Pub Date : 2025-01-25DOI: 10.1016/j.virol.2025.110437
Tanja Košutić Gulija , Maja Lang Balija , Dubravko Forčić , Ante Plećaš , Ivan Alić , Jelena Ivančić-Jelečki , Maja Jagušić
The mumps virus is a promising candidate as a vaccine vector or oncolytic therapy agent. However, its neurotropic nature, driven by molecular mechanisms that remain unclear, poses a significant obstacle to its development for these applications. This study utilizes recombinant mumps virus carrying the enhanced green fluorescent protein gene (EGFP) and two additional viruses containing, alongside EGFP, unique non-viral, non-coding 84-nucleotide inserts in the 3′ non-coding region (NCR) of the hemagglutinin-neuraminidase (HN) gene. We observed a significant increase in neurovirulence for both viruses containing inserts in the 3’ NCR of HN. The insert in HN 3′ NCR provided a replicative advantage in the brains of newborn rats and rat brain-derived cell cultures. While the viruses were able to infect rat neurons, infection of astrocytes was completely inhibited. Additionally, in infected rat brain and rat brain-derived cell cultures we detected induction of RANTES. We observed no correlation in the extent of neuronal apoptosis or the induction of pro-inflammatory cytokines between viruses with or without the HN 3′ NCR insert.
{"title":"Insertion of a short non-viral sequence in the 3′ noncoding region of the hemagglutinin-neuraminidase increases mumps virus neurovirulence","authors":"Tanja Košutić Gulija , Maja Lang Balija , Dubravko Forčić , Ante Plećaš , Ivan Alić , Jelena Ivančić-Jelečki , Maja Jagušić","doi":"10.1016/j.virol.2025.110437","DOIUrl":"10.1016/j.virol.2025.110437","url":null,"abstract":"<div><div>The mumps virus is a promising candidate as a vaccine vector or oncolytic therapy agent. However, its neurotropic nature, driven by molecular mechanisms that remain unclear, poses a significant obstacle to its development for these applications. This study utilizes recombinant mumps virus carrying the enhanced green fluorescent protein gene (EGFP) and two additional viruses containing, alongside EGFP, unique non-viral, non-coding 84-nucleotide inserts in the 3′ non-coding region (NCR) of the hemagglutinin-neuraminidase (HN) gene. We observed a significant increase in neurovirulence for both viruses containing inserts in the 3’ NCR of HN. The insert in HN 3′ NCR provided a replicative advantage in the brains of newborn rats and rat brain-derived cell cultures. While the viruses were able to infect rat neurons, infection of astrocytes was completely inhibited. Additionally, in infected rat brain and rat brain-derived cell cultures we detected induction of RANTES. We observed no correlation in the extent of neuronal apoptosis or the induction of pro-inflammatory cytokines between viruses with or without the HN 3′ NCR insert.</div></div>","PeriodicalId":23666,"journal":{"name":"Virology","volume":"604 ","pages":"Article 110437"},"PeriodicalIF":2.8,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143343455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-24DOI: 10.1016/j.virol.2025.110420
Tim Skern
Viruses were shown to encode proteinases in the 1970s. Initially, it was assumed that they would be only used for proteolytic processing of the viral proteins. Subsequent investigations showed that such proteinases could affect host metabolism to benefit viral replication. The foot-and-mouth disease virus (FMDV) leader proteinase (Lbpro) cleaves several specific cellular targets. This mini-review summarises the cellular targets of Lbpro and illustrates the protein interactions away from the canonical substrate binding sites that Lbpro has evolved to enable specific and efficient cleavage of host proteins to promote FMDV replication.
{"title":"The leader proteinase of foot-and-mouth disease virus: Efficiency through exosites","authors":"Tim Skern","doi":"10.1016/j.virol.2025.110420","DOIUrl":"10.1016/j.virol.2025.110420","url":null,"abstract":"<div><div>Viruses were shown to encode proteinases in the 1970s. Initially, it was assumed that they would be only used for proteolytic processing of the viral proteins. Subsequent investigations showed that such proteinases could affect host metabolism to benefit viral replication. The foot-and-mouth disease virus (FMDV) leader proteinase (Lb<sup>pro</sup>) cleaves several specific cellular targets. This mini-review summarises the cellular targets of Lb<sup>pro</sup> and illustrates the protein interactions away from the canonical substrate binding sites that Lb<sup>pro</sup> has evolved to enable specific and efficient cleavage of host proteins to promote FMDV replication.</div></div>","PeriodicalId":23666,"journal":{"name":"Virology","volume":"604 ","pages":"Article 110420"},"PeriodicalIF":2.8,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143070592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Porcine epidemic diarrhea virus (PEDV) is a highly contagious virus that causes acute infectious disease in swine, with mortality rates in piglets reaching up to 100%. In recent years, PEDV has led to significant economic losses in China's pig industry. As there is no specific treatment for PEDV, vaccination remains a key strategy for its prevention and control. This study utilized the EV-G replicon system to develop a nucleic acid vaccine expressing the PEDV core neutralizing epitope (COE) region, which was evaluated through immunization of Kunming mice. The results demonstrated that the vaccine successfully induced high levels of specific IgG and neutralizing antibodies in the mice, while also significantly enhanced splenic lymphocyte proliferation, and increased the expression of IL-4 and IFN-γ cytokines. These findings indicate that the constructed pBluescript-EV-G-COE-N plasmid is an effective DNA replicon vaccine. Notably, immunized with pBluescript-EV-G-COE-N replicons with chitosan resulted in higher neutralizing antibodies and IFN-γ, suggesting the enhanced immune efficacy. The successful construction and preliminary immunological evaluation of the pBluescript-EV-G-COE-N replicon highlights its potential in PEDV vaccine development and offers valuable data for future research in new PEDV vaccine formulations.
{"title":"Construction and preliminary immunological evaluation of EV-G replicon expressing PEDV-COE-N region","authors":"Lingyou Zeng , Jiaguo Bai , Jiabao Huang , Shiting Huang , Yifeng Qin , Yeshi Yin , Ying Chen , Zuzhang Wei , Weijian Huang , Kang Ouyang","doi":"10.1016/j.virol.2025.110436","DOIUrl":"10.1016/j.virol.2025.110436","url":null,"abstract":"<div><div>Porcine epidemic diarrhea virus (PEDV) is a highly contagious virus that causes acute infectious disease in swine, with mortality rates in piglets reaching up to 100%. In recent years, PEDV has led to significant economic losses in China's pig industry. As there is no specific treatment for PEDV, vaccination remains a key strategy for its prevention and control. This study utilized the EV-G replicon system to develop a nucleic acid vaccine expressing the PEDV core neutralizing epitope (COE) region, which was evaluated through immunization of Kunming mice. The results demonstrated that the vaccine successfully induced high levels of specific IgG and neutralizing antibodies in the mice, while also significantly enhanced splenic lymphocyte proliferation, and increased the expression of IL-4 and IFN-γ cytokines. These findings indicate that the constructed pBluescript-EV-G-COE-N plasmid is an effective DNA replicon vaccine. Notably, immunized with pBluescript-EV-G-COE-N replicons with chitosan resulted in higher neutralizing antibodies and IFN-γ, suggesting the enhanced immune efficacy. The successful construction and preliminary immunological evaluation of the pBluescript-EV-G-COE-N replicon highlights its potential in PEDV vaccine development and offers valuable data for future research in new PEDV vaccine formulations.</div></div>","PeriodicalId":23666,"journal":{"name":"Virology","volume":"604 ","pages":"Article 110436"},"PeriodicalIF":2.8,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143076351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-23DOI: 10.1016/j.virol.2025.110422
Yao Yao , Rui Jing , Xiang Liu , Li Kang , Pinghuang Liu
Feline infectious peritonitis (FIP), a fatal disease in cats caused by feline infectious peritonitis virus (FIPV), has limited treatment options and lacks effective vaccines. Cepharanthine (CEP), a natural isoquinoline alkaloid, possesses many medicinal properties, including antiviral activities. However, the role of CEP in management of FIPV infection remains poorly understood. Here, we identified that CEP had a potent ability to inhibit FIPV infection in vitro. CEP significantly inhibited FIPV infection when administered at different times, with co-treatment showing the most significant inhibitory effect. Time-of-addition assays demonstrated that CEP exerted antiviral activity during the post-entry stages of the FIPV infection. We also verified that CEP inhibited FIPV infection not through affecting type I interferon expression, and it could decrease pro-inflammatory factors expression induced by FIPV infection. The combination of CEP and GS-441524 exhibited synergistic antiviral effects against FIPV infection. Our findings highlight the therapeutic potential of CEP for treatment of FIP.
{"title":"Cepharanthine: A promising natural compound against feline infectious peritonitis virus infection and associated inflammation","authors":"Yao Yao , Rui Jing , Xiang Liu , Li Kang , Pinghuang Liu","doi":"10.1016/j.virol.2025.110422","DOIUrl":"10.1016/j.virol.2025.110422","url":null,"abstract":"<div><div>Feline infectious peritonitis (FIP), a fatal disease in cats caused by feline infectious peritonitis virus (FIPV), has limited treatment options and lacks effective vaccines. Cepharanthine (CEP), a natural isoquinoline alkaloid, possesses many medicinal properties, including antiviral activities. However, the role of CEP in management of FIPV infection remains poorly understood. Here, we identified that CEP had a potent ability to inhibit FIPV infection <em>in vitro</em>. CEP significantly inhibited FIPV infection when administered at different times, with co-treatment showing the most significant inhibitory effect. Time-of-addition assays demonstrated that CEP exerted antiviral activity during the post-entry stages of the FIPV infection. We also verified that CEP inhibited FIPV infection not through affecting type I interferon expression, and it could decrease pro-inflammatory factors expression induced by FIPV infection. The combination of CEP and GS-441524 exhibited synergistic antiviral effects against FIPV infection. Our findings highlight the therapeutic potential of CEP for treatment of FIP.</div></div>","PeriodicalId":23666,"journal":{"name":"Virology","volume":"604 ","pages":"Article 110422"},"PeriodicalIF":2.8,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143070577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-23DOI: 10.1016/j.virol.2025.110428
Heshanthi Herath Mudiyanselage , Ahmed Ali , Motamed Elsayed Mohmoud , Muhammad Farooq , Ishara M. Isham , Awais Ghaffar , Juan Jovel , Susantha M. Gomis , Dongyan Niu , Mohamed Faizal Abdul-Careem
Infectious bronchitis virus (IBV) is known to cause significant alterations in tracheal microbial flora in broiler chickens 5 days post-infection (dpi) and our focus is to understand the changes in both respiratory and gastrointestinal microbiome in broilers over a period of time following IBV infection. A study was conducted to characterize the tracheal and cecal microbiome in IBV infected and control broiler chickens at 6, 9 and 15 dpi. IBV genome in trachea, lung and cecal tonsils could be observed in the infected group at all the time points. Immune response parameters and histopathological lesion scores were significantly higher in IBV infected trachea and cecal tonsils at 6, 9 and 15 dpi compared to the controls. We observed that cecal microbial diversity (alpha diversity) was increased in the IBV infected group at 6 and 15 dpi. On the other hand, diversity (alpha diversity) of tracheal microbiome was elevated only at 9 dpi in the IBV infected group. Moreover, significant shift of microbial communities (beta diversity), in both cecum and trachea was observed following IBV infection. Enzyme and metabolic pathway analyses of cecum indicated an upregulation of DNA replication and cell wall synthesis pathways and a downregulation of pathways related to short chain fatty acid (SCFA) production in the IBV infected group compared to the controls. Analysis of tracheal metabolic pathways suggested initial adaptation to the infection stress and gradually shifting to enhanced microbial growth and stability. The study outcome adds to the understanding of microbiome changes secondary to histological changes and immune response following IBV infection in broiler chickens.
