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Viral-Host Cell Interactions of Animal Viruses

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

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 23473

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Special Issue Editors

Dr. Xin Yin

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Guest Editor

Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, China
Interests: zoonotic diseases; coronavirus; hepatitis viruses; innate immunity; viral egress

Prof. Dr. Bei-Bei Chu

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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 (10 papers)

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Research

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22 pages, 4872 KiB

Open AccessArticle

A Single Amino Acid Substitution in Porcine Reproductive and Respiratory Syndrome Virus Glycoprotein 2 Significantly Impairs Its Infectivity in Macrophages

by Jayeshbhai Chaudhari, Raquel Arruda Leme, Kassandra Durazo-Martinez, Sarah Sillman, Aspen M. Workman and Hiep L. X. Vu

Viruses 2022, 14(12), 2822; https://doi.org/10.3390/v14122822 - 18 Dec 2022

Viewed by 1801

Abstract

Porcine reproductive and respiratory syndrome virus (PRRSV) has a restricted tropism for macrophages and CD163 is a key receptor for infection. In this study, the PRRSV strain NCV1 was passaged on MARC-145 cells for 95 passages, and two plaque-clones (C1 and C2) were randomly selected for further analysis. The C1 virus nearly lost the ability to infect porcine alveolar macrophages (PAMs), as well as porcine kidney cells expressing porcine CD163 (PK15-pCD163), while the C2 virus replicates well in these two cell types. Pretreatment of MARC-145 cells with an anti-CD163 antibody nearly blocked C1 virus infection, indicating that the virus still required CD163 to infect cells. The C1 virus carried four unique amino acid substitutions: three in the nonstructural proteins and a K160I in GP2. The introduction of an I160K substitution in GP2 of the C1 virus restored its infectivity in PAMs and PK15-pCD163 cells, while the introduction of a K160I substitution in GP2 of the low-passaged, virulent PRRSV strain NCV13 significantly impaired its infectivity. Importantly, pigs inoculated with the rNCV13-K160I mutant exhibited lower viremia levels and lung lesions than those infected with the parental rNCV13. These results demonstrated that the K160 residue in GP2 is one of the key determinants of PRRSV tropism. Full article

(This article belongs to the Special Issue Viral-Host Cell Interactions of Animal Viruses)

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14 pages, 22905 KiB

Open AccessArticle

Identification and Characterization of Cell Lines HepG2, Hep3B217 and SNU387 as Models for Porcine Epidemic Diarrhea Coronavirus Infection

by Lilei Lv, Huaye Luo, Lingxue Yu, Wu Tong, Yifeng Jiang, Guoxin Li, Guangzhi Tong, Yanhua Li and Changlong Liu

Viruses 2022, 14(12), 2754; https://doi.org/10.3390/v14122754 - 10 Dec 2022

Cited by 1 | Viewed by 1616

Abstract

Porcine epidemic diarrhea virus (PEDV), a member of the genera alphacoronavirus, causes acute watery diarrhea and dehydration in suckling piglets and results in enormous economic losses in the swine industry worldwide. Identification and characterization of different cell lines are not only invaluable for PEDV entry and replication studies but also important for the development of various types of biological pharmaceuticals against PEDV. In this study, we present an approach to identify suitable permissive cell lines for PEDV research. Human cell lines were screened for a high correlation coefficient with the established PEDV infection model Huh7 based on RNA-seq data from the Cancer Cell Line Encyclopedia (CCLE). Experimentally testing permissiveness towards PEDV infection, three highly permissive human cell lines, HepG2, Hep3B217, and SNU387 were identified. The replication kinetics of PEDV in HepG2, Hep3B217, and SNU387 cells were similar to that in Vero and Huh7 cells. Additionally, the transcriptomes analysis showed robust induction of transcripts associated with the innate immune in response to PEDV infection in all three cell lines, including hundreds of inflammatory cytokine and interferon genes. Moreover, the expression of inflammatory cytokines and interferons were confirmed by qPCR assay. Our findings indicate that HepG2, Hep3B217, and SNU387 are suitable cell lines for PEDV replication and innate immune response studies. Full article

(This article belongs to the Special Issue Viral-Host Cell Interactions of Animal Viruses)

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11 pages, 1528 KiB

Open AccessCommunication

Essential Domains of Oxysterol-Binding Protein Required for Poliovirus Replication

by Minetaro Arita

Viruses 2022, 14(12), 2672; https://doi.org/10.3390/v14122672 - 29 Nov 2022

Cited by 1 | Viewed by 1610

Abstract

Oxysterol-binding protein (OSBP) is a host factor required for enterovirus (EV) replication. OSBP locates at membrane contact site and acts as a lipid exchanger of cholesterol and phosphatidylinositol 4-phosphate (PI4P) between cellular organelles; however, the essential domains required for the viral replication remain unknown. In this study, we define essential domains of OSBP for poliovirus (PV) replication by a functional dominance assay with a series of deletion variants of OSBP. We show that the pleckstrin homology domain (PHD) and the ligand-binding domain, but not the N-terminal intrinsically disordered domain, coiled-coil region, or the FFAT motif, are essential for PV replication. The PHD serves as the primary determinant of OSBP targeting to the replication organelle in the infected cells. These results suggest that not all the domains that support important biological functions of OSBP are essential for the viral replication. Full article

