{"title":"Mechanism of PRRSV infection and antiviral role of polyphenols.","authors":"Fructueux Modeste Amona, Yipeng Pang, Xingyu Gong, Yanhong Wang, Xingtang Fang, Chunlei Zhang, Xi Chen","doi":"10.1080/21505594.2024.2417707","DOIUrl":"10.1080/21505594.2024.2417707","url":null,"abstract":"<p><p>Porcine reproductive and respiratory syndrome (PRRS) is associated with the endemic outbreak of fever, anorexia, and abortion in pregnant sows, resulting in an enormous economic impact on the global swine industry. Current mainstream prophylactic agents and therapies have been developed to prevent PRRSV infection; however, they have limited efficacy. Therefore, there is an urgent need to develop novel antiviral strategies to prevent PRRSV infection and transmission. The identification of new PRRSV entry mediators, such as MYH9 and HSPA8; viral apoptotic mimicry; and TIM-induced macropinocytosis, to facilitate infection has led to a novel molecular understanding of the PRRSV infection mechanism, which can be utilized in the development of prophylactic agents and therapies for PRRSV infection. Polyphenols, complex chemical molecules with abundant biological activities derived from microorganisms and plants, have demonstrated great potential for controlling PRRSV infection via different mechanisms. To explore new possibilities for treating PRRSV infection with polyphenols, this review focuses on summarizing the pathogenesis of PRRSV, reviewing the potential antiviral mechanisms of polyphenols against PRRSV, and addressing the challenges associated with the widespread use of polyphenols.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11497994/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142476125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The formidable guardian: Type 3 immunity in the intestine of pigs.","authors":"Zhipeng Yang, Dou Zhang, Zhoudan Jiang, Jian Peng, Hongkui Wei","doi":"10.1080/21505594.2024.2424325","DOIUrl":"10.1080/21505594.2024.2424325","url":null,"abstract":"<p><p>Well-intestinal health is crucial for better growth performance in pigs. Type 3 immunity, which is one of the three types of immune responses in mammals, plays a vital role in maintaining intestinal homoeostasis. Therefore, we initially introduce the type 3 immune cells in the intestine of pigs, including their distribution, development, and function. We then discuss the type 3 immune response under infection, encompassing bacterial, fungal, and viral infections. It also covers two major stresses in pigs: heat stress and weaning stress. Lastly, we discuss the effects of various nutrients and feed additives on the regulation of the type 3 immune response in pigs under infection. This review aims to contribute to the understanding of the interaction between infection and type 3 immunity in pigs and to illustrate how various nutrients modulate the type 3 immune response in pigs under diverse infections.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142576832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
VirulencePub Date : 2024-12-01Epub Date: 2024-04-10DOI: 10.1080/21505594.2024.2333367
Martin Jaeger, Axel Dietschmann, Sophie Austermeier, Sude Dinçer, Pauline Porschitz, Larsen Vornholz, Ralph J A Maas, Evelien G G Sprenkeler, Jürgen Ruland, Stefan Wirtz, Tania Azam, Leo A B Joosten, Bernhard Hube, Mihai G Netea, Charles A Dinarello, Mark S Gresnigt
{"title":"Alpha1-antitrypsin impacts innate host-pathogen interactions with <i>Candida albicans</i> by stimulating fungal filamentation.","authors":"Martin Jaeger, Axel Dietschmann, Sophie Austermeier, Sude Dinçer, Pauline Porschitz, Larsen Vornholz, Ralph J A Maas, Evelien G G Sprenkeler, Jürgen Ruland, Stefan Wirtz, Tania Azam, Leo A B Joosten, Bernhard Hube, Mihai G Netea, Charles A Dinarello, Mark S Gresnigt","doi":"10.1080/21505594.2024.2333367","DOIUrl":"10.1080/21505594.2024.2333367","url":null,"abstract":"<p><p>Our immune system possesses sophisticated mechanisms to cope with invading microorganisms, while pathogens evolve strategies to deal with threats imposed by host immunity. Human plasma protein α1-antitrypsin (AAT) exhibits pleiotropic immune-modulating properties by both preventing immunopathology and improving antimicrobial host defence. Genetic associations suggested a role for AAT in candidemia, the most frequent fungal blood stream infection in intensive care units, yet little is known about how AAT influences interactions between <i>Candida albicans</i> and the immune system. Here, we show that AAT differentially impacts fungal killing by innate phagocytes. We observed that AAT induces fungal transcriptional reprogramming, associated with cell wall remodelling and downregulation of filamentation repressors. At low concentrations, the cell-wall remodelling induced by AAT increased immunogenic β-glucan exposure and consequently improved fungal clearance by monocytes. Contrastingly, higher AAT concentrations led to excessive <i>C. albicans</i> filamentation and thus promoted fungal immune escape from monocytes and macrophages. This underscores that fungal adaptations to the host protein AAT can differentially define the outcome of encounters with innate immune cells, either contributing to improved immune recognition or fungal immune escape.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11008552/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140185675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