{"title":"Delmarva (DMV1639) infectious bronchitis virus infection alters the microbiome of gastrointestinal and respiratory tracts of broiler chickens","authors":"Heshanthi Herath Mudiyanselage , Ahmed Ali , Motamed Elsayed Mohmoud , Muhammad Farooq , Ishara M. Isham , Awais Ghaffar , Juan Jovel , Susantha M. Gomis , Dongyan Niu , Mohamed Faizal Abdul-Careem","doi":"10.1016/j.virol.2025.110428","DOIUrl":"10.1016/j.virol.2025.110428","url":null,"abstract":"<div><div>Infectious bronchitis virus (IBV) is known to cause significant alterations in tracheal microbial flora in broiler chickens 5 days post-infection (dpi) and our focus is to understand the changes in both respiratory and gastrointestinal microbiome in broilers over a period of time following IBV infection. A study was conducted to characterize the tracheal and cecal microbiome in IBV infected and control broiler chickens at 6, 9 and 15 dpi. IBV genome in trachea, lung and cecal tonsils could be observed in the infected group at all the time points. Immune response parameters and histopathological lesion scores were significantly higher in IBV infected trachea and cecal tonsils at 6, 9 and 15 dpi compared to the controls. We observed that cecal microbial diversity (alpha diversity) was increased in the IBV infected group at 6 and 15 dpi. On the other hand, diversity (alpha diversity) of tracheal microbiome was elevated only at 9 dpi in the IBV infected group. Moreover, significant shift of microbial communities (beta diversity), in both cecum and trachea was observed following IBV infection. Enzyme and metabolic pathway analyses of cecum indicated an upregulation of DNA replication and cell wall synthesis pathways and a downregulation of pathways related to short chain fatty acid (SCFA) production in the IBV infected group compared to the controls. Analysis of tracheal metabolic pathways suggested initial adaptation to the infection stress and gradually shifting to enhanced microbial growth and stability. The study outcome adds to the understanding of microbiome changes secondary to histological changes and immune response following IBV infection in broiler chickens.</div></div>","PeriodicalId":23666,"journal":{"name":"Virology","volume":"604 ","pages":"Article 110428"},"PeriodicalIF":2.8,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143070582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Foot-and-mouth disease (FMD) is a severe and, highly contagious viral disease caused by FMD virus (FMDV) that primarily targets ungulates. Identifying neutralising antigenic sites on the virus is crucial for understanding the virus's antigenic characteristics. Numerous studies have pinpointed the critical residues of the neutralising antigenic sites in FMDV serotypes O, A, and C. However, information on serotype Asia 1 is very limited. This study reports the generation and characterization of forty-one monoclonal antibodies (mAbs) against FMDV serotype Asia 1 (current Indian vaccine strain). Of these, a panel of 23 neutralising mAbs was utilized to generate mAb resistant (MAR) mutants for mapping the virus's antigenic sites. New critical residues defining sites 1, 2, and 4 in FMDV serotype Asia 1 were identified. These findings significantly enhance our understanding of the antigenic nature of FMDV serotype Asia 1, and provide insights to designing broadly acting vaccines against FMD.
{"title":"Mapping novel antigenic determinants on foot-and-mouth disease virus serotype Asia 1 using neutralising monoclonal antibody resistant mutants","authors":"Rajendran Manikandan , Sivarama Krishna Gollapalli , Gopinath Shreya , Suresh Basagoudanavar , B.P. Sreenivasa , Samriddhi Dubey , V. Bhanuprakash , Aniket Sanyal , Mana Mahapatra , Satya Parida , Madhusudan Hosamani","doi":"10.1016/j.virol.2025.110421","DOIUrl":"10.1016/j.virol.2025.110421","url":null,"abstract":"<div><div>Foot-and-mouth disease (FMD) is a severe and, highly contagious viral disease caused by FMD virus (FMDV) that primarily targets ungulates. Identifying neutralising antigenic sites on the virus is crucial for understanding the virus's antigenic characteristics. Numerous studies have pinpointed the critical residues of the neutralising antigenic sites in FMDV serotypes O, A, and C. However, information on serotype Asia 1 is very limited. This study reports the generation and characterization of forty-one monoclonal antibodies (mAbs) against FMDV serotype Asia 1 (current Indian vaccine strain). Of these, a panel of 23 neutralising mAbs was utilized to generate mAb resistant (MAR) mutants for mapping the virus's antigenic sites. New critical residues defining sites 1, 2, and 4 in FMDV serotype Asia 1 were identified. These findings significantly enhance our understanding of the antigenic nature of FMDV serotype Asia 1, and provide insights to designing broadly acting vaccines against FMD.</div></div>","PeriodicalId":23666,"journal":{"name":"Virology","volume":"604 ","pages":"Article 110421"},"PeriodicalIF":2.8,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143076343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-23DOI: 10.1016/j.virol.2025.110418
Chantal Emade Nkwelle , Unique Stephens , Kimberly Liang , Joel Cassel , Joseph M. Salvino , Luis J. Montaner , Roland N. Ndip , Seraphine N. Esemu , Fidele Ntie-Kang , Ian Tietjen
J-Lat cells are derivatives of the Jurkat CD4+ T cell line that contain a non-infectious, inducible HIV provirus with a GFP tag. While these cells have substantially advanced our understanding of HIV latency, their use by many laboratories in low and middle-income countries is restricted by limited access to flow cytometry. To overcome this barrier, we describe a modified J-Lat assay using a standard microplate reader that detects HIV-GFP expression following treatment with latency-reversing agents (LRAs). We show that HIV reactivation by control LRAs like prostratin and romidepsin is readily detected with dose dependence and with significant correlation and sensitivity to standard flow cytometry. For example, 10 μM prostratin induced a 20.1 ± 3.3-fold increase in GFP fluorescence in the microplate reader assay, which corresponded to 64.2 ± 5.0% GFP-positive cells detected by flow cytometery. Similarly, 0.3 μM prostratin induced a 1.7 ± 1.2-fold increase compared to 8.7 ± 5.7% GFP-positive cells detected. Using this method, we screen 79 epigenetic modifiers and identify CUDC-101, molibresib, and quisinostat as novel LRAs. This microplate reader-based method offers accessibility to researchers in resource-limited regions to work with J-Lat cells and more actively participate in global HIV cure research efforts.
