Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

The Interaction between Cell and Virus 2.0

Special Issue Editors
Special Issue Information
Keywords
Published Papers

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Microbiology".

Deadline for manuscript submissions: 31 May 2024 | Viewed by 3358

Share This Special Issue

Special Issue Editor

Prof. Dr. Masahiro Fujimuro

E-Mail Website
Guest Editor

Department of Cell Biology, Kyoto Pharmaceutical University, Kyoto 607-8412, Japan
Interests: human herpesviruses; Kaposi's sarcoma-associated herpesvirus (KSHV); herpes simplex virus (HSV); cell signaling pathways; dengue virus (DENV); post-translational modification; proteasome; ubiquitin; protein degradation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue follows the publication of the first edition on “The Interaction between Cell and Virus” (https://www.mdpi.com/journal/ijms/special_issues/Interaction_Cell_and_Virus)”.

Viral infections cause various diseases in the host species. Antiviral medications can help to relieve the symptoms of some viruses by inhibiting viral enzymes or virus-mediated events. However, during the past half century, very few antiviral drugs (excluding anti-HCV drugs) have been developed for use in the treatment of serious and life-threatening viral infections.

A fundamental step for the effective infection and replication of all viruses is the interaction between cell and virus. This is achieved through the dysregulation and exploitation of host cell functions (e.g., gene expression, signal transduction, metabolic process, intracellular transport, organelle biogenesis or communication, apoptosis, protein degradation, and immune response) by viral molecules, such as viral proteins and microRNA. Viruses hijack the appropriate cellular functions for the establishment of infection, persistent infection, prolonging survival, control of cell proliferation, anti-apoptosis, and evasion of immune surveillance in infected cells. Viruses manipulate those cellular functions in order to create a favorable environment for the virus or the virus-infected cell. On the other hand, the host species exerts antiviral effects on virus infection through the interaction between cell and virus.

A better understanding of the interaction between viruses and host cells could provide new insights into the process of pathogenesis, immune disruption (or activation), and tumorigenesis triggered by viruses, and may provide a theoretical basis for the development of novel therapeutic interventions against infectious diseases.

For this Special Issue, original research articles, review articles and short communications are welcome. Research areas of interest include the cell–virus interaction involved in viral replication, gene expression, latent or lytic infection, viral structural protein and enzyme, virus assembly, cell signaling pathways, post-translational modification, host factors, virus immune evasion, host immune response, viral tumorigenesis or disease, antiviral medication, vaccine, animal models, and gene therapy.

Prof. Dr. Masahiro Fujimuro
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

viral replication
gene expression
lytic infection
viral structure
viral assembly
cell signaling pathway
post-translational modification
immune evasion
viral tumorigenesis
antiviral medication

Published Papers (3 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

Jump to: Review

15 pages, 2360 KiB

Open AccessCommunication

Sofosbuvir Suppresses the Genome Replication of DENV1 in Human Hepatic Huh7 Cells

by Madoka Kurosawa, Fumihiro Kato, Takayuki Hishiki, Saori Ito, Hiroki Fujisawa, Tatsuo Yamaguchi, Misato Moriguchi, Kohei Hosokawa, Tadashi Watanabe, Noriko Saito-Tarashima, Noriaki Minakawa and Masahiro Fujimuro

Int. J. Mol. Sci. 2024, 25(4), 2022; https://doi.org/10.3390/ijms25042022 - 07 Feb 2024

Viewed by 726

Abstract

Dengue virus (DENV) causes dengue fever and dengue hemorrhagic fever, and DENV infection kills 20,000 people annually worldwide. Therefore, the development of anti-DENV drugs is urgently needed. Sofosbuvir (SOF) is an effective drug for HCV-related diseases, and its triphosphorylated metabolite inhibits viral RNA synthesis by the RNA-dependent RNA polymerase (RdRp) of HCV. (2′R)-2′-Deoxy-2′-fluoro-2′-methyluridine (FMeU) is the dephosphorylated metabolite produced from SOF. The effects of SOF and FMeU on DENV1 replication were analyzed using two DENV1 replicon-based methods that we previously established. First, a replicon-harboring cell assay showed that DENV1 replicon replication in human hepatic Huh7 cells was decreased by SOF but not by FMeU. Second, a transient replicon assay showed that DENV1 replicon replication in Huh7 cells was decreased by SOF; however, in hamster kidney BHK-21 cells, it was not suppressed by SOF. Additionally, the replicon replication in Huh7 and BHK-21 cells was not affected by FMeU. Moreover, we assessed the effects of SOF on infectious DENV1 production. SOF suppressed infectious DENV1 production in Huh7 cells but not in monkey kidney Vero cells. To examine the substrate recognition of the HCV and DENV1 RdRps, the complex conformation of SOF-containing DENV1 RdRp or HCV RdRp was predicted using AlphaFold 2. These results indicate that SOF may be used as a treatment for DENV1 infection. Full article

