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3.
J Vis Exp ; (188)2022 Oct 21.
Article in English | MEDLINE | ID: covidwho-2110320

ABSTRACT

Circular RNAs (circRNAs) are a class of non-coding RNAs that are formed via back-splicing. These circRNAs are predominantly studied for their roles as regulators of various biological processes. Notably, emerging evidence demonstrates that host circRNAs can be differentially expressed (DE) upon infection with pathogens (e.g., influenza and coronaviruses), suggesting a role for circRNAs in regulating host innate immune responses. However, investigations on the role of circRNAs during pathogenic infections are limited by the knowledge and skills required to carry out the necessary bioinformatic analysis to identify DE circRNAs from RNA sequencing (RNA-seq) data. Bioinformatics prediction and identification of circRNAs is crucial before any verification, and functional studies using costly and time-consuming wet-lab techniques. To solve this issue, a step-by-step protocol of in silico prediction and characterization of circRNAs using RNA-seq data is provided in this manuscript. The protocol can be divided into four steps: 1) Prediction and quantification of DE circRNAs via the CIRIquant pipeline; 2) Annotation via circBase and characterization of DE circRNAs; 3) CircRNA-miRNA interaction prediction through Circr pipeline; 4) functional enrichment analysis of circRNA parental genes using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). This pipeline will be useful in driving future in vitro and in vivo research to further unravel the role of circRNAs in host-pathogen interactions.


Subject(s)
MicroRNAs , RNA, Circular , RNA, Circular/genetics , Sequence Analysis, RNA , MicroRNAs/genetics , Computational Biology/methods , Host-Pathogen Interactions/genetics , Gene Expression Profiling/methods
4.
Int J Mol Sci ; 23(21)2022 Oct 24.
Article in English | MEDLINE | ID: covidwho-2118281

ABSTRACT

Microorganisms can interact with plants, animals and humans in many different ways, e [...].


Subject(s)
Host-Pathogen Interactions , Plants , Humans , Animals
5.
Front Immunol ; 13: 1035559, 2022.
Article in English | MEDLINE | ID: covidwho-2109772

ABSTRACT

SARS-CoV-2 is the virus responsible for the COVID-19 pandemic. The genome of SARS-CoV-2 encodes nine accessory proteins that are involved in host-pathogen interaction. ORF8 is unique among these accessory proteins. SARS-CoV-2 ORF8 shares a surprisingly low amino acid sequence similarity with SARS-COV ORF8 (30%), and it is presumed to have originated from bat. Studies have shown that ORF8 exerts multiple different functions that interfere with host immune responses, including the downregulation of MHC class I molecules. These functions may represent strategies of host immune evasion. The x-ray crystal structure of ORF8 revealed an immunoglobulin-like domain with several distinguishing features. To date, there are numerous unanswered questions about SARS-CoV-2 ORF8 protein and its structure-function relationship that we discuss in this mini-review. A better understanding of how ORF8 interacts with components of the immune system is needed for elucidating COVID-19 pathogenesis and to develop new avenues for the treatment of the disease.


Subject(s)
COVID-19 , SARS-CoV-2 , Humans , Pandemics , Amino Acid Sequence , Host-Pathogen Interactions
6.
J Cell Biol ; 221(11)2022 Nov 07.
Article in English | MEDLINE | ID: covidwho-2097224

ABSTRACT

Viruses co-opt host proteins to carry out their lifecycle. Repurposed host proteins may thus become functionally compromised; a situation analogous to a loss-of-function mutation. We term such host proteins as viral-induced hypomorphs. Cells bearing cancer driver loss-of-function mutations have successfully been targeted with drugs perturbing proteins encoded by the synthetic lethal (SL) partners of cancer-specific mutations. Similarly, SL interactions of viral-induced hypomorphs can potentially be targeted as host-based antiviral therapeutics. Here, we use GBF1, which supports the infection of many RNA viruses, as a proof-of-concept. GBF1 becomes a hypomorph upon interaction with the poliovirus protein 3A. Screening for SL partners of GBF1 revealed ARF1 as the top hit, disruption of which selectively killed cells that synthesize 3A alone or in the context of a poliovirus replicon. Thus, viral protein interactions can induce hypomorphs that render host cells selectively vulnerable to perturbations that leave uninfected cells otherwise unscathed. Exploiting viral-induced vulnerabilities could lead to broad-spectrum antivirals for many viruses, including SARS-CoV-2.