{"title":"A high-throughput, microplate reader-based method to monitor in vitro HIV latency reversal in the absence of flow cytometry","authors":"Chantal Emade Nkwelle , Unique Stephens , Kimberly Liang , Joel Cassel , Joseph M. Salvino , Luis J. Montaner , Roland N. Ndip , Seraphine N. Esemu , Fidele Ntie-Kang , Ian Tietjen","doi":"10.1016/j.virol.2025.110418","DOIUrl":"10.1016/j.virol.2025.110418","url":null,"abstract":"<div><div>J-Lat cells are derivatives of the Jurkat CD4<sup>+</sup> T cell line that contain a non-infectious, inducible HIV provirus with a GFP tag. While these cells have substantially advanced our understanding of HIV latency, their use by many laboratories in low and middle-income countries is restricted by limited access to flow cytometry. To overcome this barrier, we describe a modified J-Lat assay using a standard microplate reader that detects HIV-GFP expression following treatment with latency-reversing agents (LRAs). We show that HIV reactivation by control LRAs like prostratin and romidepsin is readily detected with dose dependence and with significant correlation and sensitivity to standard flow cytometry. For example, 10 μM prostratin induced a 20.1 ± 3.3-fold increase in GFP fluorescence in the microplate reader assay, which corresponded to 64.2 ± 5.0% GFP-positive cells detected by flow cytometery. Similarly, 0.3 μM prostratin induced a 1.7 ± 1.2-fold increase compared to 8.7 ± 5.7% GFP-positive cells detected. Using this method, we screen 79 epigenetic modifiers and identify CUDC-101, molibresib, and quisinostat as novel LRAs. This microplate reader-based method offers accessibility to researchers in resource-limited regions to work with J-Lat cells and more actively participate in global HIV cure research efforts.</div></div>","PeriodicalId":23666,"journal":{"name":"Virology","volume":"604 ","pages":"Article 110418"},"PeriodicalIF":2.8,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143054471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-22DOI: 10.1016/j.virol.2025.110413
Richard J. Sugrue , Boon Huan Tan
Respiratory syncytial virus (RSV) particle assembly occurs on the surface of infected cells at specialized membrane domain called lipid rafts. The mature RSV particles assemble as filamentous projections called virus filaments, and these structures form on the surface of many permissive cell types indicating that this is a robust feature of the RSV particle assembly. The virus filaments also form on nasal airway organoids systems providing evidence that these structures also have a clinical relevance. Virus filaments also form on cells infected with the closely related human metapneumovirus, suggesting that virus filament formation may be a common feature of assembly process for viruses within the Pneumoviridae family. During RSV infection these virus filaments mediate the localized cell-to-cell spread of virus infection, suggesting that they play an important role in virus transmission. The current understanding of the connection between virus filament formation and virus transmission during RSV infection is presented.