(This article belongs to the Special Issue The Interaction between Cell and Virus 2.0)

► Show Figures

Figure 1

12 pages, 1874 KiB

Open AccessArticle

Culture of Human Rotaviruses in Relevant Models Shows Differences in Culture-Adapted and Nonculture-Adapted Strains

by Nazaret Peña-Gil, Walter Randazzo, Noelia Carmona-Vicente, Cristina Santiso-Bellón, Roberto Cárcamo-Cálvo, Noemi Navarro-Lleó, Vicente Monedero, María J. Yebra, Javier Buesa, Roberto Gozalbo-Rovira and Jesús Rodríguez-Díaz

Int. J. Mol. Sci. 2023, 24(24), 17362; https://doi.org/10.3390/ijms242417362 - 11 Dec 2023

Cited by 1 | Viewed by 873

Abstract

Rotavirus (RV) is the leading cause of acute gastroenteritis (AGE) in children under 5 years old worldwide, and several studies have demonstrated that histo–blood group antigens (HBGAs) play a role in its infection process. In the present study, human stool filtrates from patients diagnosed with RV diarrhea (genotyped as P[8]) were used to infect differentiated Caco-2 cells (dCaco-2) to determine whether such viral strains of clinical origin had the ability to replicate in cell cultures displaying HBGAs. The cell culture-adapted human RV Wa model strain (P[8] genotype) was used as a control. A time-course analysis of infection was conducted in dCaco-2 at 1, 24, 48, 72, and 96 h. The replication of two selected clinical isolates and Wa was further assayed in MA104, undifferentiated Caco-2 (uCaco-2), HT29, and HT29-M6 cells, as well as in monolayers of differentiated human intestinal enteroids (HIEs). The results showed that the culture-adapted Wa strain replicated more efficiently in MA104 cells than other utilized cell types. In contrast, clinical virus isolates replicated more efficiently in dCaco-2 cells and HIEs. Furthermore, through surface plasmon resonance analysis of the interaction between the RV spike protein (VP8*) and its glycan receptor (the H antigen), the V7 RV clinical isolate showed 45 times better affinity compared to VP8* from the Wa strain. These findings support the hypothesis that the differences in virus tropism between clinical virus isolates and RV Wa could be a consequence of the different HBGA contents on the surface of the cell lines employed. dCaco-2, HT29, and HT29M6 cells and HIEs display HBGAs on their surfaces, whereas MA104 and uCaco-2 cells do not. These results indicate the relevance of using non-cell culture-adapted human RV to investigate the replication of rotavirus in relevant infection models. Full article

(This article belongs to the Special Issue The Interaction between Cell and Virus 2.0)

► Show Figures

Figure 1

Review

Jump to: Research

29 pages, 830 KiB

Open AccessReview

Mcl-1 Protein and Viral Infections: A Narrative Review

by Zbigniew Wyżewski, Justyna Stępkowska, Aleksandra Maria Kobylińska, Adriana Mielcarska and Matylda Barbara Mielcarska

Int. J. Mol. Sci. 2024, 25(2), 1138; https://doi.org/10.3390/ijms25021138 - 17 Jan 2024

Viewed by 1197

Abstract

MCL-1 is the prosurvival member of the Bcl-2 family. It prevents the induction of mitochondria-dependent apoptosis. The molecular mechanisms dictating the host cell viability gain importance in the context of viral infections. The premature apoptosis of infected cells could interrupt the pathogen replication cycle. On the other hand, cell death following the effective assembly of progeny particles may facilitate virus dissemination. Thus, various viruses can interfere with the apoptosis regulation network to their advantage. Research has shown that viral infections affect the intracellular amount of MCL-1 to modify the apoptotic potential of infected cells, fitting it to the “schedule” of the replication cycle. A growing body of evidence suggests that the virus-dependent deregulation of the MCL-1 level may contribute to several virus-driven diseases. In this work, we have described the role of MCL-1 in infections caused by various viruses. We have also presented a list of promising antiviral agents targeting the MCL-1 protein. The discussed results indicate targeted interventions addressing anti-apoptotic MCL1 as a new therapeutic strategy for cancers as well as other diseases. The investigation of the cellular and molecular mechanisms involved in viral infections engaging MCL1 may contribute to a better understanding of the regulation of cell death and survival balance. Full article

(This article belongs to the Special Issue The Interaction between Cell and Virus 2.0)

► Show Figures

Journal Menu

Journal Browser

The Interaction between Cell and Virus 2.0

Share This Special Issue

Special Issue Editor

Special Issue Information

Keywords

Published Papers (3 papers)

Research

Review

Further Information

Guidelines

MDPI Initiatives

Follow MDPI