Pub Date : 2025-09-01Epub Date: 2025-07-20DOI: 10.1016/j.virusres.2025.199606
Zhen Chen , Ming Cai , Li Chai , Xia Li , Rongcheng Wen , Jinyan Jia , Huang Li , Fei Yu
Influenza virus epidemics occur annually, posing significant public health challenges. Although anti-influenza drugs are available, newly emerged viral strains frequently develop resistance, necessitating the discovery of new antiviral reagents. This study aims to evaluate the anti-influenza virus activity of Blumea Balsamifera (L.) DC. Extract (BBE) in both in vitro and in vivo settings. The antiviral activity of BBE was assessed using the CellTiter-Glo assay and the cytopathic effect (CPE) assay in Madin-Darby canine kidney (MDCK) cells, targeting influenza virus strains H1N1, H3N2, and four influenza B viruses. Specifically, BBE demonstrated significant inhibition of MDCK cell lesions caused by the A subtypes A/WSN/33 (H1N1) and A/Hong Kong/4801/2014 (H3N2), as well as the B subtypes B/Darwin/58/2019 (Yamagata), B/Phuket/3073/2013 (Yamagata), B/Sichuan Gaoxin/531/2018 (Victoria), and B/Brisbane/60/2008 (Victoria). The extract showed inhibitory concentration (IC50) values of 8.71, 11.38, 10.14, 4.66, 3.17, and 4.29 μg/mL, respectively. Time-of-drug-addition assay results indicated that BBE inhibits the early stages of influenza virus replication. Additionally, in vivo studies in murine models further confirmed the protective effects of BBE, where it reduced viral-induced weight loss, delayed mortality, and mitigated lung tissue damage. These findings suggest that Blumea Balsamifera (L.) DC. extract holds promise as a potential reagent against influenza viruses and warrants further investigation.
{"title":"Anti-influenza activity of Blumea Balsamifera (L.) DC. Extract: In vitro and in vivo evaluation against multiple influenza virus strains","authors":"Zhen Chen , Ming Cai , Li Chai , Xia Li , Rongcheng Wen , Jinyan Jia , Huang Li , Fei Yu","doi":"10.1016/j.virusres.2025.199606","DOIUrl":"10.1016/j.virusres.2025.199606","url":null,"abstract":"<div><div>Influenza virus epidemics occur annually, posing significant public health challenges. Although anti-influenza drugs are available, newly emerged viral strains frequently develop resistance, necessitating the discovery of new antiviral reagents. This study aims to evaluate the anti-influenza virus activity of Blumea Balsamifera (L.) DC. Extract (BBE) in both in vitro and in vivo settings. The antiviral activity of BBE was assessed using the CellTiter-Glo assay and the cytopathic effect (CPE) assay in Madin-Darby canine kidney (MDCK) cells, targeting influenza virus strains H1N1, H3N2, and four influenza B viruses. Specifically, BBE demonstrated significant inhibition of MDCK cell lesions caused by the A subtypes A/WSN/33 (H1N1) and A/Hong Kong/4801/2014 (H3N2), as well as the B subtypes B/Darwin/58/2019 (Yamagata), B/Phuket/3073/2013 (Yamagata), B/Sichuan Gaoxin/531/2018 (Victoria), and B/Brisbane/60/2008 (Victoria). The extract showed inhibitory concentration (IC50) values of 8.71, 11.38, 10.14, 4.66, 3.17, and 4.29 <em>μ</em>g/mL, respectively. Time-of-drug-addition assay results indicated that BBE inhibits the early stages of influenza virus replication. Additionally, in vivo studies in murine models further confirmed the protective effects of BBE, where it reduced viral-induced weight loss, delayed mortality, and mitigated lung tissue damage. These findings suggest that Blumea Balsamifera (L.) DC. extract holds promise as a potential reagent against influenza viruses and warrants further investigation.</div></div>","PeriodicalId":23483,"journal":{"name":"Virus research","volume":"359 ","pages":"Article 199606"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144691685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01Epub Date: 2025-07-30DOI: 10.1016/j.virusres.2025.199611
Qingqing Shao , Tong Liu , Bin Hu , Liuqing Chen
Autophagy and apoptosis are two pivotal programmed cell death pathways that regulate vital physiological processes, ranging from cellular development to intracellular homeostasis. These pathways also act as key battlegrounds in host-pathogen interactions during viral infection. This comprehensive review explores the dual regulatory mechanisms controlling autophagy and apoptosis triggered by clinically significant human viruses. These include DNA viruses—such as herpes simplex virus (HSV), Epstein-Barr virus (EBV), hepatitis viruses, human papillomavirus (HPV), and human bocavirus (HBoV)—and RNA viruses, including human immunodeficiency virus type 1 (HIV-1), severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), enterovirus 71 (EV71), influenza viruses, respiratory syncytial virus (RSV), Coxsackievirus B (CVB), rabies virus (RABV), and dengue virus serotype 2 (DENV2). We specifically highlight the dynamic crosstalk between autophagic and apoptotic pathways during viral pathogenesis, analyzing how viruses strategically co-opt both cellular processes to facilitate infection. By systematically elucidating these viral manipulation strategies, this review aims to provide a reference for developing targeted antiviral strategies and identifying novel therapeutic interventions.
