Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
6.4
3.3
Journals
Pathogens
Special Issues
Pathogenesis of Viral Hepatitis
share announcement

Pathogenesis of Viral Hepatitis

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Viral Pathogens".

Deadline for manuscript submissions: 28 February 2026 | Viewed by 3153

Special Issue Editor

Dr. Po-Yuan Ke

E-Mail Website
Guest Editor
Department of Biochemistry & Molecular Biology, Chang Gung University, Taoyuan 33302, Taiwan
Interests: Liver Diseases

Special Issue Information

Dear Colleagues,

Viral hepatitis leads to a significant burden on public health worldwide. Each hepatitis virus, including hepatitis A, B, C, D, and E infection, may encompass a broad and diverse spectrum of clinical symptoms, from acute liver failure to chronic end-stage liver diseases. In the past decades, research breakthroughs have promoted the development of vaccines that can successfully prevent infection by hepatitis A, B, and E as well as effective antiviral-acting agents for treating hepatitis B and C; however, the molecular progress involved in the pathogenesis of viral hepatitis is not comprehensively understood. In particular, the molecular mechanisms underlying how hepatitis B, C, and D chronic infection results in the development of late-stage liver diseases, including steatosis, fibrosis, cirrhosis, and hepatocellular carcinoma, remain unclear. This Special Issue aims to cover the current knowledge and cutting-edge research on the molecular virology of hepatitis viruses, host cell–hepatitis virus interactions, the pathogenesis of viral-hepatitis-induced liver diseases, and new directions for designing therapeutic strategies for clinical use. We invite contributions from reviews and original papers reporting recent efforts in this field.

Dr. Po-Yuan Ke
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pathogens is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • hepatitis virus
  • viral hepatitis
  • liver disease
  • steatosis
  • fibrosis
  • cirrhosis
  • liver injury
  • liver

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

31 pages, 41731 KiB  
Article
Hepatitis C Virus NS5A Activates Mitophagy Through Cargo Receptor and Phagophore Formation
by Yuan-Chao Hsiao, Chih-Wei Chang, Chau-Ting Yeh and Po-Yuan Ke
Pathogens 2024, 13(12), 1139; https://doi.org/10.3390/pathogens13121139 - 23 Dec 2024
Viewed by 1543
Abstract
Chronic HCV infection is a risk factor for end-stage liver disease, leading to a major burden on public health. Mitophagy is a specific form of selective autophagy that eliminates mitochondria to maintain mitochondrial integrity. HCV NS5A is a multifunctional protein that regulates the [...] Read more.
Chronic HCV infection is a risk factor for end-stage liver disease, leading to a major burden on public health. Mitophagy is a specific form of selective autophagy that eliminates mitochondria to maintain mitochondrial integrity. HCV NS5A is a multifunctional protein that regulates the HCV life cycle and may induce host mitophagy. However, the molecular mechanism by which HCV NS5A activates mitophagy remains largely unknown. Here, for the first time, we delineate the dynamic process of HCV NS5A-activated PINK1/Parkin-dependent mitophagy. By performing live-cell imaging and CLEM analyses of HCV NS5A-expressing cells, we demonstrate the degradation of mitochondria within autophagic vacuoles, a process that is dependent on Parkin and ubiquitin translocation onto mitochondria and PINK1 stabilization. In addition, the cargo receptors of mitophagy, NDP52 and OPTN, are recruited to the mitochondria and required for HCV NS5A-induced mitophagy. Moreover, ATG5 and DFCP1, which function in autophagosome closure and phagophore formation, are translocated near mitochondria for HCV NS5A-induced mitophagy. Furthermore, autophagy-initiating proteins, including ATG14 and ULK1, are recruited near the mitochondria for HCV NS5A-triggered mitophagy. Together, these findings demonstrate that HCV NS5A may induce PINK1/Parkin-dependent mitophagy through the recognition of mitochondria by cargo receptors and the nascent formation of phagophores close to mitochondria. Full article
(This article belongs to the Special Issue Pathogenesis of Viral Hepatitis)
►▼ Show Figures

Graphical abstract

28 pages, 5478 KiB  
Article
Role of Rab13, Protein Kinase A, and Zonula Occludens-1 in Hepatitis E Virus Entry and Cell-to-Cell Spread: Comparative Analysis of Quasi-Enveloped and Non-Enveloped Forms
by Shigeo Nagashima, Putu Prathiwi Primadharsini, Masaharu Takahashi, Takashi Nishiyama, Kazumoto Murata and Hiroaki Okamoto
Pathogens 2024, 13(12), 1130; https://doi.org/10.3390/pathogens13121130 - 20 Dec 2024
Cited by 1 | Viewed by 1086
Abstract
Hepatitis E virus (HEV) exists in two distinct forms: a non-enveloped form (neHEV), which is present in feces and bile, and a quasi-enveloped form (eHEV), found in circulating blood and culture supernatants. This study aimed to elucidate the roles of Ras-associated binding 13 [...] Read more.
Hepatitis E virus (HEV) exists in two distinct forms: a non-enveloped form (neHEV), which is present in feces and bile, and a quasi-enveloped form (eHEV), found in circulating blood and culture supernatants. This study aimed to elucidate the roles of Ras-associated binding 13 (Rab13) and protein kinase A (PKA) in the entry mechanisms of both eHEV and neHEV, utilizing small interfering RNA (siRNA) and chemical inhibitors. The results demonstrated that the entry of both viral forms is dependent on Rab13 and PKA. Further investigation into the involvement of tight junction (TJ) proteins revealed that the targeted knockdown of zonula occludens-1 (ZO-1) significantly impaired the entry of both eHEV and neHEV. In addition, in ZO-1 knockout (KO) cells inoculated with either viral form, HEV RNA levels in culture supernatants did not increase, even up to 16 days post-inoculation. Notably, the absence of ZO-1 did not affect the adsorption efficiency of eHEV or neHEV, nor did it influence HEV RNA replication. In cell-to-cell spread assays, ZO-1 KO cells inoculated with eHEV showed a lack of expression of HEV ORF2 and ORF3 proteins. In contrast, neHEV-infected ZO-1 KO cells showed markedly reduced ORF2 and ORF3 protein expression within virus-infected foci, compared to non-targeting knockout (NC KO) cells. These findings underscore the crucial role of ZO-1 in facilitating eHEV entry and mediating the cell-to-cell spread of neHEV in infected cells. Full article
(This article belongs to the Special Issue Pathogenesis of Viral Hepatitis)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop