PMC:7281546 / 7400-9214 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T13","span":{"begin":179,"end":186},"obj":"Body_part"},{"id":"T14","span":{"begin":317,"end":329},"obj":"Body_part"},{"id":"T15","span":{"begin":384,"end":395},"obj":"Body_part"},{"id":"T16","span":{"begin":427,"end":437},"obj":"Body_part"},{"id":"T17","span":{"begin":491,"end":498},"obj":"Body_part"},{"id":"T18","span":{"begin":601,"end":606},"obj":"Body_part"},{"id":"T19","span":{"begin":673,"end":677},"obj":"Body_part"},{"id":"T20","span":{"begin":799,"end":804},"obj":"Body_part"},{"id":"T21","span":{"begin":889,"end":904},"obj":"Body_part"},{"id":"T22","span":{"begin":889,"end":893},"obj":"Body_part"},{"id":"T23","span":{"begin":1462,"end":1475},"obj":"Body_part"}],"attributes":[{"id":"A13","pred":"fma_id","subj":"T13","obj":"http://purl.org/sig/ont/fma/fma67257"},{"id":"A14","pred":"fma_id","subj":"T14","obj":"http://purl.org/sig/ont/fma/fma62925"},{"id":"A15","pred":"fma_id","subj":"T15","obj":"http://purl.org/sig/ont/fma/fma62122"},{"id":"A16","pred":"fma_id","subj":"T16","obj":"http://purl.org/sig/ont/fma/fma82739"},{"id":"A17","pred":"fma_id","subj":"T17","obj":"http://purl.org/sig/ont/fma/fma67257"},{"id":"A18","pred":"fma_id","subj":"T18","obj":"http://purl.org/sig/ont/fma/fma82737"},{"id":"A19","pred":"fma_id","subj":"T19","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A20","pred":"fma_id","subj":"T20","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A21","pred":"fma_id","subj":"T21","obj":"http://purl.org/sig/ont/fma/fma86454"},{"id":"A22","pred":"fma_id","subj":"T22","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A23","pred":"fma_id","subj":"T23","obj":"http://purl.org/sig/ont/fma/fma9825"}],"text":"PEDV is the main causative pathogen of viral diarrhea in piglets. Over the years, significant work has been done to investigate PEDV pathogenesis and prevention. Aminopeptidase N protein (APN, also known as CD13) is identified as a functional receptor of PEDV and TGEV [32,33,34]. APN, a 150 KD type II transmembrane glycoprotein, is mainly expressed on the apical membrane of mature enterocytes [35]. APN binds to the 477-629 amino-acid region in the C-terminal region of PEDV spike 1 (S1) protein [34]. Apart from APN, PEDV is able to bind to sialic acids [36]. It remains unknown whether PEDV uses sugar coreceptors during viral infection [34,36]. PEDV infects multiple cell lines from different species including bat and primate (human and non-human) in vitro. The ability of PEDV to infect the cells of different species indicates that the virus utilizes the evolutionarily conserved cell components as receptors, thereby enhancing the potential for cross-species and potentially, zoonotic transmission [37,38]. The highly pathogenic variant strains of PEDV were identified in 2010 and caused a high morbidity of up to 100% in piglets, and since then, these strains become dominant, leading to most of the acute outbreaks of PED worldwide [1,7,8]. The high virulence of these strains is critically associated with the immune evasion mechanisms employed by the virus. PEDV has evolved different strategies to delicately manipulate and damage the host innate immune system for their multiplication. Clarification of these mechanisms is critical for understanding the host range, tropisms, pathogenesis, and for developing effective vaccines and antiviral drugs to curb the spread of PEDV in pigs. In this review, we provide an overview of different mechanisms used by PEDV to evade host innate immune responses."}