VirulencePub Date : 2024-12-01Epub Date: 2024-02-04DOI: 10.1080/21505594.2024.2303853
Meenakshi Kandpal, Budhadev Baral, Nidhi Varshney, Ajay Kumar Jain, Debi Chatterji, Ajay Kumar Meena, Rajan Kumar Pandey, Hem Chandra Jha
{"title":"Gut-brain axis interplay via STAT3 pathway: Implications of <i>Helicobacter pylori</i> derived secretome on inflammation and Alzheimer's disease.","authors":"Meenakshi Kandpal, Budhadev Baral, Nidhi Varshney, Ajay Kumar Jain, Debi Chatterji, Ajay Kumar Meena, Rajan Kumar Pandey, Hem Chandra Jha","doi":"10.1080/21505594.2024.2303853","DOIUrl":"10.1080/21505594.2024.2303853","url":null,"abstract":"<p><p><i>Helicobacter pylori</i> is a pathogenic bacterium that causes gastritis and gastric carcinoma. Besides gastric complications its potential link with gut-brain axis disruption and neurological disorders has also been reported. The current study investigated the plausible role and its associated molecular mechanism underlying <i>H. pylori</i> mediated gut-brain axis disruption and neuroinflammation leading to neurological modalities like Alzheimer's disease (AD). We have chosen the antimicrobial resistant and susceptible <i>H. pylori</i> strains on the basis of broth dilution method. We have observed the increased inflammatory response exerted by <i>H. pylori</i> strains in the gastric as well as in the neuronal compartment after treatment with <i>Helicobacter pylori</i> derived condition media (HPCM). Further, elevated expression of STAT1, STAT3, and AD-associated proteins- APP and APOE4 was monitored in HPCM-treated neuronal and neuron-astrocyte co-cultured cells. Excessive ROS generation has been found in these cells. The HPCM treatment to LN229 causes astrogliosis, evidenced by increased glial fibrillary acidic protein. Our results indicate the association of STAT3 as an important regulator in the <i>H. pylori-</i>mediated pathogenesis in neuronal cells. Notably, the inhibition of STAT3 by its specific inhibitor, BP-1-102, reduced the expression of pSTAT3 and AD markers in neuronal compartment induced by HPCM. Thus, our study demonstrates that <i>H. pylori</i> infection exacerbates inflammation in AGS cells and modulates the activity of STAT3 regulatory molecules. <i>H. pylori</i> secretome could affect neurological compartments by promoting STAT3 activation and inducing the expression of AD-associated signature markers. Further, pSTAT-3 inhibition mitigates the <i>H. pylori</i> associated neuroinflammation and amyloid pathology.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10854367/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139404601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
VirulencePub Date : 2024-12-01Epub Date: 2024-03-20DOI: 10.1080/21505594.2024.2329566
Eléa A Renaud, Ambre J M Maupin, Yann Bordat, Arnault Graindorge, Laurence Berry, Sébastien Besteiro
{"title":"Iron depletion has different consequences on the growth and survival of <i>Toxoplasma gondii</i> strains.","authors":"Eléa A Renaud, Ambre J M Maupin, Yann Bordat, Arnault Graindorge, Laurence Berry, Sébastien Besteiro","doi":"10.1080/21505594.2024.2329566","DOIUrl":"10.1080/21505594.2024.2329566","url":null,"abstract":"<p><p><i>Toxoplasma gondii</i> is an obligate intracellular parasite responsible for a pathology called toxoplasmosis, which primarily affects immunocompromised individuals and developing foetuses. The parasite can scavenge essential nutrients from its host to support its growth and survival. Among them, iron is one of the most important elements needed to sustain basic cellular functions as it is involved in a number of key metabolic processes, including oxygen transport, redox balance, and electron transport. We evaluated the effects of an iron chelator on the development of several parasite strains and found that they differed in their ability to tolerate iron depletion. The growth of parasites usually associated with a model of acute toxoplasmosis was strongly affected by iron depletion, whereas cystogenic strains were less sensitive as they were able to convert into persisting developmental forms that are associated with the chronic form of the disease. Ultrastructural and biochemical characterization of the impact of iron depletion on parasites also highlighted striking changes in both their metabolism and that of the host, with a marked accumulation of lipid droplets and perturbation of lipid homoeostasis. Overall, our study demonstrates that although acute iron depletion has an important effect on the growth of <i>T. gondii</i>, it has a more profound impact on actively dividing parasites, whereas less metabolically active parasite forms may be able to avoid some of the most detrimental consequences.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10962585/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140176762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
