Special Issue "Viral-Host Cell Interactions of Animal Viruses"

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Animal Viruses".

Deadline for manuscript submissions: 31 December 2022 | Viewed by 1553

Special Issue Editors

Dr. Xin Yin
E-Mail Website
Guest Editor
State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin 150069, Heilongjiang, China
Interests: zoonotic viruses; innate immunity; veterinary virology; virus-host interactions
Prof. Dr. Bei-Bei Chu
E-Mail Website
Guest Editor
College of Veterinary Medicine, Henan Agricultural University, Zhengzhou 450046, Henan, China
Interests: immunometabolism; innate immunity; virus-host interactions

Special Issue Information

Dear Colleagues,

Viruses are intracellular parasites that rely entirely on host cells to achieve their replication cycle. During infection, viruses hijack their host’s cell energy and molecular machinery to enter, multiply, and finally exit from the host cell, while the host recruits intrinsic and acquired immune pathways to counter the threat posed by viruses. Additionally, viruses have evolved multiple elegant strategies to evade these defense measures. A dramatic expansion of our knowledge of viral-host cell interactions of animal viruses has been witnessed in the past few years. These advances have provided a detailed understanding of the life cycle of viral infection as well as new insights into the disease mechanisms.

Animal viruses, especially zoonotic viruses, are on the increase and pose a significant threat to animal and human health. This Special Issue aims to collect studies on the biological arms race between animal viruses and hosts, including virus-induced physiologic changes in host cells, host antiviral responses to virus infection, immune regulation upon infection, and complex networks of virus-host proteins. It also aims to revise advanced technology to the study of viral-host cell interactions of animal viruses. All experts in the field are encouraged to contribute original research papers or propose reviews to this Special Issue of Viruses.

Dr. Xin Yin
Prof. Dr. Bei-Bei Chu
Guest Editors

Manuscript Submission Information

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Keywords

  • animal viruses
  • zoonotic viruses
  • dependency factors
  • restriction factors
  • innate immune sensing
  • interferon responses
  • immune evasion
  • receptors of animal viruses
  • virally encoded proteins
  • viral replication complexes
  • the ESCRT machinery
  • autophagy
  • adaptive immune responses to viral infection
  • immunometabolism

Published Papers (3 papers)

