Journal of Medical Virology最新文献

{"title":"A Comprehensive Molecular and Serological Investigation of Hepatitis A Virus Among Patients With Suspected Acute Hepatitis: A Brazilian Study","authors":"Ketty Gleyzer de Oliveira,&nbsp;Mariana Pinheiro Alves Vasconcelos,&nbsp;Julia Teixeira Ton,&nbsp;Silvia Naomi de Oliveira Uehara,&nbsp;Roberta Sitnik,&nbsp;Denize Ornelas Pereira Salvador de Oliveira,&nbsp;Layze Castberg,&nbsp;Ricardo Andreotti Siqueira,&nbsp;Peter James Robinson,&nbsp;Thaís Senna de Paula Domingues,&nbsp;Caroline Thomas Panico,&nbsp;César Augusto Inoue,&nbsp;Maira Marranghello Maluf,&nbsp;Fernanda de Mello Malta,&nbsp;Deyvid Amgarten,&nbsp;Erick Dorlass,&nbsp;Pedro Sebe,&nbsp;Arlene S. Pinto,&nbsp;Cirley M. D. O. Lobato,&nbsp;Adalgisa Ferreira,&nbsp;Elodie Hyppolito,&nbsp;Raymundo Paraná,&nbsp;Maria Isabel Schinoni,&nbsp;Edmundo Pessoa de Almeida Lopes,&nbsp;Magali C. Luiz,&nbsp;Raquel F. L. Garcia,&nbsp;Dennis Armando Bertolini,&nbsp;Mário Reis Álvares-da-Silva,&nbsp;Raul Salinas Arrojo,&nbsp;Eduardo Emerim,&nbsp;Gabriela P. Coral,&nbsp;Paulo R. Acosta,&nbsp;Marcello Lucena,&nbsp;Rosângela Teixeira,&nbsp;Mônica da Costa Guedes,&nbsp;Livia Melo Villar,&nbsp;Lia Lewis Ximenez,&nbsp;Clarice Gdalevici,&nbsp;Maria Cássia Jacintho Mendes-Correa,&nbsp;Flair José Carrilho,&nbsp;Gerson Sobrinho Salvador de Oliveira,&nbsp;Paulo Roberto A. Ferreira,&nbsp;Maria Lucia Gomes Ferraz,&nbsp;Ana Catharina de Seixas Santos Nastri,&nbsp;Pablo Andres Munoz Torres,&nbsp;Glória Selegatto,&nbsp;Luciana Vilas Boas Casadio,&nbsp;Simone Tenore,&nbsp;Olavo Henrique Munhoz Leite,&nbsp;Fernanda Fernandes Souza,&nbsp;Tania Reuter,&nbsp;Francisco Souto,&nbsp;Michele Nascimento-Sales,&nbsp;Ana Paula Maciel Gurski,&nbsp;Andréa Salomão,&nbsp;Bruna Emanuelle Alvarenga Fanis,&nbsp;Maria Cristina Pimenta,&nbsp;Elton Carlos de Almeida,&nbsp;Flávia Moreno Alves de Souza,&nbsp;Gerson Fernando Mendes Pereira,&nbsp;Mario Peribañez Gonzalez,&nbsp;Michele Soares Gomes-Gouvea,&nbsp;Raymundo Soares de Azevedo,&nbsp;João Renato Rebello Pinho","doi":"10.1002/jmv.70449","DOIUrl":"https://doi.org/10.1002/jmv.70449","url":null,"abstract":"<p>Hepatitis A Virus (HAV) infects millions of individuals annually and is a major cause of acute viral hepatitis worldwide. This study aims to (1) assess HAV infection in suspected acute hepatitis patients at public healthcare institutions in Brazil; (2) evaluate the proportion of immunized individuals against HAV; (3) identify HAV genotypes; (4) examine the association between HAV infection and demographic data, as well as exposure to risk factors. This is a prospective, observational multicenter study conducted in primary health services in Brazil from October 2019 to May 2023, involving 1721 patients with suspected acute hepatitis. Acute HAV infection was identified in 108 (6.3%) patients, predominantly in young men (80%) and from South and Southeast regions of Brazil (97%). Anti-HAV IgG, indicating previous exposure or vaccination, was detected in 78.6% of individuals (74% in the South to 91% in the North). Genotype I.A was found in all cases and approximately 450 mutations were identified, most of them in the structural proteins VP1-3. Two viral groups were identified and related to two introductions of the virus: cosmopolitan sequences from North America, South America, and Europe, and a minor group of Brazilian sequences similar to Asian and South American ones. The high incidence of acute HAV infections highlights the need for targeted prevention and vaccination strategies. The characterization of HAV genetic diversity and molecular epidemiology contributes to monitoring and identifying emerging outbreaks.</p>","PeriodicalId":16354,"journal":{"name":"Journal of Medical Virology","volume":"97 6","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jmv.70449","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144309124","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}