Subject(s)
Guanine Nucleotide Exchange Factors , Poliovirus , Viral Core Proteins , Humans , Guanine Nucleotide Exchange Factors/metabolism , Synthetic Lethal Mutations , Virus Replication , Gene Expression Regulation, Viral , Viral Core Proteins/genetics , Viral Core Proteins/metabolism , Host-Pathogen Interactions
7.
Iran J Immunol ; 18(1): 47-53, 2021 03.
Article in English | MEDLINE | ID: covidwho-2091347

ABSTRACT

BACKGROUND: Incidence and severity of SARS-CoV2 infection are significantly lower in children and teenagers proposing that certain vaccines, routinely administered to neonates and children may provide cross-protection against this emerging infection. OBJECTIVE: To assess the cross-protection induced by prior measles, mumps and rubella (MMR) vaccinations against COVID-19. METHODS: The antibody responses to MMR and tetanus vaccines were determined in 53 patients affected with SARS-CoV2 infection and 52 age-matched healthy subjects. Serum levels of antibodies specific for NP and RBD of SARS-CoV2 were also determined in both groups of subjects with ELISA. RESULTS: Our results revealed significant differences in anti-NP (P<0.0001) and anti-RBD (P<0.0001) IgG levels between patients and healthy controls. While the levels of rubella- and mumps specific IgG were not different in the two groups of subjects, measles-specific IgG was significantly higher in patients (P<0.01). The serum titer of anti-tetanus antibody, however, was significantly lower in patients compared to healthy individuals (P<0.01). CONCLUSION: Our findings suggest that measles vaccination triggers those B cells cross-reactive with SARS-CoV2 antigens leading to the production of increased levels of measles-specific antibody.


Subject(s)
Antibodies, Viral/blood , Antigens, Viral/immunology , COVID-19/immunology , Immunization , Immunoglobulin G/blood , Measles-Mumps-Rubella Vaccine/therapeutic use , SARS-CoV-2/immunology , Age Factors , Aged , B-Lymphocytes/immunology , B-Lymphocytes/virology , Biomarkers/blood , COVID-19/blood , COVID-19/diagnosis , COVID-19/virology , Case-Control Studies , Cross Protection , Cross Reactions , Female , Host-Pathogen Interactions , Humans , Male , Measles-Mumps-Rubella Vaccine/immunology , Middle Aged , Tetanus Toxoid/immunology , Tetanus Toxoid/therapeutic use
8.
Nat Ecol Evol ; 6(10): 1414-1422, 2022 10.
Article in English | MEDLINE | ID: covidwho-2069870

ABSTRACT

Potential interactions among co-circulating viral strains in host populations are often overlooked in the study of virus transmission. However, these interactions probably shape transmission dynamics by influencing host immune responses or altering the relative fitness among co-circulating strains. In this Review, we describe multi-strain dynamics from ecological and evolutionary perspectives, outline scales in which multi-strain dynamics occur and summarize important immunological, phylogenetic and mathematical modelling approaches used to quantify interactions among strains. We also discuss how host-pathogen interactions influence the co-circulation of pathogens. Finally, we highlight outstanding questions and knowledge gaps in the current theory and study of ecological and evolutionary dynamics of multi-strain viruses.


Subject(s)
Biological Evolution , RNA Viruses , Host-Pathogen Interactions , Phylogeny
9.
Iran J Immunol ; 18(1): 82-92, 2021 03.
Article in English | MEDLINE | ID: covidwho-2067500

ABSTRACT

BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) rapidly transmits in general population, mainly between health-care workers (HCWs) who are in close contact with patients. OBJECTIVE: To study the seropositivity of HCWs as a high-risk group compared to general population. METHODS: 72 samples were obtained from HCWs working in Masih Daneshvari hospital as one of the main COVID-19 admission centers in Tehran, during April 4 to 6, 2020. Also we collected 2021 blood samples from general population. The SARS-CoV-2 specific IgM, and IgG antibodies in the collected serum specimens were measured by commercial ELISA kits. RESULTS: Based on the clinical manifestations, 25.0%, 47.2%, and 27.8% of HCWs were categorized as symptomatic with typical symptoms, symptomatic with atypical symptoms, and asymptomatic, respectively. Symptomatic individuals with typical and atypical symptoms were 63.2% and 36.8% positive in RT-PCR test, respectively. Anti-SARS-CoV-2 IgM and IgG antibodies were detected in 15.3% and 27.8% of HCWs samples, respectively. Antibody testing in the general population indicated that SARS-CoV-2 specific IgM and IgG were found in (162/2021) 8%, and (290/2021) 14.4%, respectively. The frequency of positive cases of IgM and IgG were significantly increased in HCWs compared to general population (p= 0.028 for IgM and p= 0.002 for IgG). CONCLUSION: The frequency of SARS-CoV-2 specific antibodies in HCWs was higher than general population indicating a higher viral transmission via close exposure with COVID-19 patients.