{"title":"Interplay between autophagy and apoptosis in human viral pathogenesis","authors":"Qingqing Shao , Tong Liu , Bin Hu , Liuqing Chen","doi":"10.1016/j.virusres.2025.199611","DOIUrl":"10.1016/j.virusres.2025.199611","url":null,"abstract":"<div><div>Autophagy and apoptosis are two pivotal programmed cell death pathways that regulate vital physiological processes, ranging from cellular development to intracellular homeostasis. These pathways also act as key battlegrounds in host-pathogen interactions during viral infection. This comprehensive review explores the dual regulatory mechanisms controlling autophagy and apoptosis triggered by clinically significant human viruses. These include DNA viruses—such as herpes simplex virus (HSV), Epstein-Barr virus (EBV), hepatitis viruses, human papillomavirus (HPV), and human bocavirus (HBoV)—and RNA viruses, including human immunodeficiency virus type 1 (HIV-1), severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), enterovirus 71 (EV71), influenza viruses, respiratory syncytial virus (RSV), Coxsackievirus B (CVB), rabies virus (RABV), and dengue virus serotype 2 (DENV2). We specifically highlight the dynamic crosstalk between autophagic and apoptotic pathways during viral pathogenesis, analyzing how viruses strategically co-opt both cellular processes to facilitate infection. By systematically elucidating these viral manipulation strategies, this review aims to provide a reference for developing targeted antiviral strategies and identifying novel therapeutic interventions.</div></div>","PeriodicalId":23483,"journal":{"name":"Virus research","volume":"359 ","pages":"Article 199611"},"PeriodicalIF":2.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144765568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01Epub Date: 2025-07-19DOI: 10.1016/j.virusres.2025.199610
Madina S. Alexyuk, Andrey P. Bogoyavlenskiy, Irina A. Zaitseva, Elmira S. Omirtaeva, Yergali S. Moldakhanov, Kuralay S. Akanova, Elmira I. Anarkulova, Vladimir E. Berezin, Pavel G. Alexyuk
With the global spread of bacterial resistance and the decreasing effectiveness of antibiotics, the relevance of phage therapy is constantly growing. However, for systemic use of bacteriophages in medical practice, a complete understanding of their interaction not only with bacterial cells but also with human and animal organisms in the context of co-administered therapy is required.
This article presents the studies into the effects of lytic Escherichia coli bacteriophages on various immune response factors after their intraperitoneal administration in mice. It was found using Real-Time PCR and ELISA methods that the administration of the vB_EcoM_SCS4 and vB_EcoM_SCS57 phages did not increase the gene expression of TLR3, TLR9, IL-4, IL-5, IL-6 and the concentration of IL-2, IL-4, IL-5 and IL-6 in mice, but led to a multi-fold increase in the gene expression and concentration of IFNγ. Whereas, the injection of the vB_EcoS_SCS44 phage into mice increased the expression of the studied genes, except for the IL-5 gene, by 4 to 7 times and increased the concentration of IL-2, IL-4, IL-6 and IFNγ, except for IL-5, by 2 to 3 times. When determining the titer of virus-specific antibodies, it was found that after the administration of phages vB_EcoM_SCS4 and vB_EcoM_SCS57, the titer of IgA, IgG and IgM did not differ from that of the control animals, but the administration of phage vB_EcoS_SCS44 stimulated a twofold increase in the titer of phage-specific IgA, IgG, IgM.
