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Cladosporium cladosporioides causes asthma and superficial and deep infections, mostly in immunodeficient individuals and animals. This study aimed to investigate whether C. cladosporioides spores can enter the lungs through pulmonary circulation and influence pulmonary immune response. We intravenously injected mice with C. cladosporioides spore suspension and conducted several assays on the lungs. Pulmonary hemorrhage symptoms and congestion were most severe on days 1, 2, and 3 post-inoculation (PI). Extensive inflammatory cell infiltration occurred throughout the period of infection. More spores and hyphae colonizing the lungs were detected on days 1, 2, and 3 PI, and fewer spores and hyphae were observed within 21 d of infection. Numerous macrophages, dendritic cells, and neutrophils were observed on day 5 PI, along with upregulation of CD54, an intercellular adhesion molecule. Th1 and Th2 cells increased after infection; specifically, Th2 cells increased considerably on day 5 PI. These results suggest that days 2 and 5 PI represent the inflammatory peak in the lungs and that the Th2 and Th1 signaling pathways are potentially involved in pulmonary immune responses. In conclusion, the further adaptive immune responses played important roles in establishing effective pulmonary immunity against C. cladosporioides systemic infections based on innate immune responses.

Feline parvovirus (FPV) causes feline panleukopenia, a highly contagious disease in cats, marked by severe leukopenia, biphasic fever, diarrhea, vomiting, and hemorrhagic enteritis. Recently, FPV infection in giant pandas has increased, causing diarrhea and ultimately fatal outcomes, thereby threatening their survival and reproduction. Here, we investigated the transmission of FPV in giant pandas and its interaction with cellular receptors using an FPV strain (pFPV-sc) isolated from giant panda feces. Recombinant feline transferrin receptor 1 (fTfR1) and the giant panda ortholog (gpTfR1) were expressed in non-susceptible HEK293T and HeLa cells, while viral infection levels were measured to determine the effect of gpTfR1 on pFPV-sc replication. The findings indicated that gpTfR1 overexpression in non-susceptible cells significantly enhanced pFPV-sc replication, particularly influencing the viral attachment and internalization stages. Our data further revealed early-stage colocalization between gpTfR1 expression and virus infection, suggesting that gpTfR1 facilitates early viral infection and replication. Taken together, our study provides the first evidence on the mechanism of FPV cross-species infection in giant pandas and elucidates the interaction between gpTfR1 and FPV, which establishes a theoretical basis for the development of preventive and therapeutic strategies, thereby safeguarding the health and survival of giant panda populations from FPV.

In 2023, the detection rate of porcine rotavirus (PoRV) surpassed that of porcine epidemic diarrhea virus (PEDV) for the first time, establishing PoRV as the predominant pathogen responsible for viral diarrhea in pigs. To systematically investigate the epidemiology and molecular characteristics of PoRV in Southwest China, a total of 196 diarrheal clinical samples were collected from 29 large-scale pig farms across the region during 2024–2025. RT-qPCR results revealed a high PoRV positivity rate of 57.14% (112/196) with group A porcine rotavirus (PoRVA) being the most prevalent at 46.43%, representing the predominant group. Genotyping and phylogenetic analysis of the VP4 and VP7 genes indicated that the P genotype P[13] was most prevalent (77.78%, 21/27), while the major G genotypes were G4 (39.28%) and G9 (35.71%). The most common G/P combinations were G9P[13] and G4P[13]. Furthermore, a PoRV strain was successfully isolated and identified through whole-genome sequencing, indirect immunofluorescence assay (IFA), and transmission electron microscopy (TEM). The isolate was designated RVA/Pig-wt/SCLS-JW/2024/G1P[7], with a whole-genome constellation of G1-P[7]-I5-R1-C1-M1-A8-N1-T1-E1-H1. The structural proteins VP1-4 and VP6-7, along with nonstructural genes NSP1 and NSP5, shared high sequence identity with porcine strains, whereas the nonstructural genes NSP2–NSP4 clustered more closely with human rotaviruses. These findings indicate a higher prevalence of PoRV in southwestern China compared to other regions; the dominant circulating genotypes have shifted to G9 and G4; the isolated G1P[7] strain is relatively rare in China and might be a genetic recombinant of human and porcine rotaviruses. This study provides valuable data and theoretical support for understanding the current epidemiology of PoRV, and facilitates vaccine development and the formulation of prevention and control strategies.