(This article belongs to the Special Issue Viral-Host Cell Interactions of Animal Viruses)

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16 pages, 3074 KiB

Open AccessEditor’s ChoiceArticle

Associations between NK Cells in Different Immune Organs and Cellular SIV DNA and RNA in Regional HLADR⁻ CD4⁺ T Cells in Chronically SIV_mac239-Infected, Treatment-Naïve Rhesus Macaques

by Xinjie Li, Liyan Zhu, Yue Yin, Xueying Fan, Linting Lv, Yuqi Zhang, Yijin Pan, Yangxuanyu Yan, Hua Liang, Jing Xue and Tao Shen

Viruses 2022, 14(11), 2513; https://doi.org/10.3390/v14112513 - 13 Nov 2022

Viewed by 1515

Abstract

With the development of NK cell-directed therapeutic strategies, the actual effect of NK cells on the cellular SIV DNA levels of the virus in SIV-infected macaques in vivo remains unclear. In this study, five chronically SIV_mac239-infected, treatment-naïve rhesus macaques were euthanized, and the blood, spleen, pararectal/paracolonic lymph nodes (PaLNs), and axillary lymph nodes (ALNs) were collected. The distributional, phenotypic, and functional profiles of NK cells were detected by flow cytometry. The highest frequency of NK cells was found in PBMC, followed by the spleen, while only 0~0.5% were found in LNs. Peripheral NK cells also exhibited higher cytotoxic potential (CD56⁻ CD16⁺ NK subsets) and IFN-γ-producing capacity but low PD-1 and Tim-3 levels than those in the spleen and LNs. Our results demonstrated a significant positive correlation between the frequency of NK cells and the ratios of cellular SIV DNA/RNA in HLADR⁻ CD4⁺ T cells (r = 0.6806, p < 0.001) in SIV-infected macaques, despite no discrepancies in the cellular SIV DNA or RNA levels that were found among the blood, spleen, and LNs. These findings showed a profile of NK cell frequencies and NK cytotoxicity levels in different immune organs from chronically SIV_mac239-infected, treatment-naïve rhesus macaques. It was suggested that NK cell frequencies could be closely related to SIV DNA/RNA levels, which could affect the transcriptional activity of SIV proviruses. However, the cytotoxicity effect of NK cells on the latent SIV viral load in LNs could be limited due to the sparse abundance of NK cells in LNs. The development of NK cell-directed treatment approaches aiming for HIV clearance remains challenging. Full article

(This article belongs to the Special Issue Viral-Host Cell Interactions of Animal Viruses)

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16 pages, 4815 KiB

Open AccessArticle

Analysis of the Function of LncRNA-MSTRG.16919.1 in BHV-1-Infected Bovine Kidney Subculture Cells by Transcriptome Sequencing

by Fan Zhang, Kunsheng Jiang, Yuchun Wang, Jinzhu Ma and Baifen Song

Viruses 2022, 14(10), 2104; https://doi.org/10.3390/v14102104 - 22 Sep 2022

Viewed by 1695

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. 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−33 h, 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 2634 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)

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18 pages, 2135 KiB

Open AccessArticle

CAPG Is Required for Ebola Virus Infection by Controlling Virus Egress from Infected Cells

by Hiroyuki Mori, James P. Connell, Callie J. Donahue, RuthMabel Boytz, Yen Thi Kim Nguyen, Daisy W. Leung, Douglas J. LaCount and Robert A. Davey

Viruses 2022, 14(9), 1903; https://doi.org/10.3390/v14091903 - 28 Aug 2022

Cited by 2 | Viewed by 1757

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. 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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10 pages, 7515 KiB

Open AccessArticle

Cap Is the Protease of the Porcine Circovirus 2

by Xuechen Yang, Wei Yang, Wei Zhang, Jiamei Li, Guoyu Yang, Shuhong Zhao and Yueting Zheng

Viruses 2022, 14(7), 1550; https://doi.org/10.3390/v14071550 - 15 Jul 2022

Cited by 2 | Viewed by 1731

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 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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Review

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33 pages, 2062 KiB

Open AccessReview

Host–Pathogen Interactions Influencing Zoonotic Spillover Potential and Transmission in Humans

by Beatriz Escudero-Pérez, Alexandre Lalande, Cyrille Mathieu and Philip Lawrence