{"title":"Comparative analysis of immune responses to intraperitoneal administration of lytic E. coli bacteriophages in mice","authors":"Madina S. Alexyuk, Andrey P. Bogoyavlenskiy, Irina A. Zaitseva, Elmira S. Omirtaeva, Yergali S. Moldakhanov, Kuralay S. Akanova, Elmira I. Anarkulova, Vladimir E. Berezin, Pavel G. Alexyuk","doi":"10.1016/j.virusres.2025.199610","DOIUrl":"10.1016/j.virusres.2025.199610","url":null,"abstract":"<div><div>With the global spread of bacterial resistance and the decreasing effectiveness of antibiotics, the relevance of phage therapy is constantly growing. However, for systemic use of bacteriophages in medical practice, a complete understanding of their interaction not only with bacterial cells but also with human and animal organisms in the context of co-administered therapy is required.</div><div>This article presents the studies into the effects of lytic <em>Escherichia coli</em> bacteriophages on various immune response factors after their intraperitoneal administration in mice. It was found using Real-Time PCR and ELISA methods that the administration of the vB_EcoM_SCS4 and vB_EcoM_SCS57 phages did not increase the gene expression of TLR3, TLR9, IL-4, IL-5, IL-6 and the concentration of IL-2, IL-4, IL-5 and IL-6 in mice, but led to a multi-fold increase in the gene expression and concentration of IFNγ. Whereas, the injection of the vB_EcoS_SCS44 phage into mice increased the expression of the studied genes, except for the IL-5 gene, by 4 to 7 times and increased the concentration of IL-2, IL-4, IL-6 and IFNγ, except for IL-5, by 2 to 3 times. When determining the titer of virus-specific antibodies, it was found that after the administration of phages vB_EcoM_SCS4 and vB_EcoM_SCS57, the titer of IgA, IgG and IgM did not differ from that of the control animals, but the administration of phage vB_EcoS_SCS44 stimulated a twofold increase in the titer of phage-specific IgA, IgG, IgM.</div></div>","PeriodicalId":23483,"journal":{"name":"Virus research","volume":"359 ","pages":"Article 199610"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144683242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01Epub Date: 2025-07-14DOI: 10.1016/j.virusres.2025.199607
Eric S. Martinez , Sebastien Fuchs , Hendrik Szurmant , Xunxuan Chen , Andrew Comer , Edward Lee , Raymond Hruby , Rebecca Giusti , Brian Loveless , Julieanne P. Sees , Paula Crone , Laura J. Peek , Gary Pestano , Bin Xie , Joseph Zammuto , Sir Robert Hostoffer Jr. , Jesus Sanchez Jr.
Osteopathic manipulative treatment (OMT) has demonstrated immune augmentation in preclinical studies, but direct evidence in humans is lacking. We conducted a randomized controlled trial on the addition of OMT in subjects receiving their first Pfizer-BioNTech (BNT162b2) COVID-19 vaccination in 2021. Subjects were randomized to either receive OMT at each vaccination or not. We measured anti-spike protein, anti-nucleocapsid, and neutralizing antibodies. Primary endpoints were time-resolved and cumulative anti-SARS-CoV-2 spike protein antibody titers. Secondary endpoints were breakthrough infection symptom frequency, severity, and duration. 104 subjects were randomly assigned to control or OMT group, with 91 subjects completing the primary vaccination series. Initial antibody titers separated subjects into 51 COVID-19-naïve and 40 COVID-19-pre-exposed. COVID19-naïve subjects were selected for analysis based on data homogeneity. In this cohort, the OMT group showed significantly increased anti-SARS-CoV-2 spike protein antibody titers at 3 weeks vs controls (p = 0.038). Cumulative titers in this cohort, were significantly increased in the OMT group at 5 weeks (p = 0.046) and at 13 weeks (p = 0.009) compared to controls. An intention-to-treat (ITT) analysis of all subjects revealed significant differences in titers between the OMT group and controls at 3 weeks (p < 0.001) and at 13 weeks for AUC titers (p = 0.035) as compared to controls. The COVID-19- pre-exposed group showed no significant differences. Both groups had 10 breakthrough infections, but the OMT group experienced fewer and less severe symptoms, with symptom duration reduced from 8 days in controls to 4.5 days in the OMT group (p = 0.013). Medication duration was shorter in the OMT group, 1.5 days vs 5 days (p = 0.014). OMT-treated subjects developed quicker and stronger vaccine-induced antibody titers and had significantly shorter and less severe breakthrough symptoms, suggesting OMT may enhance immune responses to COVID19 vaccination.