VirulencePub Date : 2024-12-01Epub Date: 2024-05-26DOI: 10.1080/21505594.2024.2355201
Samuel Tong Jia Ming, Katrina Tan Yi Jun, Guillaume Carissimo
{"title":"Pathogenicity and virulence of O'nyong-nyong virus: A less studied <i>Togaviridae</i> with pandemic potential.","authors":"Samuel Tong Jia Ming, Katrina Tan Yi Jun, Guillaume Carissimo","doi":"10.1080/21505594.2024.2355201","DOIUrl":"10.1080/21505594.2024.2355201","url":null,"abstract":"<p><p>O'nyong-nyong virus (ONNV) is a neglected mosquito-borne alphavirus belonging to the <i>Togaviridae</i> family. ONNV is known to be responsible for sporadic outbreaks of acute febrile disease and polyarthralgia in Africa. As climate change increases the geographical range of known and potential new vectors, recent data indicate a possibility for ONNV to spread outside of the African continent and grow into a greater public health concern. In this review, we summarise the current knowledge on ONNV epidemiology, host-pathogen interactions, vector-virus responses, and insights into possible avenues to control risk of further epidemics. In this review, the limited ONNV literature is compared and correlated to other findings on mainly Old World alphaviruses. We highlight and discuss studies that investigate viral and host factors that determine viral-vector specificity, along with important mechanisms that determine severity and disease outcome of ONNV infection.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11135837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141155388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
VirulencePub Date : 2024-12-01Epub Date: 2024-06-24DOI: 10.1080/21505594.2024.2367652
Xianggui Yang, Jun Zeng, Dan Wang, Qin Zhou, Xuejing Yu, Zhenguo Wang, Tingting Bai, Guangxin Luan, Ying Xu
{"title":"NagZ modulates the virulence of <i>E. cloacae</i> by acting through the gene of unknown function, ECL_03795.","authors":"Xianggui Yang, Jun Zeng, Dan Wang, Qin Zhou, Xuejing Yu, Zhenguo Wang, Tingting Bai, Guangxin Luan, Ying Xu","doi":"10.1080/21505594.2024.2367652","DOIUrl":"10.1080/21505594.2024.2367652","url":null,"abstract":"<p><p>β-N-acetylglucosaminidase (NagZ), a cytosolic glucosaminidase, plays a pivotal role in peptidoglycan recycling. Previous research demonstrated that NagZ knockout significantly eradicated AmpC-dependent β-lactam resistance in <i>Enterobacter cloacae</i>. However, NagZ's role in the virulence of <i>E. cloacae</i> remains unclear. Our study, incorporating data on mouse and <i>Galleria mellonella</i> larval mortality rates, inflammation markers, and histopathological examinations, revealed a substantial reduction in the virulence of <i>E. cloacae</i> following NagZ knockout. Transcriptome sequencing uncovered differential gene expression between NagZ knockout and wild-type strains, particularly in nucleotide metabolism pathways. Further investigation demonstrated that NagZ deletion led to a significant increase in cyclic diguanosine monophosphate (c-di-GMP) levels. Additionally, transcriptome sequencing and RT-qPCR confirmed significant differences in the expression of ECL_03795, a gene with an unknown function but speculated to be involved in c-di-GMP metabolism due to its EAL domain known for phosphodiesterase activity. Interestingly, in ECL_03795 knockout strains, a notable reduction in the virulence was observed, and virulence was rescued upon complementation with ECL_03795. Consequently, our study suggests that NagZ's function on virulence is partially mediated through the ECL_03795→c-di-GMP pathway, providing insight into the development of novel therapies and strongly supporting the interest in creating highly efficient NagZ inhibitors.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11197897/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141443403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
VirulencePub Date : 2024-12-01Epub Date: 2024-07-07DOI: 10.1080/21505594.2024.2375550
Ines Ruedas-Torres, Bui Thi To Nga, Francisco J Salguero