Subject(s)
Antibodies, Viral/blood , COVID-19 Serological Testing , COVID-19/diagnosis , Health Personnel , Occupational Health , SARS-CoV-2/immunology , Adult , Aged , Biomarkers/blood , COVID-19/epidemiology , COVID-19/immunology , COVID-19/virology , Cross-Sectional Studies , Female , Host-Pathogen Interactions , Humans , Infectious Disease Transmission, Patient-to-Professional , Iran/epidemiology , Male , Middle Aged , Occupational Exposure , Predictive Value of Tests , Risk Factors , Seroepidemiologic Studies , Time Factors , Young Adult
10.
Viruses ; 14(10)2022 10 01.
Article in English | MEDLINE | ID: covidwho-2066554

ABSTRACT

Infection with SARS-CoV-2 results in Coronavirus disease 2019 (COVID-19) is known to cause mild to acute respiratory infection and sometimes progress towards respiratory failure and death. The mechanisms driving the progression of the disease and accumulation of high viral load in the lungs without initial symptoms remain elusive. In this study, we evaluated the upper respiratory tract host transcriptional response in COVID-19 patients with mild to severe symptoms and compared it with the control COVID-19 negative group using RNA-sequencing (RNA-Seq). Our results reveal an upregulated early type I interferon response in severe COVID-19 patients as compared to mild or negative COVID-19 patients. Moreover, severely symptomatic patients have pronounced induction of interferon stimulated genes (ISGs), particularly the oligoadenylate synthetase (OAS) family of genes. Our results are in concurrence with other studies depicting the early induction of IFN-I response in severe COVID-19 patients, providing novel insights about the ISGs involved.


Subject(s)
COVID-19 , Interferon Type I , Humans , SARS-CoV-2 , Transcriptome , Host-Pathogen Interactions , Antiviral Agents , Interferon Type I/genetics , Lung , Ligases , RNA
11.
Genome Med ; 14(1): 18, 2022 02 21.
Article in English | MEDLINE | ID: covidwho-1688773

ABSTRACT

BACKGROUND: Measuring host gene expression is a promising diagnostic strategy to discriminate bacterial and viral infections. Multiple signatures of varying size, complexity, and target populations have been described. However, there is little information to indicate how the performance of various published signatures compare to one another. METHODS: This systematic comparison of host gene expression signatures evaluated the performance of 28 signatures, validating them in 4589 subjects from 51 publicly available datasets. Thirteen COVID-specific datasets with 1416 subjects were included in a separate analysis. Individual signature performance was evaluated using the area under the receiving operating characteristic curve (AUC) value. Overall signature performance was evaluated using median AUCs and accuracies. RESULTS: Signature performance varied widely, with median AUCs ranging from 0.55 to 0.96 for bacterial classification and 0.69-0.97 for viral classification. Signature size varied (1-398 genes), with smaller signatures generally performing more poorly (P < 0.04). Viral infection was easier to diagnose than bacterial infection (84% vs. 79% overall accuracy, respectively; P < .001). Host gene expression classifiers performed more poorly in some pediatric populations (3 months-1 year and 2-11 years) compared to the adult population for both bacterial infection (73% and 70% vs. 82%, respectively; P < .001) and viral infection (80% and 79% vs. 88%, respectively; P < .001). We did not observe classification differences based on illness severity as defined by ICU admission for bacterial or viral infections. The median AUC across all signatures for COVID-19 classification was 0.80 compared to 0.83 for viral classification in the same datasets. CONCLUSIONS: In this systematic comparison of 28 host gene expression signatures, we observed differences based on a signature's size and characteristics of the validation population, including age and infection type. However, populations used for signature discovery did not impact performance, underscoring the redundancy among many of these signatures. Furthermore, differential performance in specific populations may only be observable through this type of large-scale validation.