{"title":"COVID-19 mRNA vaccine immune response to the addition of osteopathic manipulative treatment with lymphatic pumps: a randomized controlled trial","authors":"Eric S. Martinez , Sebastien Fuchs , Hendrik Szurmant , Xunxuan Chen , Andrew Comer , Edward Lee , Raymond Hruby , Rebecca Giusti , Brian Loveless , Julieanne P. Sees , Paula Crone , Laura J. Peek , Gary Pestano , Bin Xie , Joseph Zammuto , Sir Robert Hostoffer Jr. , Jesus Sanchez Jr.","doi":"10.1016/j.virusres.2025.199607","DOIUrl":"10.1016/j.virusres.2025.199607","url":null,"abstract":"<div><div>Osteopathic manipulative treatment (OMT) has demonstrated immune augmentation in preclinical studies, but direct evidence in humans is lacking. We conducted a randomized controlled trial on the addition of OMT in subjects receiving their first Pfizer-BioNTech (BNT162b2) COVID-19 vaccination in 2021. Subjects were randomized to either receive OMT at each vaccination or not. We measured anti-spike protein, anti-nucleocapsid, and neutralizing antibodies. Primary endpoints were time-resolved and cumulative anti-SARS-CoV-2 spike protein antibody titers. Secondary endpoints were breakthrough infection symptom frequency, severity, and duration. 104 subjects were randomly assigned to control or OMT group, with 91 subjects completing the primary vaccination series. Initial antibody titers separated subjects into 51 COVID-19-naïve and 40 COVID-19-pre-exposed. COVID19-naïve subjects were selected for analysis based on data homogeneity. In this cohort, the OMT group showed significantly increased anti-SARS-CoV-2 spike protein antibody titers at 3 weeks vs controls (<em>p</em> = 0.038). Cumulative titers in this cohort, were significantly increased in the OMT group at 5 weeks (<em>p</em> = 0.046) and at 13 weeks (<em>p</em> = 0.009) compared to controls. An intention-to-treat (ITT) analysis of all subjects revealed significant differences in titers between the OMT group and controls at 3 weeks (<em>p</em> < 0.001) and at 13 weeks for AUC titers (<em>p</em> = 0.035) as compared to controls. The COVID-19- pre-exposed group showed no significant differences. Both groups had 10 breakthrough infections, but the OMT group experienced fewer and less severe symptoms, with symptom duration reduced from 8 days in controls to 4.5 days in the OMT group (<em>p</em> = 0.013). Medication duration was shorter in the OMT group, 1.5 days vs 5 days (<em>p</em> = 0.014). OMT-treated subjects developed quicker and stronger vaccine-induced antibody titers and had significantly shorter and less severe breakthrough symptoms, suggesting OMT may enhance immune responses to COVID19 vaccination.</div></div>","PeriodicalId":23483,"journal":{"name":"Virus research","volume":"359 ","pages":"Article 199607"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144650692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-06-26DOI: 10.1016/j.virusres.2025.199599
Iván Sanz-Muñoz , Alejandro Martín-Toribio , Adrián García-Concejo , Irene Arroyo-Hernantes , Marina Toquero-Asensio , Javier Sánchez-Martínez , Carla Rodríguez-Crespo , Silvia Rojo-Rello , Marta Domínguez-Gil , Eduardo Tamayo-Gómez , Marta Hernández-Pérez , José M Eiros
The therapeutic arsenal against influenza is extremely limited and resistance often arises due to the emergence of mutations, especially in the neuraminidase (NA) gene. This study aimed to evaluate the evolution of NA mutations over 15 years in Spain. To do so, we used the GISAID database from which we downloaded a total of 11,125 influenza A(H1N1)pdm09, A(H3N2), B/Victoria and B/Yamagata NA virus sequences, and analyzed the resistance mutations using FluSurver software. Our results showed that the occurrence of NA resistance mutations remained constant in the four viruses during the 15 seasons evaluated, being around 0.5–5 %. Most of the resistance was found in the A(H1N1)pdm09 subtype (around 70 %), especially from the 2023–2024 season onwards, when a significant increase in the occurrence of S247N mutation was observed. The occurrence of this type of mutation before 2022 was rare, but in the 2023–2024 season a total of 44 influenza viruses harboring S247N mutations were detected, while in the other years, only two cases were observed. Some studies have described a significant increase in this mutation over the past two seasons and although it appears to confer only slightly reduced inhibition to oseltamivir, its increase is noteworthy and should be a reason for increased their vigilance.