{"title":"Pathogenicity and virulence of African swine fever virus.","authors":"Ines Ruedas-Torres, Bui Thi To Nga, Francisco J Salguero","doi":"10.1080/21505594.2024.2375550","DOIUrl":"10.1080/21505594.2024.2375550","url":null,"abstract":"<p><p>African swine fever (ASF) is a devastating disease with a high impact on the pork industry worldwide. ASF virus (ASFV) is a very complex pathogen, the sole member of the family <i>Asfaviridae</i>, which induces a state of immune suppression in the host through infection of myeloid cells and apoptosis of lymphocytes. Moreover, haemorrhages are the other main pathogenic effect of ASFV infection in pigs, related to the infection of endothelial cells, as well as the activation and structural changes of this cell population by proinflammatory cytokine upregulation within bystander monocytes and macrophages. There are still many gaps in the knowledge of the role of proteins produced by the ASFV, which is related to the difficulty in producing a safe and effective vaccine to combat the disease, although few candidates have been approved for use in Southeast Asia in the past couple of years.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11232652/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141555610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
VirulencePub Date : 2024-12-01Epub Date: 2024-07-30DOI: 10.1080/21505594.2024.2384553
Junhong Wang, Ming Gao, Jiarui Wang, Yan Zeng, Chunfeng Wang, Xin Cao
{"title":"<i>LGG</i> promotes activation of intestinal ILC3 through TLR2 receptor and inhibits <i>salmonella typhimurium</i> infection in mice.","authors":"Junhong Wang, Ming Gao, Jiarui Wang, Yan Zeng, Chunfeng Wang, Xin Cao","doi":"10.1080/21505594.2024.2384553","DOIUrl":"10.1080/21505594.2024.2384553","url":null,"abstract":"<p><p><i>Salmonella</i> is a foodborne pathogen that causes disruption of intestinal mucosal immunity, leading to acute gastroenteritis in the host. In this study, we found that <i>Salmonella Typhimurium</i> (<i>STM</i>) infection of the intestinal tract of mice led to a significant increase in the proportion of <i>Lacticaseibacillus</i>, while the secretion of IL-22 from type 3 innate lymphoid cells (ILC3) increased significantly. Feeding <i>Lacticaseibacillus rhamnosus GG</i> (<i>LGG</i>) effectively alleviated the infection of <i>STM</i> in the mouse intestines. TLR2<sup>-/-</sup> mice experiments found that TLR2-expressing dendritic cells (DCs) are crucial for <i>LGG</i>'s activation of ILC3. Subsequent in vitro experiments showed that heat-killed <i>LGG</i> (HK<i>-LGG</i>) could promote DCs to secrete IL-23, which in turn further promotes the activation of ILC3 and the secretion of IL-22. Finally, organoid experiments further verified that IL-22 secreted by ILC3 can enhance the intestinal mucosal immune barrier and inhibit <i>STM</i> infection. This study demonstrates that oral administration of <i>LGG</i> is a potential method for inhibiting <i>STM</i> infection.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11296546/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141856635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
VirulencePub Date : 2024-12-01Epub Date: 2024-06-04DOI: 10.1080/21505594.2024.2360130
Jiali Cao, Zehong Huang, Jing Zeng, Jumei Liu, Weilun Zuo, Zhiying Su, Yujuan Chen, Weiwei Yu, Huiming Ye
{"title":"Maternal and neonatal outcomes and clinical laboratory testing of pregnant women with COVID-19 during the BA.5.2/BF.7 surge.","authors":"Jiali Cao, Zehong Huang, Jing Zeng, Jumei Liu, Weilun Zuo, Zhiying Su, Yujuan Chen, Weiwei Yu, Huiming Ye","doi":"10.1080/21505594.2024.2360130","DOIUrl":"10.1080/21505594.2024.2360130","url":null,"abstract":"<p><p>The impact of COVID-19 on pregnant women and newborns continues to be a critical societal concern. However, the majority of research focuses on the disease resulting from the early pandemic variants, without sufficient study on the more recent BA.5.2/BF.7. We retrospectively recruited pregnant women giving birth during the surge of the BA.5.2/BF.7 and analysed the risk impact of COVID-19 on maternal and neonatal outcomes. Furthermore, subjects matched through propensity scores were used for the analysis of clinical laboratory tests. A total of 818 pregnant women were enrolled, among 276 (33.7%) were diagnosed with SARS-CoV-2 during childbirth. COVID-19 significantly increased the risk of a hospital length of stay equal to or greater than seven days and neonatal admission to the neonatal intensive care unit, with an aHR of 2.03 (95% CI, 1.22-3.38) and 1.51 (95% CI, 1.12-2.03), respectively. In the analysis of 462 matched subjects, it was found that subjects infected with SARS-CoV-2 tended slight leucopenia and coagulation abnormalities. We found that during the surge of the BA.5.2/BF.7, COVID-19 increased the risk of maternal and neonatal outcomes among Chinese pregnant women. This finding offers significant insights to guide clinical practices involving pregnant women infected with the recently emerged Omicron subvariants.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11152110/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141158791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}