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T1","span":{"begin":1462,"end":1475},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/UBERON_0002405"}],"text":"PEDV is the main causative pathogen of viral diarrhea in piglets. Over the years, significant work has been done to investigate PEDV pathogenesis and prevention. Aminopeptidase N protein (APN, also known as CD13) is identified as a functional receptor of PEDV and TGEV [32,33,34]. APN, a 150 KD type II transmembrane glycoprotein, is mainly expressed on the apical membrane of mature enterocytes [35]. APN binds to the 477-629 amino-acid region in the C-terminal region of PEDV spike 1 (S1) protein [34]. Apart from APN, PEDV is able to bind to sialic acids [36]. It remains unknown whether PEDV uses sugar coreceptors during viral infection [34,36]. PEDV infects multiple cell lines from different species including bat and primate (human and non-human) in vitro. The ability of PEDV to infect the cells of different species indicates that the virus utilizes the evolutionarily conserved cell components as receptors, thereby enhancing the potential for cross-species and potentially, zoonotic transmission [37,38]. The highly pathogenic variant strains of PEDV were identified in 2010 and caused a high morbidity of up to 100% in piglets, and since then, these strains become dominant, leading to most of the acute outbreaks of PED worldwide [1,7,8]. The high virulence of these strains is critically associated with the immune evasion mechanisms employed by the virus. PEDV has evolved different strategies to delicately manipulate and damage the host innate immune system for their multiplication. Clarification of these mechanisms is critical for understanding the host range, tropisms, pathogenesis, and for developing effective vaccines and antiviral drugs to curb the spread of PEDV in pigs. In this review, we provide an overview of different mechanisms used by PEDV to evade host innate immune responses."}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T33","span":{"begin":45,"end":53},"obj":"Disease"},{"id":"T34","span":{"begin":626,"end":641},"obj":"Disease"},{"id":"T35","span":{"begin":632,"end":641},"obj":"Disease"}],"attributes":[{"id":"A33","pred":"mondo_id","subj":"T33","obj":"http://purl.obolibrary.org/obo/MONDO_0001673"},{"id":"A34","pred":"mondo_id","subj":"T34","obj":"http://purl.obolibrary.org/obo/MONDO_0005108"},{"id":"A35","pred":"mondo_id","subj":"T35","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"}],"text":"PEDV is the main causative pathogen of viral diarrhea in piglets. Over the years, significant work has been done to investigate PEDV pathogenesis and prevention. Aminopeptidase N protein (APN, also known as CD13) is identified as a functional receptor of PEDV and TGEV [32,33,34]. APN, a 150 KD type II transmembrane glycoprotein, is mainly expressed on the apical membrane of mature enterocytes [35]. APN binds to the 477-629 amino-acid region in the C-terminal region of PEDV spike 1 (S1) protein [34]. Apart from APN, PEDV is able to bind to sialic acids [36]. It remains unknown whether PEDV uses sugar coreceptors during viral infection [34,36]. PEDV infects multiple cell lines from different species including bat and primate (human and non-human) in vitro. The ability of PEDV to infect the cells of different species indicates that the virus utilizes the evolutionarily conserved cell components as receptors, thereby enhancing the potential for cross-species and potentially, zoonotic transmission [37,38]. The highly pathogenic variant strains of PEDV were identified in 2010 and caused a high morbidity of up to 100% in piglets, and since then, these strains become dominant, leading to most of the acute outbreaks of PED worldwide [1,7,8]. The high virulence of these strains is critically associated with the immune evasion mechanisms employed by the virus. PEDV has evolved different strategies to delicately manipulate and damage the host innate immune system for their multiplication. Clarification of these mechanisms is critical for understanding the host range, tropisms, pathogenesis, and for developing effective vaccines and antiviral drugs to curb the spread of PEDV in pigs. In this review, we provide an overview of different mechanisms used by PEDV to evade host innate immune responses."