{"title":"A 15-year study of neuraminidase mutations and the increasing of S247N mutation in Spain","authors":"Iván Sanz-Muñoz , Alejandro Martín-Toribio , Adrián García-Concejo , Irene Arroyo-Hernantes , Marina Toquero-Asensio , Javier Sánchez-Martínez , Carla Rodríguez-Crespo , Silvia Rojo-Rello , Marta Domínguez-Gil , Eduardo Tamayo-Gómez , Marta Hernández-Pérez , José M Eiros","doi":"10.1016/j.virusres.2025.199599","DOIUrl":"10.1016/j.virusres.2025.199599","url":null,"abstract":"<div><div>The therapeutic arsenal against influenza is extremely limited and resistance often arises due to the emergence of mutations, especially in the neuraminidase (NA) gene. This study aimed to evaluate the evolution of NA mutations over 15 years in Spain. To do so, we used the GISAID database from which we downloaded a total of 11,125 influenza A(H1N1)pdm09, A(H3N2), B/Victoria and B/Yamagata NA virus sequences, and analyzed the resistance mutations using FluSurver software. Our results showed that the occurrence of NA resistance mutations remained constant in the four viruses during the 15 seasons evaluated, being around 0.5–5 %. Most of the resistance was found in the A(H1N1)pdm09 subtype (around 70 %), especially from the 2023–2024 season onwards, when a significant increase in the occurrence of S247N mutation was observed. The occurrence of this type of mutation before 2022 was rare, but in the 2023–2024 season a total of 44 influenza viruses harboring S247N mutations were detected, while in the other years, only two cases were observed. Some studies have described a significant increase in this mutation over the past two seasons and although it appears to confer only slightly reduced inhibition to oseltamivir, its increase is noteworthy and should be a reason for increased their vigilance.</div></div>","PeriodicalId":23483,"journal":{"name":"Virus research","volume":"358 ","pages":"Article 199599"},"PeriodicalIF":2.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144529695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-06-09DOI: 10.1016/j.virusres.2025.199594
Xia Zhou , Li Feng
Influenza infection could be associated with several systemic complications, including acute myocardial infarction (AMI); however, evidence on this association remains inconsistent. This systematic review and meta-analysis examined the influenza-AMI link, temporal AMI risk post-infection, and in-hospital outcomes and mortality in influenza-infected AMI patients. We conducted a systematic search of PubMed, EMBASE, Cochrane Library, Scopus, and Web of Science. Observational studies and self-controlled case series (SCCS) designs, were included. Data were extracted and analyzed using random-effects models to calculate pooled odds ratios (ORs), incidence rate ratios (IRRs), and 95 % confidence intervals (CIs). Subgroup analyses were performed based on exposure definitions (laboratory-confirmed influenza vs. influenza-like illness [ILI]), study design, and temporal patterns of AMI risk. In-hospital outcomes, including mortality, complications, length of stay, and costs, were also evaluated. The meta-analysis included 17 studies. A significant association was found, with a pooled adjusted OR of 2.70 (95 % CI: 1.28–5.72). ILI showed a stronger association with AMI (aOR: 2.04; 95 % CI: 1.33–3.14) compared to laboratory-confirmed influenza. Temporal analyses from SCCS studies revealed a markedly increased risk of AMI within the first week post-infection, peaking in days 1–3 (IRR: 6.83; 95 % CI: 4.66–10.01) and gradually declining thereafter. Influenza-infected AMI patients had significantly worse in-hospital outcomes, including higher mortality (OR: 1.60; 95 % CI: 1.55–1.66), and multiorgan failure (OR: 2.90; 95 % CI: 2.79–3.01). Additionally, these patients experienced longer median hospital stays (8.8 days vs. 5.5 days) and higher hospitalization costs ($20,678 vs. $18,269) compared to non-influenza AMI patients. This study confirms a strong link between influenza and AMI, especially early post-infection. Influenza-infected AMI patients experience worse outcomes, longer hospital stays, and higher costs. These findings highlight the importance of influenza prevention strategies, including vaccination, particularly in high-risk groups, to reduce AMI risk and its cardiovascular burden.
