesis, the partial restoration of hepatic homeostasis following DAA-induced cure, and the clinical implications for surveillance and management in the post-HCV era. By integrating insights from molecular virology, immunopathogenesis, and clinical hepatology, the review highlights how persistent epigenetic and inflammatory footprints may sustain oncogenic potential even after viral clearance. A comprehensive understanding of these processes is essential for optimizing HCC prevention strategies, guiding surveillance policies, and advancing future therapeutic innovations aimed at complete hepatic recovery. Full article
(This article belongs to the Special Issue Viral Hepatitis: Diagnosis, Treatment and Management—2nd Edition)
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