{"title":"H13N8 and H16N3 AIV Isolated From Shorebirds Can Replicate in the Rectum of Mice","authors":"Jiaqi Lan,&nbsp;Lanlan Liu,&nbsp;Xiang Li,&nbsp;Ru Ding,&nbsp;Jiali Zhu,&nbsp;Fengyi Qu,&nbsp;Boyu Zhai,&nbsp;Jinyan Wu,&nbsp;Yajun Wang,&nbsp;Siyuan Yang,&nbsp;Hongliang Chai,&nbsp;Xiangwei Zeng","doi":"10.1002/jmv.70455","DOIUrl":"https://doi.org/10.1002/jmv.70455","url":null,"abstract":"<div>\u0000 \u0000 <p>To investigate the pathogenicity and cross-species transmission potential of H13 and H16-subtype of low pathogenic avian influenza viruses (LPAIVs), two strains of H13N8 and H16N3 isolated from shorebirds were used to infect mice. Clinical signs were observed, and viral loads and cytokine expression levels were measured. The results showed that both H13N8 and H16N3 AIV exhibited low pathogenicity in mice and could replicate efficiently in the rectum of mice without prior adaptation. Compared with the PBS group, six cytokines were expressed at low levels, further confirming the low pathogenicity of the H13N8 and H16N3 strains in mice. The results indicate that both strains have the potential for cross-species transmission to mammals.</p></div>","PeriodicalId":16354,"journal":{"name":"Journal of Medical Virology","volume":"97 6","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144300439","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}

{"title":"Single-Cell RNA Sequencing Reveals Macrophage–Endothelial Cell Crosstalk in Viral Myocarditis","authors":"Yingnan You,&nbsp;Kaiyin Guo,&nbsp;Mengjie Ma,&nbsp;Xiuyun Duan,&nbsp;Yaxue Xie,&nbsp;Yanjie Jiang,&nbsp;Hailin Jia,&nbsp;Bo Han","doi":"10.1002/jmv.70440","DOIUrl":"https://doi.org/10.1002/jmv.70440","url":null,"abstract":"<div>\u0000 \u0000 <p>Viral myocarditis is characterized by inflammatory cell infiltration and myocardial damage. However, the involvement of immune cells and the interaction between immune cells and stromal cells remain poorly understood. We successfully established a mouse model of viral myocarditis induced by Coxsackievirus B3 (CVB3) and systematically analyzed immune cell infiltration and myocardial injury at different time points. Single-cell RNA sequencing (scRNA-seq) was performed at the peak of immune cell infiltration to characterize the immune landscape of infected cardiac tissue and peripheral blood mononuclear cells (PBMCs). Macrophage depletion and vascular endothelial growth factor receptor (VEGFR) inhibition were performed to validate the immune-stromal crosstalk. Peak immune cell infiltration and myocardial injury occurred on the 7th day of infection. scRNA-seq revealed that endothelial cells and mononuclear phagocytes (MNPs) were the most substantially expanded cell populations in the hearts of mice with viral infection. Trem2 macrophage, characterized by tissue repair gene signatures, was the predominant MNP subcluster in the infected heart, while tip cells and capillaries were the most expanded endothelial cell clusters. Cell–cell communication analysis identified increased macrophage–endothelial cell interactions during CVB3 infection. Macrophage-derived VEGFA secretion, partially induced by CVB3 infection and apoptotic cardiomyocyte debris, promoted angiogenesis, while macrophage depletion resulted in reduced VEGFA secretion and endothelial proliferation. Moreover, inhibition of VEGFR exacerbated cardiac dysfunction, highlighting the protective role of angiogenesis in myocarditis progression. In summary, these results elucidated a cardioprotective role of macrophage-driven angiogenesis via vascular endothelial growth factor signaling during viral myocarditis, providing new insights into therapeutic strategies for inflammatory heart diseases.</p></div>","PeriodicalId":16354,"journal":{"name":"Journal of Medical Virology","volume":"97 6","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144300440","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}