{"title":"The association between influenza infection and acute myocardial infarction: A comprehensive systematic review and meta-analysis","authors":"Xia Zhou , Li Feng","doi":"10.1016/j.virusres.2025.199594","DOIUrl":"10.1016/j.virusres.2025.199594","url":null,"abstract":"<div><div>Influenza infection could be associated with several systemic complications, including acute myocardial infarction (AMI); however, evidence on this association remains inconsistent. This systematic review and meta-analysis examined the influenza-AMI link, temporal AMI risk post-infection, and in-hospital outcomes and mortality in influenza-infected AMI patients. We conducted a systematic search of PubMed, EMBASE, Cochrane Library, Scopus, and Web of Science. Observational studies and self-controlled case series (SCCS) designs, were included. Data were extracted and analyzed using random-effects models to calculate pooled odds ratios (ORs), incidence rate ratios (IRRs), and 95 % confidence intervals (CIs). Subgroup analyses were performed based on exposure definitions (laboratory-confirmed influenza vs. influenza-like illness [ILI]), study design, and temporal patterns of AMI risk. In-hospital outcomes, including mortality, complications, length of stay, and costs, were also evaluated. The meta-analysis included 17 studies. A significant association was found, with a pooled adjusted OR of 2.70 (95 % CI: 1.28–5.72). ILI showed a stronger association with AMI (aOR: 2.04; 95 % CI: 1.33–3.14) compared to laboratory-confirmed influenza. Temporal analyses from SCCS studies revealed a markedly increased risk of AMI within the first week post-infection, peaking in days 1–3 (IRR: 6.83; 95 % CI: 4.66–10.01) and gradually declining thereafter. Influenza-infected AMI patients had significantly worse in-hospital outcomes, including higher mortality (OR: 1.60; 95 % CI: 1.55–1.66), and multiorgan failure (OR: 2.90; 95 % CI: 2.79–3.01). Additionally, these patients experienced longer median hospital stays (8.8 days vs. 5.5 days) and higher hospitalization costs ($20,678 vs. $18,269) compared to non-influenza AMI patients. This study confirms a strong link between influenza and AMI, especially early post-infection. Influenza-infected AMI patients experience worse outcomes, longer hospital stays, and higher costs. These findings highlight the importance of influenza prevention strategies, including vaccination, particularly in high-risk groups, to reduce AMI risk and its cardiovascular burden.</div></div>","PeriodicalId":23483,"journal":{"name":"Virus research","volume":"358 ","pages":"Article 199594"},"PeriodicalIF":2.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144276030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-06-04DOI: 10.1016/j.virusres.2025.199589
Hong Hong , Xintong Han , Qiuxiang Hu , Huafeng Song , Bing Han
Background & aim
Chronic hepatitis B (CHB) is a global public health problem affecting hundreds of millions of people and is associated with significant morbidity and mortality of liver cancer. Exosomes originate from cells and their detection in biofluids provides valuable insights into cellular and tissue alterations, thus reflecting underlying pathological states. The aim of this study was to provide exosomal RNA biomarkers of CHB and develop a machine learning model for the non-invasive diagnosis of CHB patients.
Methods
The differentially expressed genes (DEGs) were screened according to the RNA-seq data of normal and CHB liver tissues. The biomarkers were selected according to the analysis of pathway enrichment and functional annotation. The correlation of biomarkers’ expression level with the inflammation stage of CHB patients was analyzed. The non-invasive diagnostic value of the potential RNA biomarkers was evaluated by checking their different expression level in the plasma exosome of healthy individuals and CHB patients. A machine learning model was constructed to diagnose CHB by combining three identified biomarkers.
Results
A total of 1,006 differential expressed genes (569 upregulated and 437 downregulated) were screened between normal and CHB tissues. The GO and KEGG results showed the DEGs were mainly enriched in inflammation-related pathways. Among these genes, the expression of 4 upregulated genes and 27 downregulated genes showed consistent trends with the inflammation stage utilizing an independent CHB dataset. Three (PXN-AS1, RAD9A, SLC17A9) of 27 downregulated genes were found significantly decreased in plasma exosome of CHB patients. ROC analysis revealed that PXN-AS1, RAD9A and SLC17A9 exhibited moderate diagnostic performance in distinguishing CHB from healthy controls, with AUC values of 0.743, 0.762, and 0.665 respectively. A machine learning model, Adaboost classifier, was constructed to detect CHB by combining exosomal expression of PXN-AS1, RAD9A and SLC17A9. The AUC of the model was 0.983 and 0.924 for CHB detection in train and test dataset respectively.