Background Marek's disease (MD) is an economically important viral disease of chickens caused by Marek's disease virus (MDV), an oncogenic herpesvirus. This disease was well controlled since the widespread use of commercial vaccines, but field MDVs have shown continuous increasing in virulence and acquired the ability to overcome the immune response induced by vaccines. Nowadays, MD continues to be a serious threat to poultry industry, isolation and characterization of MDVs are essential for monitoring changes of viruses and evaluating the effectiveness of existing vaccines. Results Between 2008 and 2010, 18 field MDV strains were isolated from vaccinated chicken flocks in Sichuan province, China. Three oncogenic genes including Meq, pp38 and vIL-8 genes of the 18 isolates were amplified and sequenced. Homology analysis showed that the deduced amino acid sequences of these three genes exhibit 95.0-98.8%, 99.3-100% and 97.0-98.5% homology respectively with these of other reference strains published in GenBank. Alignment analysis of the nucleotide and deduced amino acid sequences showed that four amino acid mutations in Meq gene and two amino acid mutations in vIL-8 gene displayed perfect regularity in MDVs circulating in China, which could be considered as features of field MDVs prevalent in recent years in China. In addition, one amino acid mutation in pp38 gene can be considered as a feature of virulent MDVs from USA, and three amino acid mutations in Meq gene were identified and unique in very virulent plus (vv+) MDVs. Phylogenetic analysis based on Meq and vIL-8 protein sequences revealed that field MDVs in China evolved independently. Virulence studies showed that CVI988 could provide efficient protection against the field MDVs epidemic recently in China. Conclusions This study and other published data in the GenBank have demonstrated the features of Meq, pp38 and vIL-8 genes of MDVs circulating in recent years in Sichuan, China. Mutations, deletions or insertions were observed in these three genes, and some mutations could be considered as the unique marks of the MDVs circulating presently in China. The paper supplies some valuable information concerning the evolution of MDV which is useful for the vaccine development and control of MD in China.

Thioester-containing proteins (TEPs), which are distinguished by the thioester motif (GCGEQ), are essential to arthropods' defense against infections. Although TEPs have been extensively investigated in , , and , their functions in mosquitoes remain inadequately explored. Interestingly, we discovered that TEPs exhibit functional antagonism to their orthologs in other species, actively facilitating viral infection in this vector. In this study, we identified nine genes in , three of which were found to critically facilitate (JEV) infection, with exhibiting the most pronounced proviral effect. Mechanistically, TEP27 may have suppressed the production of several antimicrobial peptides (AMPs), which increased JEV replication. Our work also highlights the potential of targeting susceptibility factors such as TEP27 to block pathogen acquisition. Notably, the rate of mosquito infection was significantly decreased by membrane blood feeding antisera against TEP27. Therefore, vaccination against TEP27 offers a workable method of avoiding JEV infection. According to our research, TEP27 is a promising target for the development of vaccines that prevent JEV transmission. By preventing viral infection in mosquitoes that feed on immunized hosts, this approach can directly disrupt the natural transmission cycle, offering a novel strategy to reduce the disease burden.

Glaesserella parasuis cytolethal distending toxin ( Gp CDT) is a bacterial genotoxin whose main action is to activate DNA damage responses, induce cell cycle arrest, and induce the apoptosis of host cells. In our previous studies, we reported that cells incubated with Gp CDT exhibited changes in the expression of ferroptosis-related proteins; thus, we hypothesized that, in addition to apoptosis, Gp CDT may also cause ferroptosis, a novel mode of cell death. Here, we observed that treatment of 3D4/21 cells with Gp CDT resulted in cytoplasmic iron overload, depletion of GSH (reduced glutathione), and overproduction of reactive oxygen species (ROS) and malondialdehyde (MDA), indicating that Gp CDT disrupted iron metabolism and redox homeostasis in these cells. These phenomena were counteracted by the specific ferroptosis inhibitor ferrostatin-1 and the iron chelator deferoxamine mesylate. In vitro infection with the Glaesserella parasuis field isolate strain SC1401 (CDT positive) induced changes in the expression of ferroptosis biomarkers and proteins. Infection of C57BL/6 mice yielded similar results. Our results suggest that ferroptosis may play a substantial role in Gp CDT-induced cellular injury.

Swine acute diarrhoea syndrome coronavirus (SADS-CoV), a novel HKU2-related coronavirus of bat origin, is a newly emerged swine enteropathogenic coronavirus that causes severe diarrhoea in piglets. SADS-CoV has a broad cell tropism with the capability to infect a wide variety of cells from human and diverse animals, which implicates its ability to hold high risks of cross-species transmission. The intracellular antiviral immunity, comprised of the intrinsic and innate immunity, represents the first line of host defence against viral infection prior to the onset of adaptive immunity. To date, there are no vaccines and drugs approved to prevent or treat SADS-CoV infection. Understanding of the mutual relationship between SADS-CoV infection and host immunity is crucial for the development of novel vaccines and drugs against SADS-CoV. Here, we review recent advancements in our understanding of the interplay between SADS-CoV infection and the host intrinsic and innate immunity. The extensive and in-depth investigation on their interactive relationship will contribute to the identification of new targets for developing intervention strategies to control SADS-CoV infection.