Subject(s)
Bacterial Infections/diagnosis , Datasets as Topic/statistics & numerical data , Host-Pathogen Interactions/genetics , Transcriptome , Virus Diseases/diagnosis , Adult , Bacterial Infections/epidemiology , Bacterial Infections/genetics , Biomarkers/analysis , COVID-19/diagnosis , COVID-19/genetics , Child , Cohort Studies , Diagnosis, Differential , Gene Expression Profiling/statistics & numerical data , Genetic Association Studies/statistics & numerical data , Humans , Publications/statistics & numerical data , SARS-CoV-2/pathogenicity , Validation Studies as Topic , Virus Diseases/epidemiology , Virus Diseases/genetics
13.
Front Cell Infect Microbiol ; 12: 1002856, 2022.
Article in English | MEDLINE | ID: covidwho-2065455
14.
Sci Adv ; 8(38): eabm6668, 2022 09 23.
Article in English | MEDLINE | ID: covidwho-2053083

ABSTRACT

Viruses exploit host cell machinery to support their replication. Defining the cellular proteins and processes required for a virus during infection is crucial to understanding the mechanisms of virally induced disease and designing host-directed therapeutics. Here, we perform a genome-wide CRISPR-Cas9-based screening in lung epithelial cells infected with the PR/8/NS1-GFP virus and use GFPhi cell as a unique screening marker to identify host factors that inhibit influenza A virus (IAV) infection. We discovered that APOE affects influenza virus infection both in vitro and in vivo. Cell deficiency in APOE conferred substantially increased susceptibility to IAV; mice deficient in APOE manifested more severe lung pathology, increased virus load, and decreased survival rate. Mechanistically, lack of cell-produced APOE results in impaired cell cholesterol homeostasis, enhancing influenza virus attachment. Thus, we identified a previously unrecognized role of APOE in restraining IAV infection.


Subject(s)
Communicable Diseases , Influenza A virus , Influenza, Human , Orthomyxoviridae Infections , Animals , Apolipoproteins , Apolipoproteins E/genetics , Cholesterol , Host-Pathogen Interactions , Humans , Influenza, Human/genetics , Mice , Orthomyxoviridae Infections/genetics , Virus Replication
15.
Science ; 369(6511): 1586-1592, 2020 09 25.
Article in English | MEDLINE | ID: covidwho-2038226

ABSTRACT

Intervention strategies are urgently needed to control the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic. The trimeric viral spike (S) protein catalyzes fusion between viral and target cell membranes to initiate infection. Here, we report two cryo-electron microscopy structures derived from a preparation of the full-length S protein, representing its prefusion (2.9-angstrom resolution) and postfusion (3.0-angstrom resolution) conformations, respectively. The spontaneous transition to the postfusion state is independent of target cells. The prefusion trimer has three receptor-binding domains clamped down by a segment adjacent to the fusion peptide. The postfusion structure is strategically decorated by N-linked glycans, suggesting possible protective roles against host immune responses and harsh external conditions. These findings advance our understanding of SARS-CoV-2 entry and may guide the development of vaccines and therapeutics.


Subject(s)
Host-Pathogen Interactions/immunology , Spike Glycoprotein, Coronavirus/chemistry , Angiotensin-Converting Enzyme 2 , Cryoelectron Microscopy , HEK293 Cells , Humans , Peptidyl-Dipeptidase A/chemistry , Protein Domains , Protein Multimerization , Protein Structure, Secondary , Receptors, Virus/chemistry , Virus Internalization
16.
Proc Natl Acad Sci U S A ; 119(35): e2122851119, 2022 08 30.
Article in English | MEDLINE | ID: covidwho-2001002

ABSTRACT

Disease transmission prediction across wildlife is crucial for risk assessment of emerging infectious diseases. Susceptibility of host species to pathogens is influenced by the geographic, environmental, and phylogenetic context of the specific system under study. We used machine learning to analyze how such variables influence pathogen incidence for multihost pathogen assemblages, including one of direct transmission (coronaviruses and bats) and two vector-borne systems (West Nile Virus [WNV] and birds, and malaria and birds). Here we show that this methodology is able to provide reliable global spatial susceptibility predictions for the studied host-pathogen systems, even when using a small amount of incidence information (i.e., [Formula: see text] of information in a database). We found that avian malaria was mostly affected by environmental factors and by an interaction between phylogeny and geography, and WNV susceptibility was mostly influenced by phylogeny and by the interaction between geographic and environmental distances, whereas coronavirus susceptibility was mostly affected by geography. This approach will help to direct surveillance and field efforts providing cost-effective decisions on where to invest limited resources.