{"title":"The link between respiratory syncytial virus (RSV) morphogenesis and virus transmission: Towards a paradigm for understanding RSV transmission in the upper airway","authors":"Richard J. Sugrue , Boon Huan Tan","doi":"10.1016/j.virol.2025.110413","DOIUrl":"10.1016/j.virol.2025.110413","url":null,"abstract":"<div><div>Respiratory syncytial virus (RSV) particle assembly occurs on the surface of infected cells at specialized membrane domain called lipid rafts. The mature RSV particles assemble as filamentous projections called virus filaments, and these structures form on the surface of many permissive cell types indicating that this is a robust feature of the RSV particle assembly. The virus filaments also form on nasal airway organoids systems providing evidence that these structures also have a clinical relevance. Virus filaments also form on cells infected with the closely related human metapneumovirus, suggesting that virus filament formation may be a common feature of assembly process for viruses within the <em>Pneumoviridae</em> family. During RSV infection these virus filaments mediate the localized cell-to-cell spread of virus infection, suggesting that they play an important role in virus transmission. The current understanding of the connection between virus filament formation and virus transmission during RSV infection is presented.</div></div>","PeriodicalId":23666,"journal":{"name":"Virology","volume":"604 ","pages":"Article 110413"},"PeriodicalIF":2.8,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143054559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-22DOI: 10.1016/j.virol.2025.110425
Linlin Du , Tao Li , Wei Guo , ChenYang Li , Ying Lan , Feng Lin , Kai Xu , Jiban Kumar Kundu , Yijun Zhou , Yunyue Wang , Tong Zhou
Rice is a staple food in East and Southeast Asian countries, rice disease surveillance and warning is particularly important. Rice stripe disease and southern rice black-streaked dwarf virus disease are the insect-borne viral diseases that easily break out and quickly become epidemic. It is important to improve the efficiency of the virus detection method. In this work, a colloidal gold strip assay (CGSA) was used in mixed samples to detect rice stripe virus (RSV) and southern rice black-streaked dwarf virus (SRBSDV) in small brown planthoppers (SBPH) and white-backed planthoppers (WBPH), respectively. The results show that RSV could be detected in 9, 19 and 49 SBPHs mixed with a single positive SBPH sample, and SRBSDV could be detected in 9 WBPHs mixed with a single positive WBPH sample. The mixed sample detection technology presented in this article can significantly reduce the cost of detection and fulfil the requirements for large-scale, real-time virus surveillance in sentinel surveillance.
{"title":"Research on mixed sample test for the rapid detection of rice stripe virus and southern rice black-streaked dwarf virus in vector","authors":"Linlin Du , Tao Li , Wei Guo , ChenYang Li , Ying Lan , Feng Lin , Kai Xu , Jiban Kumar Kundu , Yijun Zhou , Yunyue Wang , Tong Zhou","doi":"10.1016/j.virol.2025.110425","DOIUrl":"10.1016/j.virol.2025.110425","url":null,"abstract":"<div><div>Rice is a staple food in East and Southeast Asian countries, rice disease surveillance and warning is particularly important. Rice stripe disease and southern rice black-streaked dwarf virus disease are the insect-borne viral diseases that easily break out and quickly become epidemic. It is important to improve the efficiency of the virus detection method. In this work, a colloidal gold strip assay (CGSA) was used in mixed samples to detect rice stripe virus (RSV) and southern rice black-streaked dwarf virus (SRBSDV) in small brown planthoppers (SBPH) and white-backed planthoppers (WBPH), respectively. The results show that RSV could be detected in 9, 19 and 49 SBPHs mixed with a single positive SBPH sample, and SRBSDV could be detected in 9 WBPHs mixed with a single positive WBPH sample. The mixed sample detection technology presented in this article can significantly reduce the cost of detection and fulfil the requirements for large-scale, real-time virus surveillance in sentinel surveillance.</div></div>","PeriodicalId":23666,"journal":{"name":"Virology","volume":"604 ","pages":"Article 110425"},"PeriodicalIF":2.8,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143070587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-21DOI: 10.1016/j.virol.2025.110419
Jie Zhao , Qianhong Dai , Haoyu Sun , Beiyi Zhou , Xiaoyuan Lan , Yonghui Qiu , Qianqian Zhang , Dedong Wang , Yongqiu Cui , Jinshuo Guo , Lei Hou , Jue Liu , Jianwei Zhou
Porcine circovirus type 3 (PCV3) is an emerging pathogen that causes porcine dermatitis, and reproductive failure. PCV3 Cap interacts with DExD/H-box helicase 36 (DHX36), a protein that functions primarily through regulating interferon (IFN)-β production. However, how the interaction between DHX36 and PCV3 Cap regulates viral replication remains unknown. Herein, we observed impaired PCV3 proliferation after DHX36 overexpression as indicated by decreased Rep protein expression and virus production. In contrast, PCV3 replication increased upon small interfering RNA-mediated DHX36 depletion. Furthermore, DHX36 positively regulated IFN-β production and interferon-stimulated genes (ISGs) expression. Mechanistically, PCV3 Cap interacted with DHX36, and the PCV3 Cap-NLS and DHX36-NTD were essential for the interaction. Furthermore, DHX36 may get degraded because its binding cellular partners became ubiquitinated and then reduced, and PCV3 Cap-(35-100aa) also promoted the degradation of DHX36 through the K48-linked ubiquitination. Taken together, these results show that DHX36 antagonizes PCV3 replication by interacting with PCV3 Cap and activating IFN-β response, which provides important insight on the prevention and controlling of PCV3 infection.
