Journal of Virology最新文献

{"title":"LncRNA <i>JINR1</i> regulates <i>miR-216b-5p/</i>GRP78 and <i>miR-1-3p/</i>DDX5 axis to promote JEV infection and cell death.","authors":"Shraddha Tripathi, Suryansh Sengar, Anirban Basu, Vivek Sharma","doi":"10.1128/jvi.00066-25","DOIUrl":"10.1128/jvi.00066-25","url":null,"abstract":"<p><p>Japanese encephalitis virus (JEV) infection in the central nervous system (CNS) leads to neuroinflammation and neuronal cell death. Several long non-coding RNAs (lncRNAs) are differentially expressed during viral infection and regulate multiple aspects of viral pathogenesis. Previously, we have shown that JEV/West Nile virus (WNV) infection promotes JEV-induced non-coding RNA 1 (<i>JINR1</i>) expression in SH-SY5Y cells, and it interacts with RNA-binding motif protein 10 (RBM10) to enhance cell death and viral replication. In this study, we show that JEV or WNV infection of the SH-SY5Y cells inhibits the expression of microRNAs (miRNAs) <i>miR-216b-5p</i> and <i>miR-1-3p</i>. These miRNAs bind to the JEV/WNV genome, and their overexpression during JEV/WNV infection reduces viral replication and cell death. Depleting <i>JINR1</i> or RBM10 during viral infection prevents the downregulation of <i>miR-216b-5p</i> and <i>miR-1-3p</i>. In addition, <i>JINR1</i> or RBM10 knockdown during JEV/WNV infection enhances the binding of RNA Pol II and H3K4me3 at the promoters of <i>miR-216b-5p</i> and <i>miR-1-3p. JINR1</i> or RBM10 depletion also prevents the binding of H3K27me3 at the promoters of these miRNAs, suggesting that <i>JINR1</i> and RBM10 are involved in their transcription repression. Interestingly<i>, JINR1</i> also acts as a competing endogenous RNA (ceRNA) that directly binds to <i>miR-216b-5p</i> and <i>miR-1-3p,</i> resulting in the upregulation of their targets glucose-regulated protein 78 (GRP78) and DEAD-Box Helicase 5 (DDX5), respectively, which are involved in regulating viral replication. Our findings suggest that <i>JINR1</i> uses multiple mechanisms to promote JEV and WNV infection in neuronal cells.</p><p><strong>Importance: </strong>Infection of the central nervous system (CNS) by Japanese encephalitis virus (JEV) or West Nile virus (WNV) leads to neuroinflammation and neuronal cell death. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) regulate viral infection by regulating the expression of host genes. However, knowledge about the interplay between lncRNAs and miRNAs during JEN/WNV infection is limited. We show that JEV/WNV infection inhibits the expression of anti-viral host miRNAs <i>miR-216b-5p</i> and <i>miR-1-3p</i>. These miRNAs inhibit the JEV and WNV replication by directly binding with their genome. <i>JINR1</i> and its interacting protein, RBM10, inhibit the transcription of <i>miR-216b-5p</i> and <i>miR-1-3p</i>. Interestingly, <i>JINR1</i> also binds and sequesters <i>miR-216b-5p</i> and <i>miR-1-3p</i>, resulting in upregulation of their targets GRP78 and DDX5, respectively, which promote viral infection. Our findings suggest that lncRNA <i>JINR1</i> is a potential target for developing anti-virals against JEV/WNV infection.</p>","PeriodicalId":17583,"journal":{"name":"Journal of Virology","volume":" ","pages":"e0006625"},"PeriodicalIF":4.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12090723/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144026764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LDHA-lactate axis modulates mitophagy inhibiting CSFV replication.","authors":"Sen Zeng, Zipeng Luo, Wenhui Zhu, Zhanhui Zhang, Ruibo Zhao, Shuaiqi Zhu, Qi Qiu, Nan Cao, Xinliang Fu, Wenjun Liu, Shuangqi Fan, Cheng Fu","doi":"10.1128/jvi.00268-25","DOIUrl":"10.1128/jvi.00268-25","url":null,"abstract":"<p><p>Lactate dehydrogenase A (LDHA) plays a crucial role in regulating lactate synthesis in various biological processes. Lactate, a byproduct of glycometabolism, has been recognized as a unique molecule with implications in both metabolism and immunity. Classical swine fever (CSF), caused by the classical swine fever virus (CSFV), is a highly contagious and severe infectious disease that primarily affects pigs. Prior research has shown that CSFV infection disrupts the normal glycolytic process, leading to an accumulation of lactate within the host. Nevertheless, it remains unclear whether there is mutual regulation between the CSFV and LDHA-lactate axis. Here, we have found that CSFV infection increases LDHA expression <i>in vivo</i> and <i>in vitro</i>, which may be attributed to attenuated ISGylation of LDHA. Furthermore, CSFV infection induces L-lactate production via LDHA dependence <i>in vitro</i>. The cellular biology research on LDHA has revealed that LDHA not only