Subject(s)
Animals, Wild , Communicable Diseases, Emerging , Disease Susceptibility , Animals , Animals, Wild/parasitology , Animals, Wild/virology , Bird Diseases/epidemiology , Bird Diseases/transmission , Chiroptera/virology , Communicable Diseases, Emerging/epidemiology , Communicable Diseases, Emerging/transmission , Communicable Diseases, Emerging/veterinary , Coronavirus , Coronavirus Infections/epidemiology , Coronavirus Infections/transmission , Coronavirus Infections/veterinary , Databases, Factual , Environment , Epidemiological Monitoring , Geography , Host-Pathogen Interactions , Incidence , Machine Learning , Malaria/epidemiology , Malaria/transmission , Malaria/veterinary , Phylogeny , Risk Assessment , West Nile Fever/epidemiology , West Nile Fever/transmission , West Nile Fever/veterinary , West Nile virus
17.
Int J Mol Sci ; 23(15)2022 Aug 01.
Article in English | MEDLINE | ID: covidwho-1994084

ABSTRACT

Tuberculosis remains a major threat to global public health, with more than 1.5 million deaths recorded in 2020. Improved interventions against tuberculosis are urgently needed, but there are still gaps in our knowledge of the host-pathogen interaction that need to be filled, especially at the site of infection. With a long history of infection in humans, Mycobacterium tuberculosis (Mtb) has evolved to be able to exploit the microenvironment of the infection site to survive and grow. The immune cells are not only reliant on immune signalling to mount an effective response to Mtb invasion but can also be orchestrated by their metabolic state. Cellular metabolism was often overlooked in the past but growing evidence of its importance in the functions of immune cells suggests that it can no longer be ignored. This review aims to gain a better understanding of mucosal immunometabolism of resident effector cells, such as alveolar macrophages and mucosal-associated invariant T cells (MAIT cells), in response to Mtb infection and how Mtb manipulates them for its survival and growth, which could address our knowledge gaps while opening up new questions, and potentially be applied for future vaccination and therapeutic strategies.


Subject(s)
Mucosal-Associated Invariant T Cells , Mycobacterium tuberculosis , Tuberculosis , Host-Pathogen Interactions , Humans , Immunity, Innate , Tuberculosis/microbiology
18.
PLoS Pathog ; 18(7): e1010660, 2022 07.
Article in English | MEDLINE | ID: covidwho-1993526

ABSTRACT

Coxiella burnetii is the etiological agent of the zoonotic disease Q fever, which is featured by its ability to replicate in acid vacuoles resembling the lysosomal network. One key virulence determinant of C. burnetii is the Dot/Icm system that transfers more than 150 effector proteins into host cells. These effectors function to construct the lysosome-like compartment permissive for bacterial replication, but the functions of most of these effectors remain elusive. In this study, we used an affinity tag purification mass spectrometry (AP-MS) approach to generate a C. burnetii-human protein-protein interaction (PPI) map involving 53 C. burnetii effectors and 3480 host proteins. This PPI map revealed that the C. burnetii effector CBU0425 (designated CirB) interacts with most subunits of the 20S core proteasome. We found that ectopically expressed CirB inhibits hydrolytic activity of the proteasome. In addition, overexpression of CirB in C. burnetii caused dramatic inhibition of proteasome activity in host cells, while knocking down CirB expression alleviated such inhibitory effects. Moreover, we showed that a region of CirB that spans residues 91-120 binds to the proteasome subunit PSMB5 (beta 5). Finally, PSMB5 knockdown promotes C. burnetii virulence, highlighting the importance of proteasome activity modulation during the course of C. burnetii infection.


