A novel strain of porcine epidemic diarrhea virus in Vietnamese pigs

Kim, Yong Kwan; Lim, Suk-Kyung; Lim, Ji-Ae; Cho, In‐Soo; Park, Eunhye; Le, Van Phan; Hien, Nguyen Ba; Thach, Pham Ngoc; Quynh, Do Hai; Vui, Tran Quang; Tien, Nguyen Trung; An, Dong-Jun

doi:10.1007/s00705-015-2411-5

Cited by 28 publications

(25 citation statements)

References 26 publications

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“…In comparison with the S protein of CV777, all Vietnamese strains in G2‐1 and G2‐2 examined in this study had insertions (a 4‐amino acid insertion between positions 55 and 56 and a 1‐amino acid insertion between positions 134 and 135) and a 2‐amino acid deletion at positions 158–159. These insertions and deletions were identical to those of previously reported strains isolated after 2010, in which the mutations were found in the hypervariable domain in the N‐terminus of the S protein (Kim, Lim et al., ; Temeeyasen et al., ; Vui, Tung, Inui, Slater, & Nilubol, ). In comparison with the sequence of the initial prototype strains in North America (high virulent NA prototype strains), the Vietnamese field strains VN262/HB/2014 and VN232/2013 possessed three deletions (a 1‐nucleotide deletion at position 166, an 11‐nucleotide deletion at positions 172–182 and a 3‐nucleotide deletion at positions 414–416) and a 6‐nucleotide insertion between positions 474 and 475 in the S gene.…”

Section: Resultssupporting

confidence: 87%

“…Six PEDV Vietnamese strains in our study were included in subgroup G2‐1. Four of these strains (VN292/HN/2014, VN367/VP/2014, VN‐K2/HY/2015 and VN‐TH15/HY/2015) formed a monophyletic branch, and they were closely related to the previously reported Vietnamese strains HUA‐PED45 and HUA‐PED47 (Kim, Lim et al., ). The other Vietnamese strain in this subgroup, namely VN02/HY/2013, was closely grouped with reference strains recently isolated in Japan (13JM‐291), Thailand (BRC2) and Vietnam (VN/VAP1113_1/2013/VungTau, VN/KCHY_310113/2013/KhoaiChau and VN/JFP1013_1/2013/VinhAn).…”

Section: Resultssupporting

confidence: 63%

“…In a previous study (Kim, Lim et al., ), five PEDV strains isolated in a central province (Quang Tri) of Vietnam were clustered into the S INDEL type of PEDV. Consistent with those data, in this study, we identified a strain (VN232/HB/2013) belonging to this type that was collected in a northern province (Hoa Binh) of Vietnam.…”

Section: Discussionmentioning

confidence: 98%

“…Two recent studies reported that five Vietnamese PEDV strains isolated in 2013 and early 2014 including VN/JFP1013_1/2013/Vinh An/Vietnam, VN/VAP1113_1/2013/Vung Tua/Vietnam, VN/KCHY‐310113/2013/KhoaiChau/HungYen/Vietnam (Vui et al., ), HUA‐PED45 and HUA‐PED47 2010 (Kim, Lim et al., ) were related to new Chinese variants that have emerged since 2010. The Vietnamese PEDV strain HUA‐14PED96 (accession number KT941120), which was identified in a Northern province, was reported to have a unique 72‐nucleotide deletion in the ORF1a gene (Choe et al., ).…”

Section: Discussionmentioning

confidence: 99%

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Appearance of US-like porcine epidemic diarrhoea virus (PEDV) strains before US outbreaks and genetic heterogeneity of PEDVs collected in Northern Vietnam during 2012-2015

Diep

Sueyoshi

Izzati

et al. 2017

Transbound Emerg Dis

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Summary Porcine epidemic diarrhoea virus (PEDV) is the aetiologic agent of porcine epidemic diarrhoea (PED), a highly contagious enteric disease that is threatening the swine industry globally. Since PED was first reported in Southern Vietnam in 2009, the disease has spread throughout the country and caused substantial economic losses. To identify PEDVs responsible for the recent outbreaks, the full‐length spike (S) gene of 25 field PEDV strains collected from seven northern provinces of Vietnam was sequenced and analysed. The sequence analysis revealed that the S genes of Vietnamese PEDVs were heterogeneous and classified into four genotypes, namely North America and Asian non‐S INDEL, Asian non‐S INDEL, new S INDEL and classical S INDEL. This study reported the pre‐existence of US‐like PEDV strains in Vietnam. Thirteen Vietnamese variants had a truncated S protein that was 261 amino acids shorter than the normal protein. We also detected one novel variant with an 8‐amino acid insertion located in the receptor‐binding region for porcine aminopeptidase N. Compared to the commercial vaccine strains, the emerging Vietnamese strains were genetically distant and had various amino acid differences in epitope regions and N‐glycosylation sites in the S protein. The development of novel vaccines based on the emerging Vietnamese strains may be contributive to the control of the current PED outbreaks.