}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T44","span":{"begin":99,"end":102},"obj":"http://purl.obolibrary.org/obo/CLO_0051582"},{"id":"T45","span":{"begin":230,"end":231},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T46","span":{"begin":286,"end":287},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T47","span":{"begin":365,"end":373},"obj":"http://purl.obolibrary.org/obo/UBERON_0000158"},{"id":"T48","span":{"begin":397,"end":399},"obj":"http://purl.obolibrary.org/obo/CLO_0001000"},{"id":"T49","span":{"begin":487,"end":489},"obj":"http://purl.obolibrary.org/obo/CLO_0050050"},{"id":"T50","span":{"begin":500,"end":502},"obj":"http://purl.obolibrary.org/obo/CLO_0001302"},{"id":"T51","span":{"begin":559,"end":561},"obj":"http://purl.obolibrary.org/obo/CLO_0001313"},{"id":"T52","span":{"begin":673,"end":683},"obj":"http://purl.obolibrary.org/obo/CLO_0000031"},{"id":"T53","span":{"begin":717,"end":720},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_9397"},{"id":"T54","span":{"begin":725,"end":732},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_9443"},{"id":"T55","span":{"begin":734,"end":739},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_9606"},{"id":"T56","span":{"begin":748,"end":753},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_9606"},{"id":"T57","span":{"begin":799,"end":804},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T58","span":{"begin":845,"end":850},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T59","span":{"begin":889,"end":893},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T60","span":{"begin":1098,"end":1099},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T61","span":{"begin":1365,"end":1370},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T62","span":{"begin":1377,"end":1380},"obj":"http://purl.obolibrary.org/obo/CLO_0051582"},{"id":"T63","span":{"begin":1462,"end":1475},"obj":"http://purl.obolibrary.org/obo/UBERON_0002405"}],"text":"PEDV is the main causative pathogen of viral diarrhea in piglets. Over the years, significant work has been done to investigate PEDV pathogenesis and prevention. Aminopeptidase N protein (APN, also known as CD13) is identified as a functional receptor of PEDV and TGEV [32,33,34]. APN, a 150 KD type II transmembrane glycoprotein, is mainly expressed on the apical membrane of mature enterocytes [35]. APN binds to the 477-629 amino-acid region in the C-terminal region of PEDV spike 1 (S1) protein [34]. Apart from APN, PEDV is able to bind to sialic acids [36]. It remains unknown whether PEDV uses sugar coreceptors during viral infection [34,36]. PEDV infects multiple cell lines from different species including bat and primate (human and non-human) in vitro. The ability of PEDV to infect the cells of different species indicates that the virus utilizes the evolutionarily conserved cell components as receptors, thereby enhancing the potential for cross-species and potentially, zoonotic transmission [37,38]. The highly pathogenic variant strains of PEDV were identified in 2010 and caused a high morbidity of up to 100% in piglets, and since then, these strains become dominant, leading to most of the acute outbreaks of PED worldwide [1,7,8]. The high virulence of these strains is critically associated with the immune evasion mechanisms employed by the virus. PEDV has evolved different strategies to delicately manipulate and damage the host innate immune system for their multiplication. Clarification of these mechanisms is critical for understanding the host range, tropisms, pathogenesis, and for developing effective vaccines and antiviral drugs to curb the spread of PEDV in pigs. In this review, we provide an overview of different mechanisms used by PEDV to evade host innate immune responses."