localizes to the mitochondria but also inhibits PINK1-Parkin-mediated mitophagy. Through various experimental techniques such as western blot to detect mitophagy marker proteins, laser confocal microscopy to observe the flow of mitophagy, and transmission electron microscopy to assess changes in the number of mitochondria enclosed within autophagosome-like vesicles, it has been discovered that the addition of exogenous lactate can inhibit PINK1-Parkin-mediated mitophagy. Importantly, we have observed that lactate activates the JAK1-STAT1-ISG15 network and suppresses CSFV replication by antagonizing CCCP-induced mitophagy. These results represent the first report on the mechanisms through which the LDHA-lactate axis regulates mitophagy, the JAK-STAT pathway, and CSFV replication. This study provides novel insights into the roles of the LDHA-lactate axis in glycometabolism and viral replication.</p><p><strong>Importance: </strong>This research unveils how CSFV interacts with cellular metabolism through LDHA. By revealing LDHA's dual role and how lactate influences cellular processes during CSFV infection, this study uncovers new pathways for viral replication. These findings not only deepen our understanding of viral-host interactions but also open doors for innovative antiviral strategies centered around manipulating cellular metabolism.</p>","PeriodicalId":17583,"journal":{"name":"Journal of Virology","volume":" ","pages":"e0026825"},"PeriodicalIF":4.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12090782/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144042310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel tobamo-like mycovirus with filamentous particles replicates in plant cells.","authors":"Meilian Hong, Fengjuan Tian, Zhenmei Song, Hongmei Liu, Yigang Tong, Tingting Zhang","doi":"10.1128/jvi.02102-24","DOIUrl":"10.1128/jvi.02102-24","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Parasitic and symbiotic plant-fungus relationships have existed for millions of years, and phylogenetic analyses of certain virus families indicate transmission between plants and fungi. A group of tobamo-like viruses from various fungi has recently been identified. Tobamo-like viruses are homologous to plant viruses of the &lt;i&gt;Tobamovirus&lt;/i&gt; genus in the &lt;i&gt;Virgaviridae&lt;/i&gt; family, but it was unknown whether they form typical virus particles and can replicate and exhibit cell-to-cell movement in plants. Here, a novel tobamo-like virus, Nigrospora aurantiaca tobamo-like virus 1 (NaTLV1), obtained from the phytopathogenic fungus &lt;i&gt;Nigrospora aurantiaca&lt;/i&gt;, was characterized. Its genome (10,301 nucleotides) comprises four open reading frames (ORFs) and a poly(A) tail. ORF1 encodes a methyltransferase and helicase, and ORF2 encodes RNA-dependent RNA polymerase, which are closely related to proteins of &lt;i&gt;Virgaviridae&lt;/i&gt; viruses. ORF3 encodes a putative movement protein, and ORF4 encodes a putative coat protein, which are closely related to proteins of &lt;i&gt;Gammaflexiviridae&lt;/i&gt; and &lt;i&gt;Betaflexiviridae&lt;/i&gt; viruses. NaTLV1 formed filamentous virus particles and could replicate in &lt;i&gt;Nicotiana benthamiana&lt;/i&gt;. However, the cell-to-cell movement of NaTLV1 was not observed in &lt;i&gt;N. benthamiana&lt;/i&gt; but could not be ruled out. NaTLV1 underwent horizontal and vertical transmissions via hyphal anastomosis and conidia, respectively. There were no significant differences in phenotype or virulence between NaTLV1-infected (A4) and NaTLV1-free (V1) &lt;i&gt;N. aurantiaca&lt;/i&gt; strains. In general, our findings may be useful in elucidating the origination and evolution of tobamo-like viruses, plant virus families (&lt;i&gt;Virgaviridae&lt;/i&gt; and &lt;i&gt;Betaflexiviridae&lt;/i&gt;), and a fungal virus family (&lt;i&gt;Gammaflexiviridae&lt;/i&gt;).IMPORTANCECross-kingdom infections involving plant- and fungal-associated viruses have been directly observed in nature, and some of these viruses share a high degree of genetic similarity. A group of novel tobamo-like viruses with nonsegmented single-stranded RNA genomes was recently isolated from diverse fungal groups. Here, we identified a novel virus, Nigrospora aurantiaca tobamo-like virus 1 (NaTLV1), in the phytopathogenic fungus &lt;i&gt;Nigrospora aurantiaca&lt;/i&gt;. NaTLV1 was phylogenetically related to other tobamo-like viruses, plant-associated viruses in the &lt;i&gt;Virgaviridae&lt;/i&gt; and &lt;i&gt;Betaflexiviridae&lt;/i&gt; families, and fungus-associated viruses in the &lt;i&gt;Gammaflexiviridae&lt;/i&gt; family. NaTLV1 formed filamentous virus particles and could replicate in &lt;i&gt;Nicotiana benthamiana,&lt;/i&gt; but the cell-to-cell movement of NaTLV1 was not observed. This study provides potential insights into the origins and evolution of mycoviruses originating from plant viruses and indicates that tobamo-like viruses may have adapted to an intracellular lifestyle during evolution. The identification of novel tobamo-like viruses is crucial for understanding fungal and plant virus evo","PeriodicalId":17583,"journal":{"name":"Journal of Virology","volume":" ","pages":"e0210224"},"PeriodicalIF":4.