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Research

Article
Analysis of the Function of LncRNA-MSTRG.16919.1 in BHV-1-infected Bovine Kidney Subculture Cells by Transcriptome Sequencing
Viruses 2022, 14(10), 2104; https://doi.org/10.3390/v14102104 - 22 Sep 2022
Viewed by 266
Abstract
Infection of cattle with bovine herpesvirus type 1 (BHV−1) can lead to upper respiratory tract disease, conjunctivitis, or genital disease and cause serious economic losses to the cattle industry worldwide. The role of long noncoding RNAs in BHV−1 infection is not well understood. [...] Read more.
Infection of cattle with bovine herpesvirus type 1 (BHV−1) can lead to upper respiratory tract disease, conjunctivitis, or genital disease and cause serious economic losses to the cattle industry worldwide. The role of long noncoding RNAs in BHV−1 infection is not well understood. To explore the role of lncRNA−MSTRG.16919.1 in bovine herpes virus type I (BHV−1) infected MDBK cells, the lncRNA−MSTRG.16919.1 gene was silenced and sequenced transcriptome and sequencing data were analyzed by Edge R software, Gene Ontology (GO), the Kyoto Encyclopedia of Genes and Genomes (KEGG), and an interaction network of proteins. Real−time quantitative PCR (RT−qPCR) and Western blotting were used to verify the results of bioinformatic analyses. The results showed that 1151 differential genes were obtained in the siRNA−MSTRG.16919.1 group compared with an NC group. Compared with BHV−33h, 6586 differentially expressed genes were obtained. A total of 498 differentially expressed genes were screened from the two groups. To verify the accuracy of the sequencing, six genes were randomly selected for RT−qPCR, and the results showed that the expression trend of selected genes was consistent with the sequencing results. GO enrichment analysis showed that the differential genes were related to such biological processes as nucleotide binding, enzyme binding, cell cycle, and glial macromolecule metabolism. KEGG analysis enriched 378 and 2,634 signaling pathways, respectively, that were associated with virus infection, ubiquitin−mediated protein hydrolysis, phosphoinositol metabolism, apoptosis, and other metabolic pathways. The STRING protein interaction database was used to analyze the interaction network of proteins encoded by differential genes, and the degree algorithm in Cytoscape was used to screen the top 20 proteins. The results showed that SKIV2L2, JAK2, PIK3CB, and MAPK8 were related to virus infection. Western blot analysis of TNF, NF−κB, MAPK8, MAPK9, and MAPK10 proteins showed that lncRNA−MSTRG.16919.1 was involved in regulating the expression of these functional proteins. The results of this study provide basic information for exploring the function and regulatory mechanism of lncRNA−MSTRG.16919.1 in organisms and help for further studying the interaction between virus and host. Full article
(This article belongs to the Special Issue Viral-Host Cell Interactions of Animal Viruses)
Article
CAPG Is Required for Ebola Virus Infection by Controlling Virus Egress from Infected Cells
Viruses 2022, 14(9), 1903; https://doi.org/10.3390/v14091903 - 28 Aug 2022
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Abstract
The replication of Ebola virus (EBOV) is dependent upon actin functionality, especially at cell entry through macropinocytosis and at release of virus from cells. Previously, major actin-regulatory factors involved in actin nucleation, such as Rac1 and Arp2/3, were shown important in both steps. [...] Read more.
The replication of Ebola virus (EBOV) is dependent upon actin functionality, especially at cell entry through macropinocytosis and at release of virus from cells. Previously, major actin-regulatory factors involved in actin nucleation, such as Rac1 and Arp2/3, were shown important in both steps. However, downstream of nucleation, many other cell factors are needed to control actin dynamics. How these regulate EBOV infection remains largely unclear. Here, we identified the actin-regulating protein, CAPG, as important for EBOV replication. Notably, knockdown of CAPG specifically inhibited viral infectivity and yield of infectious particles. Cell-based mechanistic analysis revealed a requirement of CAPG for virus production from infected cells. Proximity ligation and split-green fluorescent protein reconstitution assays revealed strong association of CAPG with VP40 that was mediated through the S1 domain of CAPG. Overall, CAPG is a novel host factor regulating EBOV infection through connecting actin filament stabilization to viral egress from cells. Full article
(This article belongs to the Special Issue Viral-Host Cell Interactions of Animal Viruses)
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Article
Cap Is the Protease of the Porcine Circovirus 2
Viruses 2022, 14(7), 1550; https://doi.org/10.3390/v14071550 - 15 Jul 2022
Viewed by 502
Abstract
Circoviruses are the smallest single-stranded DNA viruses that infect mammalian species, avian species, fish, and insects. The infections of circoviruses are known to be associated with a series of fatal diseases, but the protease of circovirus still remains unknown. In this research, we [...] Read more.
Circoviruses are the smallest single-stranded DNA viruses that infect mammalian species, avian species, fish, and insects. The infections of circoviruses are known to be associated with a series of fatal diseases, but the protease of circovirus still remains unknown. In this research, we identified viral capsid protein (Cap) as the protease of porcine circovirus type 2 (PCV2), to our knowledge the first circoviruses protease to be reported. First, we found that the expression of host proteins is affected due to PCV2 infection in the porcine kidney (PK-15) cells. Then, by proteomic analysis, 253 host proteins that were down regulated were identified due to direct or indirect effects of PCV2. Further, Cap expression, but not other ORFs of PCV2, significantly reduced both JMJD6 (bifunctional arginine demethylase and lysyl-hydroxylase) and CCT5 (the chaperonin containing TCP1 subunit 5) in PK-15 cells. Finally, the results in vitro hydrolysis assays demonstrated that Cap could directly degraded either JMJD6 or CCT5 with different catalytic efficiency. In summary, our study expands repertoire of PCV2 Cap and promotes the development of inhibitors toward the anti-PCV2. Full article
(This article belongs to the Special Issue Viral-Host Cell Interactions of Animal Viruses)
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