{"title":"Molecular Epidemiology of Sapovirus Infection in Japanese Children With Acute Gastroenteritis Before and After the COVID-19 Pandemic","authors":"Shoko Okitsu,&nbsp;Pattara Khamrin,&nbsp;Toshiyuki Hikita,&nbsp;Yuko Onda,&nbsp;Sheikh Ariful Hoque,&nbsp;Satoshi Hayakawa,&nbsp;Shihoko Komine-Aizawa,&nbsp;Niwat Maneekarn,&nbsp;Hiroshi Ushijima","doi":"10.1002/jmv.70450","DOIUrl":"https://doi.org/10.1002/jmv.70450","url":null,"abstract":"<div>\u0000 \u0000 <p>Sapovirus (SaV) is one of the pathogens associated with sporadic acute gastroenteritis in infants and children, and also with foodborne outbreaks in all age groups. This study investigated the molecular detection and characterization of SaV in Japanese children with acute gastroenteritis from July 2017 to June 2024, and the results were compared with those of the previous study conducted in 2014–2017. The study period of this study encompassed the period before, during, and after the COVID-19 pandemic in Japan. During the COVID-19 pandemic, both the number of collected samples and SaV-positive samples decreased remarkably. Among 931 samples included in this study, the rate of SaV infection was 7.5% (70/931), which was higher than the previous study at 5.0%, especially the rates of infection after the pandemic increased to 9.8% in 2022–2023 and 16.4% in 2023–2024. Regarding the SaV genotype distribution, GI.1 was the most predominant genotype at 37.1% comparable to those of the previous study during 2014–2017, followed by GII.3, GI.2, GII.1, GII.2 and GIV.1, GV.1, and GII.5 genotypes. In 2022–2023, GII.3 instead of GI.1 was the most common genotype; however, GI.1 resumed the most dominant genotype again the following year. The findings suggested that SaV infection in Japanese children was remarkable after the COVID-19 pandemic, and the systematic surveillance should be conducted continuously in Japan.</p>\u0000 </div>","PeriodicalId":16354,"journal":{"name":"Journal of Medical Virology","volume":"97 6","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144291890","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}

{"title":"Pleiotropic Effects of Metformin on the Chemotherapy Response of HPV-Positive Cancer Cells","authors":"Alicia Avenhaus,&nbsp;Bianca J. Kuhn,&nbsp;Milica Velimirović,&nbsp;Tobias D. Strobel,&nbsp;Julia Bulkescher,&nbsp;Claudia Lohrey,&nbsp;Jeroen Krijgsveld,&nbsp;Felix Hoppe-Seyler,&nbsp;Karin Hoppe-Seyler","doi":"10.1002/jmv.70434","DOIUrl":"https://doi.org/10.1002/jmv.70434","url":null,"abstract":"<p>Improved treatment strategies for HPV-positive cancers are urgently required. The viral E6/E7 oncoproteins are essential for the proliferation of HPV-positive cancer cells and considered attractive therapeutic targets. Metformin is proposed to be repurposed for cancer therapy, but this is under controversial debate. We previously demonstrated that E6/E7 expression and the proliferation of HPV-positive cancer cells are repressed by Metformin. Here, we explore the effects of Metformin on the phenotype of HPV-positive cancer cells in detail, either applied as monotreatment or in combination with chemotherapeutic agents. We provide evidence that the downregulation of E6/E7 is not the primary mechanism underlying Metformin's growth-inhibitory effect in HPV-positive cancer cells. Specifically, compared to targeted E6/E7 repression by RNA interference (RNAi), Metformin treatment differently altered the expression of growth regulatory proteins, exerted different effects on the cell cycle, and was able to suppress growth even in the presence of E6/E7. Furthermore, we found that cancer cells pre-treated with Metformin become resistant to senescence induction by the pro-senescent chemotherapeutic agent Etoposide, likely as a secondary effect of Metformin-induced growth inhibition. Finally, depending on experimental conditions, we uncover divergent, even opposing, effects on the proliferation of HPV-positive cancer cells when Metformin is combined with Cisplatin, with p53 playing a key role in these processes. Collectively, our results show that Metformin exerts complex effects on the phenotype of HPV-positive cancer cells, which are critically influenced by experimental conditions. Our findings may also explain the discrepant results in the literature, reporting agonistic or antagonistic effects upon combining Metformin with Cisplatin.</p>","PeriodicalId":16354,"journal":{"name":"Journal of Medical Virology","volume":"97 6","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jmv.70434","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144299683","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}