}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T18","span":{"begin":179,"end":186},"obj":"Chemical"},{"id":"T19","span":{"begin":292,"end":294},"obj":"Chemical"},{"id":"T20","span":{"begin":300,"end":302},"obj":"Chemical"},{"id":"T21","span":{"begin":317,"end":329},"obj":"Chemical"},{"id":"T22","span":{"begin":427,"end":432},"obj":"Chemical"},{"id":"T23","span":{"begin":433,"end":437},"obj":"Chemical"},{"id":"T24","span":{"begin":491,"end":498},"obj":"Chemical"},{"id":"T25","span":{"begin":545,"end":557},"obj":"Chemical"},{"id":"T26","span":{"begin":552,"end":557},"obj":"Chemical"},{"id":"T27","span":{"begin":1648,"end":1663},"obj":"Chemical"},{"id":"T28","span":{"begin":1648,"end":1657},"obj":"Chemical"},{"id":"T29","span":{"begin":1658,"end":1663},"obj":"Chemical"}],"attributes":[{"id":"A18","pred":"chebi_id","subj":"T18","obj":"http://purl.obolibrary.org/obo/CHEBI_36080"},{"id":"A19","pred":"chebi_id","subj":"T19","obj":"http://purl.obolibrary.org/obo/CHEBI_73601"},{"id":"A20","pred":"chebi_id","subj":"T20","obj":"http://purl.obolibrary.org/obo/CHEBI_74067"},{"id":"A21","pred":"chebi_id","subj":"T21","obj":"http://purl.obolibrary.org/obo/CHEBI_17089"},{"id":"A22","pred":"chebi_id","subj":"T22","obj":"http://purl.obolibrary.org/obo/CHEBI_46882"},{"id":"A23","pred":"chebi_id","subj":"T23","obj":"http://purl.obolibrary.org/obo/CHEBI_37527"},{"id":"A24","pred":"chebi_id","subj":"T24","obj":"http://purl.obolibrary.org/obo/CHEBI_36080"},{"id":"A25","pred":"chebi_id","subj":"T25","obj":"http://purl.obolibrary.org/obo/CHEBI_26667"},{"id":"A26","pred":"chebi_id","subj":"T26","obj":"http://purl.obolibrary.org/obo/CHEBI_37527"},{"id":"A27","pred":"chebi_id","subj":"T27","obj":"http://purl.obolibrary.org/obo/CHEBI_36044"},{"id":"A28","pred":"chebi_id","subj":"T28","obj":"http://purl.obolibrary.org/obo/CHEBI_22587"},{"id":"A29","pred":"chebi_id","subj":"T29","obj":"http://purl.obolibrary.org/obo/CHEBI_23888"}],"text":"PEDV is the main causative pathogen of viral diarrhea in piglets. Over the years, significant work has been done to investigate PEDV pathogenesis and prevention. Aminopeptidase N protein (APN, also known as CD13) is identified as a functional receptor of PEDV and TGEV [32,33,34]. APN, a 150 KD type II transmembrane glycoprotein, is mainly expressed on the apical membrane of mature enterocytes [35]. APN binds to the 477-629 amino-acid region in the C-terminal region of PEDV spike 1 (S1) protein [34]. Apart from APN, PEDV is able to bind to sialic acids [36]. It remains unknown whether PEDV uses sugar coreceptors during viral infection [34,36]. PEDV infects multiple cell lines from different species including bat and primate (human and non-human) in vitro. The ability of PEDV to infect the cells of different species indicates that the virus utilizes the evolutionarily conserved cell components as receptors, thereby enhancing the potential for cross-species and potentially, zoonotic transmission [37,38]. The highly pathogenic variant strains of PEDV were identified in 2010 and caused a high morbidity of up to 100% in piglets, and since then, these strains become dominant, leading to most of the acute outbreaks of PED worldwide [1,7,8]. The high virulence of these strains is critically associated with the immune evasion mechanisms employed by the virus. PEDV has evolved different strategies to delicately manipulate and damage the host innate immune system for their multiplication. Clarification of these mechanisms is critical for understanding the host range, tropisms, pathogenesis, and for developing effective vaccines and antiviral drugs to curb the spread of PEDV in pigs. In this review, we provide an overview of different mechanisms used by PEDV to evade host innate immune responses."