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12090730/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human cytomegalovirus gH/gL/gO binding to PDGFRα provides a regulatory signal activating the fusion protein gB that can be blocked by neutralizing antibodies.","authors":"Eric P Schultz, Lars Ponsness, Jean-Marc Lanchy, Matthias Zehner, Florian Klein, Brent J Ryckman","doi":"10.1128/jvi.00035-25","DOIUrl":"10.1128/jvi.00035-25","url":null,"abstract":"<p><p>Herpesviruses require membrane fusion for entry and spread, a process facilitated by the fusion glycoprotein B (gB) and the regulatory factor gH/gL. The human cytomegalovirus (HCMV) gH/gL can be modified by the accessory protein gO, or the set of proteins UL128, UL130, and UL131. While the binding of the gH/gL/gO and gH/gL/UL128-131 complexes to cellular receptors, including PDGFRα and NRP2, has been well-characterized structurally, the specific role of receptor engagements by the gH/gL/gO and gH/gL/UL128-131 in regulation of fusion has remained unclear. We describe a cell-cell fusion assay that can quantitatively measure fusion on a timescale of minutes and demonstrate that binding of gH/gL/gO to PDGFRα dramatically enhances gB-mediated cell-cell fusion. In contrast, gH/gL/pUL128-131-regulated fusion is significantly slower, and gH/gL alone cannot promote gB fusion activity within this timescale. The genetic diversity of gO influenced the observed cell-cell fusion rates, correlating with previously reported effects on HCMV infectivity. Mutations in gL that had no effect on the formation of gH/gL/gO or binding to PDGFRa dramatically reduced the cell-cell fusion rate, suggesting that gL plays a critical role in linking the gH/gL/gO-PDGFRa receptor binding to activation of gB. Several neutralizing human monoclonal antibodies were found to potently block gH/gL/gO-PDGFRa-regulated cell-cell fusion, suggesting this mechanism as a therapeutic target.</p><p><strong>Importance: </strong>Development of vaccines and therapeutics targeting the fusion apparatus of human cytomegalovirus (HCMV) has been limited by the lack of an <i>in vitro</i> cell-cell fusion assay that faithfully models the receptor-dependent fusion characteristic of HCMV entry. The cell-cell fusion assay described here demonstrated that the binding of gH/gL/gO to its receptor, PDGFRα, serves to regulate the activity of the fusion protein gB, and this is specifically vulnerable to inhibition by neutralizing antibodies. Moreover, the measurement of fusion kinetics allows for mutational studies of the fusion mechanism, assessing the influence of genetic diversity among the viral glycoproteins and studying the mechanism of neutralizing antibodies.</p>","PeriodicalId":17583,"journal":{"name":"Journal of Virology","volume":" ","pages":"e0003525"},"PeriodicalIF":4.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12090739/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL3 depletion blocks vesicular stomatitis virus replication in pancreatic cancer cells through the establishment of an intrinsic antiviral state.","authors":"Cassandra Catacalos-Goad, Jacob Hawkins, Quinton Krueger, Nathaniel Foret, Valery Z Grdzelishvili","doi":"10.1128/jvi.02284-24","DOIUrl":"10.1128/jvi.02284-24","url":null,"abstract":"<p><p>Vesicular stomatitis virus (VSV) is a promising oncolytic virus (OV) against different malignancies, including pancreatic ductal adenocarcinoma (PDAC). In this study, we examined the role of methyltransferase-like 3 (METTL3), a catalytic subunit of the cellular writer complex that is responsible for N6-methyladenosine (m6A) RNA modification, as a potential host factor of VSV replication in PDAC cells. METTL3 was previously shown to be upregulated in PDAC, where it promotes cancer cell proliferation, invasion, and chemoresistance. The impact of METTL3 on life cycles of different viruses varies depending on both the virus and the cell type. Additionally, METTL3 plays a positive role in VSV replication in non-PDAC cells via m6A modification of VSV RNAs, which attenuates innate antiviral responses. In this study, we examined the role of METTL3 in 10 different human PDAC cell lines and