{"title":"Molecular Characterization of Parvovirus B19 in Pregnant Women During the 2024 Outbreak in Belgium","authors":"Florence Lemaitre,&nbsp;Clara Chivasso,&nbsp;Laurent Debaisieux,&nbsp;Marie-Hélène Jurion,&nbsp;Marie-Luce Delforge","doi":"10.1002/jmv.70443","DOIUrl":"https://doi.org/10.1002/jmv.70443","url":null,"abstract":"<div>\u0000 \u0000 <p>Since the beginning of 2024, several countries in Europe have faced an increase in the detection of <i>Parvovirus B19</i> (B19V). The present study aimed to investigate the B19V outbreak in Belgium, focusing on molecular features and transmission dynamics among pregnant women. A total of 86 biological samples collected all over the country during the period between January and October 2024 were tested for B19V, and positive ones (<i>n</i> = 35) were used for molecular sequence investigations. An abnormal resurgence of B19V infections was first documented in February, and a significant decline was observed in October 2024. Phylogenetic analysis of all 35 sequences covering the nonstructural protein 1 (NS1)/capsid viral protein 1 (VP1) unique region junction showed that the genotype was 1a, which was in line with global patterns. The data showed that Belgian sequences clustered with strains from neighboring countries, indicating widespread circulation. The hypothesis involves the COVID-19 pandemic, which may have contributed to this outbreak, creating an immunity gap. This study highlights the importance of monitoring B19V, especially for high-risk groups, accentuating the importance of laboratory confirmation. Based on the results obtained, it is very unlikely that B19's emerging molecular features are responsible for the detection of an increasing number of cases in Belgium.</p></div>","PeriodicalId":16354,"journal":{"name":"Journal of Medical Virology","volume":"97 6","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144291891","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}

{"title":"Papain-Like Protease of SARS-CoV-2 Induces Intestinal Inflammation via the ISG15 Pathway: Identification of Natural Compound Inhibitors","authors":"Fang Wu,&nbsp;Zhaoyong Zhang,&nbsp;Qili Lun,&nbsp;Xu Hong,&nbsp;Jiantao Chen,&nbsp;Xinfeng Xu,&nbsp;Xinyi Xiong,&nbsp;Ying Zhang,&nbsp;Dmitry N. Shcherbakov,&nbsp;Shuwen Liu,&nbsp;Yaoqi Zhou,&nbsp;Yanqun Wang,&nbsp;Jian Zhan,&nbsp;Jincun Zhao,&nbsp;Wei Xu","doi":"10.1002/jmv.70448","DOIUrl":"https://doi.org/10.1002/jmv.70448","url":null,"abstract":"<div>\u0000 \u0000 <p>The SARS-CoV-2 papain-like protease (PLpro) is a multifunctional viral protein that facilitates viral assembly and disrupts host immune responses by removing interferon-stimulated gene 15 (ISG15) modifications from target proteins. However, the mechanisms by which PLpro-mediated immune evasion leads to inflammatory responses are not well understood. In this study, we demonstrate for the first time that PLpro induces inflammation in colonic epithelial cells and colonic inflammation in a mouse model, acting through the ISG15 signaling pathway. Using high-throughput screening, we identified two natural product-derived compounds, coptisine sulfate and (+)-shikonin, that inhibit the interaction between PLpro and ISG15 at the PLpro/ISG15 interface. We further investigated the mechanism of action of these two inhibitors using surface plasmon resonance, thermal shift assays, molecular docking, and molecular simulation studies. Importantly, both coptisine sulfate and (+)-shikonin were able to reduce intestinal inflammation in the PLpro-induced mouse model. These findings provide novel insights into how the SARS-CoV-2 PLpro can drive inflammatory responses and introduce two natural compound-based inhibitors that may offer a new approach to alleviate gastrointestinal complications associated with COVID-19 infection. Our results highlight the potential of targeting the PLpro/ISG15 interaction as a therapeutic strategy against SARS-CoV-2.</p></div>","PeriodicalId":16354,"journal":{"name":"Journal of Medical Virology","volume":"97 6","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144291889","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}