Conclusion
Based on multiple RNA-seq data of tissues and plasma exosomes, we identified PXN-AS1, RAD9A, SLC17A9 as diagnostic biomarkers for CHB detection. The model based on three biomarkers showed potential diagnostic value for detecting CHB. Additional validation with a larger sample size is essential to thoroughly assess the reliability of these three biomarkers and the model's performance.
{"title":"Identification and evaluation of biomarkers for diagnosis of chronic hepatitis B using RNA-seq","authors":"Hong Hong , Xintong Han , Qiuxiang Hu , Huafeng Song , Bing Han","doi":"10.1016/j.virusres.2025.199589","DOIUrl":"10.1016/j.virusres.2025.199589","url":null,"abstract":"<div><h3>Background & aim</h3><div>Chronic hepatitis B (CHB) is a global public health problem affecting hundreds of millions of people and is associated with significant morbidity and mortality of liver cancer. Exosomes originate from cells and their detection in biofluids provides valuable insights into cellular and tissue alterations, thus reflecting underlying pathological states. The aim of this study was to provide exosomal RNA biomarkers of CHB and develop a machine learning model for the non-invasive diagnosis of CHB patients.</div></div><div><h3>Methods</h3><div>The differentially expressed genes (DEGs) were screened according to the RNA-seq data of normal and CHB liver tissues. The biomarkers were selected according to the analysis of pathway enrichment and functional annotation. The correlation of biomarkers’ expression level with the inflammation stage of CHB patients was analyzed. The non-invasive diagnostic value of the potential RNA biomarkers was evaluated by checking their different expression level in the plasma exosome of healthy individuals and CHB patients. A machine learning model was constructed to diagnose CHB by combining three identified biomarkers.</div></div><div><h3>Results</h3><div>A total of 1,006 differential expressed genes (569 upregulated and 437 downregulated) were screened between normal and CHB tissues. The GO and KEGG results showed the DEGs were mainly enriched in inflammation-related pathways. Among these genes, the expression of 4 upregulated genes and 27 downregulated genes showed consistent trends with the inflammation stage utilizing an independent CHB dataset. Three (<em>PXN-AS1, RAD9A, SLC17A9</em>) of 27 downregulated genes were found significantly decreased in plasma exosome of CHB patients. ROC analysis revealed that <em>PXN-AS1, RAD9A</em> and <em>SLC17A9</em> exhibited moderate diagnostic performance in distinguishing CHB from healthy controls, with AUC values of 0.743, 0.762, and 0.665 respectively. A machine learning model, Adaboost classifier, was constructed to detect CHB by combining exosomal expression of <em>PXN-AS1, RAD9A</em> and <em>SLC17A9</em>. The AUC of the model was 0.983 and 0.924 for CHB detection in train and test dataset respectively.</div></div><div><h3>Conclusion</h3><div>Based on multiple RNA-seq data of tissues and plasma exosomes, we identified <em>PXN-AS1, RAD9A, SLC17A9</em> as diagnostic biomarkers for CHB detection. The model based on three biomarkers showed potential diagnostic value for detecting CHB. Additional validation with a larger sample size is essential to thoroughly assess the reliability of these three biomarkers and the model's performance.</div></div>","PeriodicalId":23483,"journal":{"name":"Virus research","volume":"358 ","pages":"Article 199589"},"PeriodicalIF":2.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144249826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-06-21DOI: 10.1016/j.virusres.2025.199601
Kairui Yang
Emerging pathogens underscore an urgent need for rapidly developed vaccines to minimize mortality and societal disruption. Traditional vaccine development requires time spans of years, making it ill-suited to fast evolving viruses that can overwhelm healthcare systems and economies. In response, plug-and-play vaccine platforms offer a more agile solution. By reusing proven backbones, they reduce the repetitive safety and production steps otherwise required for each new pathogen, thus accelerating both regulatory approval and large-scale manufacturing. In parallel, artificial intelligence and computational tools enable faster antigen and epitope identification, more accurate immune response modeling, and improved vaccine design. These innovations have already shortened timelines and enhanced efficacy.
