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The Interaction between Cell and Virus, 2nd Edition
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The Interaction between Cell and Virus, 2nd Edition

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: closed (30 September 2024) | Viewed by 7065

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

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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.

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Keywords

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

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Published Papers (5 papers)

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Research

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15 pages, 4797 KiB  
Article
Genomic Landscape and Regulation of RNA Editing in Pekin Ducks Susceptible to Duck Hepatitis A Virus Genotype 3 Infection
by Haonao Zhao, Zifang Wu, Zezhong Wang, Jinlong Ru, Shuaiqin Wang, Yang Li, Shuisheng Hou, Yunsheng Zhang and Xia Wang
Int. J. Mol. Sci. 2024, 25(19), 10413; https://doi.org/10.3390/ijms251910413 - 27 Sep 2024
Viewed by 494
Abstract
RNA editing is increasingly recognized as a post-transcriptional modification that directly affects viral infection by regulating RNA stability and recoding proteins. the duck hepatitis A virus genotype 3 (DHAV-3) infection is seriously detrimental to the Asian duck industry. However, the landscape and roles [...] Read more.
RNA editing is increasingly recognized as a post-transcriptional modification that directly affects viral infection by regulating RNA stability and recoding proteins. the duck hepatitis A virus genotype 3 (DHAV-3) infection is seriously detrimental to the Asian duck industry. However, the landscape and roles of RNA editing in the susceptibility and resistance of Pekin ducks to DHAV-3 remain unclear. Here, we profiled dynamic RNA editing events in liver tissue and investigated their potential functions during DHAV-3 infection in Pekin ducks. We identified 11,067 informative RNA editing sites in liver tissue from DHAV-3-susceptible and -resistant ducklings at three time points during virus infection. Differential RNA editing sites (DRESs) between S and R ducks were dynamically changed during infection, which were enriched in genes associated with vesicle-mediated transport and immune-related pathways. Moreover, we predicted and experimentally verified that RNA editing events in 3′-UTR could result in loss or gain of miRNA–mRNA interactions, thereby changing the expression of target genes. We also found a few DRESs in coding sequences (CDSs) that altered the amino acid sequences of several proteins that were vital for viral infection. Taken together, these data suggest that dynamic RNA editing has significant potential to tune physiological processes in response to virus infection in Pekin ducks, thus contributing to host differential susceptibility to DHAV-3. Full article
(This article belongs to the Special Issue The Interaction between Cell and Virus, 2nd Edition)
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19 pages, 10538 KiB  
Article
Poxvirus A51R Proteins Negatively Regulate Microtubule-Dependent Transport by Kinesin-1
by Dahee Seo, Yang Yue, Shin Yamazaki, Kristen J. Verhey and Don B. Gammon
Int. J. Mol. Sci. 2024, 25(14), 7825; https://doi.org/10.3390/ijms25147825 - 17 Jul 2024
Viewed by 844
Abstract
Microtubule (MT)-dependent transport is a critical means of intracellular movement of cellular cargo by kinesin and dynein motors. MT-dependent transport is tightly regulated by cellular MT-associated proteins (MAPs) that directly bind to MTs and either promote or impede motor protein function. Viruses have [...] Read more.
Microtubule (MT)-dependent transport is a critical means of intracellular movement of cellular cargo by kinesin and dynein motors. MT-dependent transport is tightly regulated by cellular MT-associated proteins (MAPs) that directly bind to MTs and either promote or impede motor protein function. Viruses have been widely shown to usurp MT-dependent transport to facilitate their virion movement to sites of replication and/or for exit from the cell. However, it is unclear if viruses also negatively regulate MT-dependent transport. Using single-molecule motility and cellular transport assays, we show that the vaccinia virus (VV)-encoded MAP, A51R, inhibits kinesin-1-dependent transport along MTs in vitro and in cells. This inhibition is selective as the function of kinesin-3 is largely unaffected by VV A51R. Interestingly, we show that A51R promotes the perinuclear accumulation of cellular cargo transported by kinesin-1 such as lysosomes and mitochondria during infection. Moreover, A51R also regulates the release of specialized VV virions that exit the cell using kinesin-1-dependent movement. Using a fluorescently tagged rigor mutant of kinesin-1, we show that these motors accumulate on A51R-stabilized MTs, suggesting these stabilized MTs may form a “kinesin-1 sink” to regulate MT-dependent transport in the cell. Collectively, our findings uncover a new mechanism by which viruses regulate host cytoskeletal processes. Full article
(This article belongs to the Special Issue The Interaction between Cell and Virus, 2nd Edition)
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15 pages, 2360 KiB  
Communication
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 - 7 Feb 2024
Viewed by 1387
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 [...] Read more.
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, 2nd Edition)
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12 pages, 1874 KiB  
Article
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 1359
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 [...] Read more.
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, 2nd Edition)
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Review

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29 pages, 830 KiB  
Review
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
Cited by 2 | Viewed by 2144
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 [...] Read more.
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, 2nd Edition)
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