Viruses 2023, 15(3), 599; https://doi.org/10.3390/v15030599 - 22 Feb 2023

Cited by 6 | Viewed by 5074

Abstract

Emerging infectious diseases of zoonotic origin are an ever-increasing public health risk and economic burden. The factors that determine if and when an animal virus is able to spill over into the human population with sufficient success to achieve ongoing transmission in humans are complex and dynamic. We are currently unable to fully predict which pathogens may appear in humans, where and with what impact. In this review, we highlight current knowledge of the key host–pathogen interactions known to influence zoonotic spillover potential and transmission in humans, with a particular focus on two important human viruses of zoonotic origin, the Nipah virus and the Ebola virus. Namely, key factors determining spillover potential include cellular and tissue tropism, as well as the virulence and pathogenic characteristics of the pathogen and the capacity of the pathogen to adapt and evolve within a novel host environment. We also detail our emerging understanding of the importance of steric hindrance of host cell factors by viral proteins using a “flytrap”-type mechanism of protein amyloidogenesis that could be crucial in developing future antiviral therapies against emerging pathogens. Finally, we discuss strategies to prepare for and to reduce the frequency of zoonotic spillover occurrences in order to minimize the risk of new outbreaks. Full article

(This article belongs to the Special Issue Viral-Host Cell Interactions of Animal Viruses)

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22 pages, 2787 KiB

Open AccessReview

Tough Way In, Tough Way Out: The Complex Interplay of Host and Viral Factors in Nucleocytoplasmic Trafficking during HIV-1 Infection

by Satarupa Sarkar, Kannan Balakrishnan, Kumaraswami Chintala, Krishnaveni Mohareer, Tom Luedde, Ananda Ayyappan Jaguva Vasudevan, Carsten Münk and Sharmistha Banerjee

Viruses 2022, 14(11), 2503; https://doi.org/10.3390/v14112503 - 12 Nov 2022

Cited by 4 | Viewed by 2256

Abstract

Human immunodeficiency virus-1 (HIV-1) is a retrovirus that integrates its reverse-transcribed genome as proviral DNA into the host genome to establish a successful infection. The viral genome integration requires safeguarding the subviral complexes, reverse transcription complex (RTC) and preintegration complex (PIC), in the cytosol from degradation, presumably effectively secured by the capsid surrounding these complexes. An intact capsid, however, is a large structure, which raises concerns about its translocation from cytoplasm to nucleus crossing the nuclear membrane, guarded by complex nuclear pore structures, which do not allow non-specific transport of large molecules. In addition, the generation of new virions requires the export of incompletely processed viral RNA from the nucleus to the cytoplasm, an event conventionally not permitted through mammalian nuclear membranes. HIV-1 has evolved multiple mechanisms involving redundant host pathways by liaison with the cell’s nucleocytoplasmic trafficking system, failure of which would lead to the collapse of the infection cycle. This review aims to assemble the current developments in temporal and spatial events governing nucleocytoplasmic transport of HIV-1 factors. Discoveries are anticipated to serve as the foundation for devising host-directed therapies involving selective abolishment of the critical interactomes between viral proteins and their host equivalents. Full article

(This article belongs to the Special Issue Viral-Host Cell Interactions of Animal Viruses)

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13 pages, 1429 KiB

Open AccessReview

Host Cell Receptors Implicated in the Cellular Tropism of BVDV

by Shuhui Qi, Lijing Wo, Chao Sun, Juan Zhang, Quanhai Pang and Xin Yin

Viruses 2022, 14(10), 2302; https://doi.org/10.3390/v14102302 - 20 Oct 2022

Cited by 1 | Viewed by 3381

Abstract

Bovine viral diarrhea virus (BVDV) is one of the most hazardous viruses, which causes huge economic losses in the cattle industry around the world. In recent years, there has been a continuous increase in the diversity of pestivirus worldwide. As a member of the genus Pestivirus in the Flaviviridae family, BVDV has a wide range of host animals including cattle, goat, sheep, pig, camel and other cloven-hoofed animals, and it has multi-tissue tropism as well. The recognition of their permissive cells by viruses via interaction with the cellular receptors is a prerequisite for successful infection. So far, little is known about the cellular receptors essential for BVDV entry and their detailed functions during BVDV infection. Thus, discovery of the cellular receptors involved in the entry of BVDV and other pestiviruses is significant for development of the novel intervention. The viral envelope glycoprotein E^rns and E2 are crucial determinants of the cellular tropism of BVDV. The cellular proteins bound with E^rns and E2 potentially participate in BVDV entry, and their abundance might determine the cellular tropism of BVDV. Here, we summarize current knowledge regarding the cellular molecules have been described for BVDV entry, such as, complement regulatory protein 46 (CD46), heparan sulfate (HS), the low-density lipoprotein (LDL) receptor, and a disintegrin and metalloproteinase 17 (ADAM17). Furthermore, we focus on their implications of the recently identified cellular receptors for pestiviruses in BVDV life cycle. This knowledge provides a theoretical basis for BVDV prevention and treatment by targeting the cellular receptors essential for BVDV infection. Full article

(This article belongs to the Special Issue Viral-Host Cell Interactions of Animal Viruses)

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