Importance
Porcine circovirus type 3 (PCV3) is a newly discovered pathogen associated with multiple clinicopathological signs. Clarifying the mechanisms that host factors modulate PCV3 replication helps understanding of the viral pathogenesis. The PCV3 capsid (Cap) protein has been shown to interact with DExD/H-box helicase 36 (DHX36) (Zhou et al., 2022b), a crucial protein that regulates virus replication. Herein, we further demonstrated that DHX36 protein is degraded in PCV3-infected cells and antagonizes the replication of PCV3 and that DHX36 increases interferon-β and interferon-stimulated gene levels by binding to PCV3 Cap. In addition, PCV3 infection could decrease DHX36 expression levels to antagonize its antiviral activity. These results reveal a molecular mechanism by which DHX36 antagonizes PCV3 replication by binding to PCV3 Cap protein and activating IFN signals, thereby providing important targets for preventing and controlling PCV3 infection.
{"title":"Ubiquitination-dependent degradation of DHX36 mediated by porcine circovirus type 3 capsid protein","authors":"Jie Zhao , Qianhong Dai , Haoyu Sun , Beiyi Zhou , Xiaoyuan Lan , Yonghui Qiu , Qianqian Zhang , Dedong Wang , Yongqiu Cui , Jinshuo Guo , Lei Hou , Jue Liu , Jianwei Zhou","doi":"10.1016/j.virol.2025.110419","DOIUrl":"10.1016/j.virol.2025.110419","url":null,"abstract":"<div><div>Porcine circovirus type 3 (PCV3) is an emerging pathogen that causes porcine dermatitis, and reproductive failure. PCV3 Cap interacts with DExD/H-box helicase 36 (DHX36), a protein that functions primarily through regulating interferon (IFN)-β production. However, how the interaction between DHX36 and PCV3 Cap regulates viral replication remains unknown. Herein, we observed impaired PCV3 proliferation after DHX36 overexpression as indicated by decreased Rep protein expression and virus production. In contrast, PCV3 replication increased upon small interfering RNA-mediated <em>DHX36</em> depletion. Furthermore, DHX36 positively regulated IFN-β production and interferon-stimulated genes (ISGs) expression. Mechanistically, PCV3 Cap interacted with DHX36, and the PCV3 Cap-NLS and DHX36-NTD were essential for the interaction. Furthermore, DHX36 may get degraded because its binding cellular partners became ubiquitinated and then reduced, and PCV3 Cap-(35-100aa) also promoted the degradation of DHX36 through the K48-linked ubiquitination. Taken together, these results show that DHX36 antagonizes PCV3 replication by interacting with PCV3 Cap and activating IFN-β response, which provides important insight on the prevention and controlling of PCV3 infection.</div></div><div><h3>Importance</h3><div>Porcine circovirus type 3 (PCV3) is a newly discovered pathogen associated with multiple clinicopathological signs. Clarifying the mechanisms that host factors modulate PCV3 replication helps understanding of the viral pathogenesis. The PCV3 capsid (Cap) protein has been shown to interact with DExD/H-box helicase 36 (DHX36) (Zhou et al., 2022b), a crucial protein that regulates virus replication. Herein, we further demonstrated that DHX36 protein is degraded in PCV3-infected cells and antagonizes the replication of PCV3 and that DHX36 increases interferon-β and interferon-stimulated gene levels by binding to PCV3 Cap. In addition, PCV3 infection could decrease DHX36 expression levels to antagonize its antiviral activity. These results reveal a molecular mechanism by which DHX36 antagonizes PCV3 replication by binding to PCV3 Cap protein and activating IFN signals, thereby providing important targets for preventing and controlling PCV3 infection.</div></div>","PeriodicalId":23666,"journal":{"name":"Virology","volume":"604 ","pages":"Article 110419"},"PeriodicalIF":2.8,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143044011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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