}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T19","span":{"begin":45,"end":53},"obj":"Phenotype"}],"attributes":[{"id":"A19","pred":"hp_id","subj":"T19","obj":"http://purl.obolibrary.org/obo/HP_0002014"}],"text":"PEDV is the main causative pathogen of viral diarrhea in piglets. Over the years, significant work has been done to investigate PEDV pathogenesis and prevention. Aminopeptidase N protein (APN, also known as CD13) is identified as a functional receptor of PEDV and TGEV [32,33,34]. APN, a 150 KD type II transmembrane glycoprotein, is mainly expressed on the apical membrane of mature enterocytes [35]. APN binds to the 477-629 amino-acid region in the C-terminal region of PEDV spike 1 (S1) protein [34]. Apart from APN, PEDV is able to bind to sialic acids [36]. It remains unknown whether PEDV uses sugar coreceptors during viral infection [34,36]. PEDV infects multiple cell lines from different species including bat and primate (human and non-human) in vitro. The ability of PEDV to infect the cells of different species indicates that the virus utilizes the evolutionarily conserved cell components as receptors, thereby enhancing the potential for cross-species and potentially, zoonotic transmission [37,38]. The highly pathogenic variant strains of PEDV were identified in 2010 and caused a high morbidity of up to 100% in piglets, and since then, these strains become dominant, leading to most of the acute outbreaks of PED worldwide [1,7,8]. The high virulence of these strains is critically associated with the immune evasion mechanisms employed by the virus. PEDV has evolved different strategies to delicately manipulate and damage the host innate immune system for their multiplication. Clarification of these mechanisms is critical for understanding the host range, tropisms, pathogenesis, and for developing effective vaccines and antiviral drugs to curb the spread of PEDV in pigs. In this review, we provide an overview of different mechanisms used by PEDV to evade host innate immune responses."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T16","span":{"begin":133,"end":145},"obj":"http://purl.obolibrary.org/obo/GO_0009405"},{"id":"T17","span":{"begin":626,"end":641},"obj":"http://purl.obolibrary.org/obo/GO_0016032"},{"id":"T18","span":{"begin":1262,"end":1271},"obj":"http://purl.obolibrary.org/obo/GO_0016032"},{"id":"T19","span":{"begin":1262,"end":1271},"obj":"http://purl.obolibrary.org/obo/GO_0009405"},{"id":"T20","span":{"begin":1323,"end":1337},"obj":"http://purl.obolibrary.org/obo/GO_0042783"},{"id":"T21","span":{"begin":1455,"end":1468},"obj":"http://purl.obolibrary.org/obo/GO_0045087"},{"id":"T22","span":{"begin":1592,"end":1604},"obj":"http://purl.obolibrary.org/obo/GO_0009405"},{"id":"T23","span":{"begin":1790,"end":1813},"obj":"http://purl.obolibrary.org/obo/GO_0045087"}],"text":"PEDV is the main causative pathogen of viral diarrhea in piglets. Over the years, significant work has been done to investigate PEDV pathogenesis and prevention. Aminopeptidase N protein (APN, also known as CD13) is identified as a functional receptor of PEDV and TGEV [32,33,34]. APN, a 150 KD type II transmembrane glycoprotein, is mainly expressed on the apical membrane of mature enterocytes [35]. APN binds to the 477-629 amino-acid region in the C-terminal region of PEDV spike 1 (S1) protein [34]. Apart from APN, PEDV is able to bind to sialic acids [36]. It remains unknown whether PEDV uses sugar coreceptors during viral infection [34,36]. PEDV infects multiple cell lines from different species including bat and primate (human and non-human) in vitro. The ability of PEDV to infect the cells of different species indicates that the virus utilizes the evolutionarily conserved cell components as receptors, thereby enhancing the potential for cross-species and potentially, zoonotic transmission [37,38]. The highly pathogenic variant strains of PEDV were identified in 2010 and caused a high morbidity of up to 100% in piglets, and since then, these strains become dominant, leading to most of the acute outbreaks of PED worldwide [1,7,8]. The high virulence of these strains is critically associated with the immune evasion mechanisms employed by the virus. PEDV has evolved different strategies to delicately manipulate and damage the host innate immune system for their multiplication. Clarification of these mechanisms is critical for understanding the host range, tropisms, pathogenesis, and for developing effective vaccines and antiviral drugs to curb the spread of PEDV in pigs. In this review, we provide an overview of different mechanisms used by PEDV to evade host innate immune responses."}