{"title":"Accelerating vaccine development: Plug-and-play platforms for emerging infectious diseases","authors":"Kairui Yang","doi":"10.1016/j.virusres.2025.199601","DOIUrl":"10.1016/j.virusres.2025.199601","url":null,"abstract":"<div><div>Emerging pathogens underscore an urgent need for rapidly developed vaccines to minimize mortality and societal disruption. Traditional vaccine development requires time spans of years, making it ill-suited to fast evolving viruses that can overwhelm healthcare systems and economies. In response, plug-and-play vaccine platforms offer a more agile solution. By reusing proven backbones, they reduce the repetitive safety and production steps otherwise required for each new pathogen, thus accelerating both regulatory approval and large-scale manufacturing. In parallel, artificial intelligence and computational tools enable faster antigen and epitope identification, more accurate immune response modeling, and improved vaccine design. These innovations have already shortened timelines and enhanced efficacy.</div></div>","PeriodicalId":23483,"journal":{"name":"Virus research","volume":"358 ","pages":"Article 199601"},"PeriodicalIF":2.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144476896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-07-07DOI: 10.1016/j.virusres.2025.199604
Chadwic De’Sean Mears , Koshiro Tabata , Takuma Ariizumi , Bernard M. Hang'ombe , Yongjin Qiu , Hayato Harima , Masahiro Kajihara , William W. Hall , Michihito Sasaki , Hirofumi Sawa , Yasuko Orba
Alphaviruses in the family Togaviridae include zoonotic arthropod-borne viruses, including Sindbis virus (SINV), chikungunya virus, as well as insect-specific viruses such as Eilat virus (EILV). Previous investigations of alphaviruses in Zambia have identified a novel insect-specific alphavirus, Mwinilunga alphavirus in mosquitoes. Further ongoing surveillance resulted in the isolation of EILV and SINV for the first time in Zambia. Here, these alphaviruses were characterized in terms of growth kinetics in cells, and molecular phylogenetic relatedness to other alphaviruses. Zambian EILV (strain zmq19_M44) exhibited a close phylogenetic relationship with other insect-specific alphaviruses and shared a close nucleotide identity to those of EILV isolate (90.4 %) and Mwinilunga alphavirus (75.5 %). EILV zmq19_M44 attained a saturating titer in C6/36 cells at 6–8-days post infection but was unable to replicate in mammalian cells. Phylogenetic analysis revealed the Zambian SINV (strain zmq17_M115) belongs in Clade D of SINV Genotype 1 along with the Kenyan isolate BONI 584 from Central Africa. The growth of the SINV zmq17_M115 was comparable to that of the prototype SINV strain AR339 in mammalian cells but was statistically different in insect cells. Our findings will contribute to public health measures for the control of alphaviral diseases in Zambia.
{"title":"Mosquito-borne alphaviruses in Zambia: Isolation and characterization of Eilat and Sindbis viruses","authors":"Chadwic De’Sean Mears , Koshiro Tabata , Takuma Ariizumi , Bernard M. Hang'ombe , Yongjin Qiu , Hayato Harima , Masahiro Kajihara , William W. Hall , Michihito Sasaki , Hirofumi Sawa , Yasuko Orba","doi":"10.1016/j.virusres.2025.199604","DOIUrl":"10.1016/j.virusres.2025.199604","url":null,"abstract":"<div><div>Alphaviruses in the family <em>Togaviridae</em> include zoonotic arthropod-borne viruses, including Sindbis virus (SINV), chikungunya virus, as well as insect-specific viruses such as Eilat virus (EILV). Previous investigations of alphaviruses in Zambia have identified a novel insect-specific alphavirus, Mwinilunga alphavirus in mosquitoes. Further ongoing surveillance resulted in the isolation of EILV and SINV for the first time in Zambia. Here, these alphaviruses were characterized in terms of growth kinetics in cells, and molecular phylogenetic relatedness to other alphaviruses. Zambian EILV (strain zmq19_M44) exhibited a close phylogenetic relationship with other insect-specific alphaviruses and shared a close nucleotide identity to those of EILV isolate (90.4 %) and Mwinilunga alphavirus (75.5 %). EILV zmq19_M44 attained a saturating titer in C6/36 cells at 6–8-days post infection but was unable to replicate in mammalian cells. Phylogenetic analysis revealed the Zambian SINV (strain zmq17_M115) belongs in Clade D of SINV Genotype 1 along with the Kenyan isolate BONI 584 from Central Africa. The growth of the SINV zmq17_M115 was comparable to that of the prototype SINV strain AR339 in mammalian cells but was statistically different in insect cells. Our findings will contribute to public health measures for the control of alphaviral diseases in Zambia.</div></div>","PeriodicalId":23483,"journal":{"name":"Virus research","volume":"358 ","pages":"Article 199604"},"PeriodicalIF":2.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144596283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}