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Section: Resultssupporting

confidence: 87%

Section: Resultssupporting

confidence: 63%

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Appearance of US-like porcine epidemic diarrhoea virus (PEDV) strains before US outbreaks and genetic heterogeneity of PEDVs collected in Northern Vietnam during 2012-2015

Diep

Sueyoshi

Izzati

et al. 2017

Transbound Emerg Dis

View full text Add to dashboard Cite

show abstract

“…Porcine epidemic diarrhea virus (PEDV) has been identified as the etiologic agent of porcine epidemic diarrhea (PED), and it causes diarrhea, vomiting, and dehydration in infected swine (3,4). Outbreaks of PED have occurred frequently in many swine-raising countries in Europe, Asia, and America, resulting in considerable economic losses (5)(6)(7)(8)(9)(10).…”

mentioning

confidence: 99%

Tight Junction Protein Occludin Is a Porcine Epidemic Diarrhea Virus Entry Factor

Luo

Guo

Zhang

et al. 2017

J Virol

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Porcine epidemic diarrhea virus (PEDV), the causative agent of porcine epidemic diarrhea, has caused huge economic losses in pig-producing countries. Although PEDV was long believed to replicate in the intestinal epithelium by using aminopeptidase N as a receptor, the mechanisms of PEDV infection are not fully characterized. In this study, we found that PEDV infection of epithelial cells results in disruption of the tight junctional distribution of occludin to its intracellular location. Overexpression of occludin in target cells makes them more susceptible to PEDV infection, whereas ablation of occludin expression by use of small interfering RNA (siRNA) in target cells significantly reduces their susceptibility to virus infection. However, the results observed with occludin siRNA indicate that occludin is not required for virus attachment. We conclude that occludin plays an essential role in PEDV infection at the postbinding stages. Furthermore, we observed that macropinocytosis inhibitors blocked occludin internalization and virus entry, indicating that virus entry and occludin internalization are closely coupled. However, the macropinocytosis inhibitors could not impede virus replication once the virus had entered host cells. This suggests that occludin internalization by macropinocytosis or a macropinocytosis-like process is involved in the virus entry events. Immunofluorescence confocal microscopy showed that PEDV was trapped at cellular junctional regions upon macropinocytosis inhibitor treatment, indicating that occludin may serve as a scaffold in the vicinity of virus entry. Collectively, these data show that occludin plays an essential role in PEDV infection during late entry events. Our observation may provide novel insights into PEDV infection and related pathogenesis.IMPORTANCE Tight junctions are highly specialized membrane domains whose main function is to attach adjacent cells to each other, thereby forming intercellular seals. Here we investigate, for the first time, the role of the tight junction protein occludin in PEDV infection. We observed that PEDV infection induced the internalization of occludin. By using genetic modification methods, we demonstrate that occludin plays an essential role in PEDV infection. Moreover, PEDV entry and occludin internalization seem to be closely coupled. Our findings reveal a new mechanism of PEDV infection.KEYWORDS PEDV, occludin, tight junction C oronaviruses are a group of positive-strand RNA viruses belonging to the family Coronaviridae in the order Nidovirales. They are broadly distributed among mammalian and avian species, and they cause acute and persistent infections. In most cases, coronaviruses are generally associated with significant respiratory and/or intestinal tract diseases (1, 2). Porcine epidemic diarrhea virus (PEDV) has been identified as the etiologic agent of porcine epidemic diarrhea (PED), and it causes diarrhea, vomiting, and dehydration in infected swine (3, 4). Outbreaks of PED have occurred frequently in

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Genetic characterization of the spike gene of porcine epidemic diarrhea viruses (PEDVs) circulating in Vietnam from 2015 to 2016

Than

Choe

et al. 2020

Veterinary Medicine & Sci

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Background Porcine epidemic diarrhea (PED) is a highly contagious swine disease caused by the PED virus (PEDV), which is a member of the family Coronaviridae . Since the first outbreaks in Belgium and the United Kingdom were reported in 1971, PED has spread throughout many countries around the world and causing significant economic loss. This study was conducted to investigate the recent distribution of PEDV strains in Vietnam during the 2015–2016 seasons. Methods A total of 30 PED‐specific PCR‐positive intestinal and faecal samples were collected from unvaccinated piglets in Vietnam during the 2015–2016 seasons. The full length of the spike (S) gene of these PEDV strains were analysed to determine their phylogeny and genetic relationship with other available PEDV strains globally. Results Phylogenetic analysis of the complete S gene sequences revealed that the 28 Vietnamese PEDV strains collected in the northern and central regions clustered in the G2 group (both G2a and G2b sub‐groups), while the other 2 PEDV strains (HUA‐PED176 and HUA‐PED254) collected in the southern region were clustered in the G1/G1b group/sub‐group. The nucleotide (nt) and deduced amino acid (aa) analyses based on the complete S gene sequences showed that the Vietnamese PEDV strains were closely related to each other, sharing nt and aa homology of 93.2%–99.9% and 92.6%–99.9%, respectively. The N‐glycosylation patterns and mutations in the antigenic region were observed in Vietnamese PEDV strains. Conclusions This study provides, for the first time, up‐to‐date information on viral circulation and genetic distribution, as well as evidence to assist in the development of effective PEDV vaccines in Vietnam.

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A novel strain of porcine epidemic diarrhea virus in Vietnamese pigs

Cited by 28 publications

References 26 publications

Appearance of US-like porcine epidemic diarrhoea virus (PEDV) strains before US outbreaks and genetic heterogeneity of PEDVs collected in Northern Vietnam during 2012-2015

Appearance of US-like porcine epidemic diarrhoea virus (PEDV) strains before US outbreaks and genetic heterogeneity of PEDVs collected in Northern Vietnam during 2012-2015

Tight Junction Protein Occludin Is a Porcine Epidemic Diarrhea Virus Entry Factor

Genetic characterization of the spike gene of porcine epidemic diarrhea viruses (PEDVs) circulating in Vietnam from 2015 to 2016

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