{"project":"LitCovid-sentences","denotations":[{"id":"T49","span":{"begin":0,"end":65},"obj":"Sentence"},{"id":"T50","span":{"begin":66,"end":161},"obj":"Sentence"},{"id":"T51","span":{"begin":162,"end":280},"obj":"Sentence"},{"id":"T52","span":{"begin":281,"end":401},"obj":"Sentence"},{"id":"T53","span":{"begin":402,"end":504},"obj":"Sentence"},{"id":"T54","span":{"begin":505,"end":563},"obj":"Sentence"},{"id":"T55","span":{"begin":564,"end":650},"obj":"Sentence"},{"id":"T56","span":{"begin":651,"end":764},"obj":"Sentence"},{"id":"T57","span":{"begin":765,"end":1016},"obj":"Sentence"},{"id":"T58","span":{"begin":1017,"end":1252},"obj":"Sentence"},{"id":"T59","span":{"begin":1253,"end":1371},"obj":"Sentence"},{"id":"T60","span":{"begin":1372,"end":1501},"obj":"Sentence"},{"id":"T61","span":{"begin":1502,"end":1699},"obj":"Sentence"},{"id":"T62","span":{"begin":1700,"end":1814},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"PEDV is the main causative pathogen of viral diarrhea in piglets. Over the years, significant work has been done to investigate PEDV pathogenesis and prevention. Aminopeptidase N protein (APN, also known as CD13) is identified as a functional receptor of PEDV and TGEV [32,33,34]. APN, a 150 KD type II transmembrane glycoprotein, is mainly expressed on the apical membrane of mature enterocytes [35]. APN binds to the 477-629 amino-acid region in the C-terminal region of PEDV spike 1 (S1) protein [34]. Apart from APN, PEDV is able to bind to sialic acids [36]. It remains unknown whether PEDV uses sugar coreceptors during viral infection [34,36]. PEDV infects multiple cell lines from different species including bat and primate (human and non-human) in vitro. The ability of PEDV to infect the cells of different species indicates that the virus utilizes the evolutionarily conserved cell components as receptors, thereby enhancing the potential for cross-species and potentially, zoonotic transmission [37,38]. The highly pathogenic variant strains of PEDV were identified in 2010 and caused a high morbidity of up to 100% in piglets, and since then, these strains become dominant, leading to most of the acute outbreaks of PED worldwide [1,7,8]. The high virulence of these strains is critically associated with the immune evasion mechanisms employed by the virus. PEDV has evolved different strategies to delicately manipulate and damage the host innate immune system for their multiplication. Clarification of these mechanisms is critical for understanding the host range, tropisms, pathogenesis, and for developing effective vaccines and antiviral drugs to curb the spread of PEDV in pigs. In this review, we provide an overview of different mechanisms used by PEDV to evade host innate immune responses."}

{"project":"2_test","denotations":[{"id":"32403318-17467767-82827250","span":{"begin":270,"end":272},"obj":"17467767"},{"id":"32403318-20074871-82827251","span":{"begin":273,"end":275},"obj":"20074871"},{"id":"32403318-26907329-82827252","span":{"begin":276,"end":278},"obj":"26907329"},{"id":"32403318-18603472-82827253","span":{"begin":397,"end":399},"obj":"18603472"},{"id":"32403318-26907329-82827254","span":{"begin":500,"end":502},"obj":"26907329"},{"id":"32403318-25787280-82827255","span":{"begin":559,"end":561},"obj":"25787280"},{"id":"32403318-26907329-82827256","span":{"begin":643,"end":645},"obj":"26907329"},{"id":"32403318-25787280-82827257","span":{"begin":646,"end":648},"obj":"25787280"},{"id":"32403318-23486053-82827258","span":{"begin":1009,"end":1011},"obj":"23486053"},{"id":"32403318-23486063-82827259","span":{"begin":1012,"end":1014},"obj":"23486063"},{"id":"32403318-22261231-82827260","span":{"begin":1245,"end":1246},"obj":"22261231"},{"id":"32403318-22840964-82827261","span":{"begin":1247,"end":1248},"obj":"22840964"},{"id":"32403318-23797760-82827262","span":{"begin":1249,"end":1250},"obj":"23797760"}],"text":"PEDV