Subject(s)
Coxiella burnetii , Q Fever , Bacterial Proteins/genetics , Bacterial Proteins/metabolism , Host-Pathogen Interactions , Humans , Proteasome Endopeptidase Complex/genetics , Proteasome Endopeptidase Complex/metabolism , Protein Interaction Maps , Q Fever/metabolism , Vacuoles/metabolism
19.
Antioxid Redox Signal ; 35(16): 1376-1392, 2021 12.
Article in English | MEDLINE | ID: covidwho-1342795

ABSTRACT

Significance: It is estimated that close to 50 million cases of sepsis result in over 11 million annual fatalities worldwide. The pathognomonic feature of sepsis is a dysregulated inflammatory response arising from viral, bacterial, or fungal infections. Immune recognition of pathogen-associated molecular patterns is a hallmark of the host immune defense to combat microbes and to prevent the progression to sepsis. Mitochondrial antiviral signaling protein (MAVS) is a ubiquitous adaptor protein located at the outer mitochondrial membrane, which is activated by the cytosolic pattern recognition receptors, retinoic acid-inducible gene I (RIG-I) and melanoma differentiation associated gene 5 (MDA5), following binding of viral RNA agonists. Recent Advances: Substantial progress has been made in deciphering the activation of the MAVS pathway with its interacting proteins, downstream signaling events (interferon [IFN] regulatory factors, nuclear factor kappa B), and context-dependent type I/III IFN response. Critical Issues: In the evolutionary race between pathogens and the host, viruses have developed immune evasion strategies for cleavage, degradation, or blockade of proteins in the MAVS pathway. For example, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) M protein and ORF9b protein antagonize MAVS signaling and a protective type I IFN response. Future Directions: The role of MAVS as a sensor for nonviral pathogens, host cell injury, and metabolic perturbations awaits better characterization in the future. New technical advances in multidimensional single-cell analysis and single-molecule methods will accelerate the rate of new discoveries. The ultimate goal is to manipulate MAVS activities in the form of immune-modulatory therapies to combat infections and sepsis. Antioxid. Redox Signal. 35, 1376-1392.


Subject(s)
Adaptor Proteins, Signal Transducing/immunology , Sepsis/immunology , Signal Transduction/immunology , Virus Diseases/immunology , Animals , Host-Pathogen Interactions/immunology , Humans , Immune Evasion/immunology , Sepsis/virology
20.
Arch Microbiol ; 204(8): 536, 2022 Aug 01.
Article in English | MEDLINE | ID: covidwho-1976800

ABSTRACT

The present study aimed to explore if bovine coronavirus nucleocapsid (BCoV N) impacts IFN-ß production in the host cells and to reveal further molecular mechanism of BCoV pathogenesis. Human embryonic kidney (HEK) 293 T cells were transiently transfected with pMyc-BCoV-N recombinant plasmids, then infected with the vesicular stomatitis virus (VSV). Expression levels of beta interferon (IFN-ß) mRNA were detected using RT-qPCR. The results showed that BCoV N gene was 1347 bp that was consistent with the expected size. pMyc-BCoV-N recombinant protein was 1347 bp which was successfully transcribed and overexpressed in HEK 293 T cells. BCoV-N recombinant protein inhibited dose-dependently VSV-induced IFN-ß production (p < 0.01). MDA5, MAVS, TBK1 and IRF3 could promote transcription levels of IFN-ß mRNA. But, BCoV-N protein demoted IFN-ß transcription levels induced by MDA5, MAVS, TBK1 and IRF3. Furthermore, expression levels of MDA5, MAVS, TBK1 and IRF3 mRNAs were reduced in RIG-I-like receptor (RLR) pathway. In conclusion, BCoV-N reduced IFN-ß levels in RIG-I-like receptor (RLR) pathway in HEK 293 T cells which were induced by MDA5, MAVS, TBK1 and IRF3(5D). BCoV-N protein inhibited IFN-ß production and activation of RIG-I-like receptors (RLRs) signal pathway. Our findings demonstrated BCoV N protein is an IFN-ß antagonist through inhibition of MDA5, MAVS, TBK1 and IRF3(5D) in RLRs pathway, also revealed a new mechanism of BCoV N protein to evade host innate immune response by inhibiting type I IFN production, which is beneficial to developing novel prevention strategy for BCoV disease in the animals and humans.


Subject(s)
Coronavirus, Bovine , Animals , Cattle , Coronavirus, Bovine/genetics , HEK293 Cells , Host-Pathogen Interactions , Humans , Interferon-beta/genetics , Nucleocapsid , RNA, Messenger , Recombinant Proteins
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