uncovered two distinct outcomes. METTL3 depletion did not affect VSV replication in PDAC cell lines with defective innate antiviral signaling, suggesting that METTL3 is not directly involved in VSV replication. In contrast, METTL3 depletion dramatically inhibited VSV replication in PDAC cell lines with functional antiviral signaling. We show that this result is due to the RIG-I-dependent induction of a virus-independent, intrinsic antiviral state in METTL3-depleted PDAC cells. This intrinsic antiviral state was marked by type-III (but not type I or II) interferon secretion and constitutive overexpression of antiviral sensors [RIG-I (DDX58), MDA5 (IFIH1), and LGP2 (DHX58)], transactivators (STAT1, IRF7, and IRF9), and a diverse subset of antiviral effectors, including MX1, OAS1/2/3, and IFIT1/3.IMPORTANCEPancreatic cancer is a deadly and extremely challenging disease, making it essential to develop new treatment options and improve patient survival rates. One promising approach is the use of replication-competent \"oncolytic viruses\" designed to specifically target and destroy cancer cells while sparing healthy ones. To create effective oncolytic virus therapies for pancreatic cancer, it is crucial to identify host factors that influence the successful infection of cancer cells by these viruses. Here, we demonstrate that the cellular protein METTL3, which was previously shown to promote pancreatic cancer cell proliferation, invasion, and resistance to chemotherapy, plays a positive role in oncolytic virus replication in most of the tested human pancreatic cancer cell lines. We demonstrate that METTL3 depletion induces a chronic antiviral state that dramatically inhibits viral replication. Our study is important for understanding and improving oncolytic virus-based therapies.</p>","PeriodicalId":17583,"journal":{"name":"Journal of Virology","volume":" ","pages":"e0228424"},"PeriodicalIF":4.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12090749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144017209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction for Yan et al., \"Molecular Determinants of Hepatitis B and D Virus Entry Restriction in Mouse Sodium Taurocholate Cotransporting Polypeptide\".","authors":"Huan Yan, Bo Peng, Wenhui He, Guocai Zhong, Yonghe Qi, Bijie Ren, Zhenchao Gao, Zhiyi Jing, Mei Song, Guangwei Xu, Jianhua Sui, Wenhui Li","doi":"10.1128/jvi.00445-25","DOIUrl":"10.1128/jvi.00445-25","url":null,"abstract":"","PeriodicalId":17583,"journal":{"name":"Journal of Virology","volume":" ","pages":"e0044525"},"PeriodicalIF":4.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12090734/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144029618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activated blood-derived human primary T cells support replication of HAdV C5 and virus transmission to polarized human primary epithelial cells.","authors":"Daniela Policarpo Sequeira, Maarit Suomalainen, Patrick C Freitag, Andreas Plückthun, Michael Klingenbrunner, Lucy Fischer, Silvio Hemmi, Christian Münz, Romain Volle, Urs F Greber","doi":"10.1128/jvi.01825-24","DOIUrl":"10.1128/jvi.01825-24","url":null,"abstract":"<p><p>Human adenoviruses (HAdVs) cause self-limiting disease but are life-threatening to immunocompromised individuals. HAdV-C5 infects epithelial cells of the airways and eyes through aerosols, contaminated hands, or medical instruments, as well as fecal-oral contacts, gives rise to viremia, persisting in lymphoid cells of the gastrointestinal tract. Here, we show that pre-activated human primary blood-derived T cells can be infected with HAdV-C5 <i>in vitro</i>, upon incubation of the virus with a mixture of three distinct homotrimeric adapter proteins that target the virus to T cells. Each of the adapter proteins can bind 1 of the 12 fiber knobs of the virion through a designed ankyrin repeat protein. Two of the adapters contained a single-chain antibody fragment to T cell surface proteins CD3 or CD28, and the third one contained the cytokine interleukin-2. These adapters mediated efficient infection of primary T cells by HAdV-C5 and infectious progeny release, albeit with donor-to-donor variability. Co-culture of well-polarized air-liquid interface human bronchial epithelial cells with infected CD3⁺ T cells gave rise to progressively increased viral titers from replicating but not from replication-defective E1-deleted HAdV-C5, notably with similar kinetics as cell-free virus infections, suggesting that progeny virus from T cells was further amplified in epithelial cells. This study provides a platform to explore interactions between epithelial and immune cells in acute and persistent HAdV-C5 infection