is the main causative pathogen of viral diarrhea in piglets. Over the years, significant work has been done to investigate PEDV pathogenesis and prevention. Aminopeptidase N protein (APN, also known as CD13) is identified as a functional receptor of PEDV and TGEV [32,33,34]. APN, a 150 KD type II transmembrane glycoprotein, is mainly expressed on the apical membrane of mature enterocytes [35]. APN binds to the 477-629 amino-acid region in the C-terminal region of PEDV spike 1 (S1) protein [34]. Apart from APN, PEDV is able to bind to sialic acids [36]. It remains unknown whether PEDV uses sugar coreceptors during viral infection [34,36]. PEDV infects multiple cell lines from different species including bat and primate (human and non-human) in vitro. The ability of PEDV to infect the cells of different species indicates that the virus utilizes the evolutionarily conserved cell components as receptors, thereby enhancing the potential for cross-species and potentially, zoonotic transmission [37,38]. The highly pathogenic variant strains of PEDV were identified in 2010 and caused a high morbidity of up to 100% in piglets, and since then, these strains become dominant, leading to most of the acute outbreaks of PED worldwide [1,7,8]. The high virulence of these strains is critically associated with the immune evasion mechanisms employed by the virus. PEDV has evolved different strategies to delicately manipulate and damage the host innate immune system for their multiplication. Clarification of these mechanisms is critical for understanding the host range, tropisms, pathogenesis, and for developing effective vaccines and antiviral drugs to curb the spread of PEDV in pigs. In this review, we provide an overview of different mechanisms used by PEDV to evade host innate immune responses."}

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Over the years, significant work has been done to investigate PEDV pathogenesis and prevention. Aminopeptidase N protein (APN, also known as CD13) is identified as a functional receptor of PEDV and TGEV [32,33,34]. APN, a 150 KD type II transmembrane glycoprotein, is mainly expressed on the apical membrane of mature enterocytes [35]. APN binds to the 477-629 amino-acid region in the C-terminal region of PEDV spike 1 (S1) protein [34]. Apart from APN, PEDV is able to bind to sialic acids [36]. It remains unknown whether PEDV uses sugar coreceptors during viral infection [34,36]. PEDV infects multiple cell lines from different species including bat and primate (human and non-human) in vitro. The ability of PEDV to infect the cells of different species indicates that the virus utilizes the evolutionarily conserved cell components as receptors, thereby enhancing the potential for cross-species and potentially, zoonotic transmission [37,38]. The highly pathogenic variant strains of PEDV were identified in 2010 and caused a high morbidity of up to 100% in piglets, and since then, these strains become dominant, leading to most of the acute outbreaks of PED worldwide [1,7,8]. The high virulence of these strains is critically associated with the immune evasion mechanisms employed by the virus. PEDV has evolved different strategies to delicately manipulate and damage the host innate immune system for their multiplication. Clarification of these mechanisms is critical for understanding the host range, tropisms, pathogenesis, and for developing effective vaccines and antiviral drugs to curb the spread of PEDV in pigs. In this review, we provide an overview of different mechanisms used by PEDV to evade host innate immune responses."}