{"title":"CircCBP Inhibits Influenza A Virus Replication by Interfering the vRNP Activity and Enhancing Antiviral Immune Response","authors":"Xinli Yao,&nbsp;Mingge Wang,&nbsp;Xiaomei Tong,&nbsp;Dandan Qi,&nbsp;Xin Ye","doi":"10.1002/jmv.70442","DOIUrl":"https://doi.org/10.1002/jmv.70442","url":null,"abstract":"<div>\u0000 \u0000 <p>Influenza A virus (IAV) is an essential pathogen which can cause pandemic and seasonal flu. Host factors, including noncoding RNAs have been found to be participated in the replication of IAV. However, the mechanism by which circular RNAs (circRNAs) regulating IAV replication remains unclear. By taking the approach of RNA deep sequencing to analyze the circRNA profiles of A549 cells upon IAV infection, we identified that circular CREB binding protein (circCBP) is significantly upregulated after IAV infection or interferon (IFN) treatment. Overexpression of circCBP inhibited IAV replication, while knockdown of circCBP promoted viral replication, indicating that circCBP inhibits IAV replication. We found that circCBP interacts with the viral nucleoprotein (NP) and reduces its interaction with viral polymerase subunits PB1 and PB2, and consequently blocks the vRNP activity. CircCBP can also bind with nonstructural protein 1 (NS1) and alleviate the inhibitory effect of NS1 on antiviral immune response. In addition, circCBP binds with the major stress granule proteins such as G3BP1. Further study revealed that circCBP enhances the oligomerization of G3BP1, which in turn promotes the formation of stress granules and the transcription of IFN-β. Our study reveals the novel functions of circCBP in regulating virus replication and stress granule-related antiviral immune response, providing a new clue to develop circRNA-based antiviral inhibitors.</p>\u0000 </div>","PeriodicalId":16354,"journal":{"name":"Journal of Medical Virology","volume":"97 6","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144264514","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}

{"title":"Long Term Sequelae of Mild RSV Infections in Healthy Children Aged 0–3 Years in the Primary Care Setting—A Prospective Two Year Follow Up Observational Study","authors":"Paulina Ehlmaier,&nbsp;Peter Voitl,&nbsp;Angela Riepl,&nbsp;Lena Lischka,&nbsp;Julian J. M. Voitl,&nbsp;Klara Langer,&nbsp;Ulrike Kuzio,&nbsp;Alexandra Mühl-Riegler,&nbsp;Bernhard Mühl,&nbsp;Susanne C. Diesner-Treiber","doi":"10.1002/jmv.70441","DOIUrl":"https://doi.org/10.1002/jmv.70441","url":null,"abstract":"<p>Children with an early severe respiratory syncytial virus (RSV) infection have an increased risk of wheezing later in life. This longitudinal study aimed to investigate whether children with a mild RSV infection taken care of in a primary health care setting had an increased incidence of wheezing in the 2 years following infection compared to children with other respiratory infections (RSV-negative). Nasal swabs of children with acute respiratory infections were examined for 23 pathogens by multiplex PCR. 216 RSV-positive and RSV-negative (<i>N</i> = 201) matched for age, gender and time of diagnosis were followed for 2 years using telemedical control to record the occurrence of wheezing, hospitalization and frequency of respiratory tract infections. RSV-positive patients showed a 48% lower risk (OR 0.520, <i>p</i> = 0.03) of developing wheezing in the 2-year observation period compared to the RSV-negative group; Rhinovirus-positive patients had a trendwise increased risk (OR 1.47, <i>p</i> = 0.0872). These data were also reflected in a reduced prescription rate of short acting beta agonists in the RSV group. In conclusion, mild RSV infections led to fewer wheezing episodes in RSV-positive compared to RSV-negative patients. Rhinovirus infections appear to increase wheezing. Our data are consistent with the idea that there could be a dose-effect relationship with RSV infections.</p>","PeriodicalId":16354,"journal":{"name":"Journal of Medical Virology","volume":"97 6","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jmv.70441","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144264483","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}

{"title":"ACE1 rs1799752 Polymorphism Is not Associated With the Presence of Post-COVID-19 Condition","authors":"César Fernández-de-las-Peñas,&nbsp;Lars Arendt-Nielsen,&nbsp;Antonio Gil-Crujera,&nbsp;Stella M. Gómez-Sánchez,&nbsp;Silvia Ambite-Quesada,&nbsp;Maria A. Palomar-Gallego,&nbsp;Oscar J. Pellicer-Valero,&nbsp;Rocco Giordano,&nbsp;Gema Díaz-Gil","doi":"10.1002/jmv.70438","DOIUrl":"https://doi.org/10.1002/jmv.70438","url":null,"abstract":"","PeriodicalId":16354,"journal":{"name":"Journal of Medical Virology","volume":"97 6","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144255941","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}