settings.IMPORTANCEMany human adenoviruses (HAdV), including HAdV-C5, infect and propagate to high titers in epithelial cells of the airways. Virus ends up in lymphoid cells of the gastrointestinal and respiratory mucosa, where it can persist subclinically for years, restricted by memory T cells and humoral immune defense. In immunodeficient patients or newborns, however, HAdV can be fatal, coincident with lymphocytopenia and virus proliferation in epithelial cells. Here, we show that activated blood-derived human primary T lymphocytes can be productively infected with HAdV-C5 coated with trimerized adapter proteins targeting CD3, CD28, and the interleukin 2 receptors. A co-culture model of infected T cells and primary human bronchial epithelial cells in the absence of HAdV-specific immune cells showed that progeny virus from T cells was transferred to epithelial cells and led to increased progeny production compared to infected T cells alone, a situation potentially mimicking persistently infected mucosal lymphoid cells in immunosuppressed patients.</p>","PeriodicalId":17583,"journal":{"name":"Journal of Virology","volume":" ","pages":"e0182524"},"PeriodicalIF":4.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12090788/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144033386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"2024 Acknowledgment of <i>Journal of Virology Ad Hoc</i> Reviewers.","authors":"Felicia Goodrum, Stacey Schultz-Cherry","doi":"10.1128/jvi.00552-25","DOIUrl":"https://doi.org/10.1128/jvi.00552-25","url":null,"abstract":"","PeriodicalId":17583,"journal":{"name":"Journal of Virology","volume":"99 5","pages":"e0055225"},"PeriodicalIF":4.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144111138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recognizing the Top Peer Reviewers in 2024 for the <i>Journal of Virology</i>.","authors":"Felicia Goodrum, Stacey Schultz-Cherry","doi":"10.1128/jvi.00539-25","DOIUrl":"https://doi.org/10.1128/jvi.00539-25","url":null,"abstract":"","PeriodicalId":17583,"journal":{"name":"Journal of Virology","volume":"99 5","pages":"e0053925"},"PeriodicalIF":4.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144111140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endemic coronavirus infection is associated with SARS-CoV-2 Fc receptor-binding antibodies.","authors":"David J Bean, Yan Mei Liang, Frida Avila, Xianbao He, Archana Asundi, Manish Sagar","doi":"10.1128/jvi.00550-25","DOIUrl":"10.1128/jvi.00550-25","url":null,"abstract":"<p><p>Recent documented infection with an endemic coronavirus (eCoV) is associated with less severe coronavirus disease 2019 (COVID-19), yet the immune mechanism behind this protection has not been fully explored. We measured both antibody and T-cell responses against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in SARS-CoV-2-naïve individuals, classified into two groups: those with or without presumed recent eCoV infections. There was no difference in neutralizing antibodies and T-cell responses against SARS-CoV-2 antigens between the two groups. SARS-CoV-2-naïve individuals with recent presumed eCoV infection, however, had higher and significantly correlated levels of Fc receptor (FcR)-binding antibodies against eCoV spikes (S) and SARS-CoV-2 S2. Recent eCoV infection boosts cross-reactive antibodies that can mediate Fc effector functions, and this may play a role in the observed heterotypic immune protection against severe COVID-19.</p><p><strong>Importance: </strong>With the recent emergence of SARS-CoV-2 and other pathogenic coronaviruses, it is important to understand how the immune system may protect against disease from future coronavirus outbreaks. We investigated the adaptive immune responses elicited from a \"common cold\" eCoV and measured the cross-reactivity against SARS-CoV-2 in individuals classified as having or not having a recent eCoV infection. Although both groups had similar cross-reactive T-cell and neutralizing antibody responses, individuals with a recent eCoV infection had higher antibody levels capable of Fc receptor binding. Antibodies with enhanced Fc receptor binding could mediate the killing of virally infected cells through mechanisms such as antibody-dependent cellular cytotoxicity, which may reduce the severity of COVID-19. Antibodies capable of mediating Fc effector functions may be critical for therapies and vaccines against future pathogenic coronavirus outbreaks.</p>","PeriodicalId":17583,"journal":{"name":"Journal of Virology","volume":" ","pages":"e0055025"},"PeriodicalIF":4.0,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144094078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}