Porcine deltacoronavirus (PDCoV) is a newly emerging enteric pathogen in swine that causes diarrhea in neonatal piglets and creates an additional economic burden on porcine industries in Asia and North America. In this study, a PDCoV isolate, CHN-SC2015, was isolated from Sichuan Province in southwest China. The isolate was characterized by a cytopathic effect, immunofluorescence, and electron microscopy. CHN-SC2015 titers in LLC-PK cells ranged from 104.31 to 108.22 TCID50/mL during the first 30 passages. During serial passage, 11 nucleotide mutations occurred in the S gene, resulting in nine amino acid changes. A whole genome sequencing analysis demonstrated that CHN-SC2015 shares 97.5%–99.1% identity with 59 reference strains in GenBank. Furthermore, CHN-SC2015 contained 6-nt deletion and 9-nt insertion in the ORF1ab gene, 3-nt deletion in the S gene and 11-nt deletion in its 3′UTR compared with other reference strains available in GenBank. A phylogenetic analysis showed that CHN-SC2015 is more closely related to other PDCoV strains in China than to the strains from Southeast Asia, USA, Japan, and South Korea, indicating the diversity of genetic relationships and regional and epidemic characteristics among these strains. A recombination analysis indicated that CHN-SC2015 experienced recombination events between SHJS/SL/2016 and TT-1115. In vivo infection demonstrated that CHN-SC2015 is highly pathogenic to sucking piglets, causing diarrhea, vomiting, dehydration, and death. Virus was shed daily in the feces of infected piglets and upon necropsy, was found distributed in the gastrointestinal tract and in multiple organs. CHN-SC2015 is the first systematically characterized strain from southwest China hitherto reported. Our results enrich the body of information on the epidemiology, pathogenicity and molecular evolution associated with PDCoV.

The Chinese poultry industry has experienced outbreaks of Newcastle disease (ND) dating back to the 1920s. However, the epidemic has exhibited a downtrend in recent years. In this study, both observational and genetic data [fusion (F) and haemagglutinin-neuraminidase genes (HN)] were analyzed, and phylogeographic analysis based on prevalent genotypes of Newcastle disease virus (NDV) was conducted for better understanding of the evolution and spatiotemporal dynamics of ND in China. In line with the observed trend of epidemic outbreaks, the effective population size of F and HN genes of circulating NDV is no longer growing since 2000, which is supported by 95% highest posterior diversity (HPD) intervals. Phylogeographic analysis indicated that the two eastern coastal provinces, Shandong and Jiangsu were the most relevant hubs for NDV migration, and the geographical regions with active NDV diffusion seemed to be constrained to southern and eastern China. The live poultry trade may play an important role in viral spread. Interestingly, no migration links from wild birds to poultry received Bayes factor support (BF > 3), while the migration links from poultry to wild birds accounted for 64% in all effective migrations. This may indicate that the sporadic cases of ND in wild bird likely spillover events from poultry. These findings contribute to predictive models of NDV transmission, and potentially help in the prevention of future outbreaks.

Cytolethal Distending Toxin (CDT) is the only exotoxin that ( ) can secrete. CDT ( CDT) triggers DNA damage responses, leading to irreversible cell cycle arrest and apoptosis, playing an important role in the pathogenic process of . Currently, research on the host cell receptors of CDT remains limited. Screening and identification of host cell receptors that interact with CDT are crucial for systematically elucidating the cytotoxic mechanisms induced by this toxin. This study employed Co-immunoprecipitation (Co-IP) combined with Liquid Chromatography-Tandem Mass Spectrometry (LC-MS/MS) to identify potential host proteins interacting with CDT in PK15 cells. Nine Proteins were selected for further evaluation based on subcellular localization and Gene Ontology classification. Eukaryotic expression and Co-IP validated four interacting proteins. Subsequently, heterozygous knockout PK15 cell lines for these genes were generated via CRISPR/Cas9, and CCK-8 assays identified TM9SF4 as having the most significant impact on CDT virulence. Therefore, a homozygous knockout PK15 cell line (KO) was generated via limited dilution, and a stable -overexpressing PK15 cell line (OE) was established through lentiviral packaging. Western blotting and qRT-PCR confirmed protein and gene expression, and CCK-8 assays combined with cytopathic effect (CPE) observation determined the role of TM9SF4 in CDT-induced cytotoxicity. Finally, indirect immunofluorescence was performed to assess co-localization of TM9SF4 with CDT. We identified 287 proteins in PK15 cells that potentially interact with CDT, among which 58 were localized to the plasma membrane or extracellular. Nine proteins were selected for further investigation. Among them, EPHB4, LITAF, TM9SF4, SLC12A4 interacted with CDT, but only the deficiency of TM9SF4 significantly inhibited the virulence of the CDT. Results from CCK-8 and CPE showed that KO cells exhibited significantly higher survival rates and suppressed CDT-induced cellular distention and cell death, whereas OE cells showed decreased survival rates and typical cytopathic change. Finally, indirect immunofluorescence confirmed strong co-localization between TM9SF4 and CDT. We initially proposed TM9SF4 as a receptor for CDT in PK15 cells, essential for CDT binding and cytotoxicity. This study may provide a new theoretical basis for targeted prevention and treatment of swine Glässer's disease.