In vivo morphogenesis of a new porcine enteric coronavirus, CV 777

Ducatelle, Richard; Coussement, W.; Pensaert, Maurice; Debouck, P.; Hoorens, J.

doi:10.1007/bf01315165

Cited by 50 publications

(42 citation statements)

References 12 publications

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“…Porcine epidemic diarrhea virus (PEDV), a member of genus Alphacoronavirus, family Coronaviridae Zhou et al, 1988), is the causative agent of porcine epidemic diarrhea (PED), an acute and highly contagious enteric disease in swine characterized by severe enteritis, vomiting and watery diarrhea (Ducatelle et al, 1981). The virus causes villus atrophy and destroys villus enterocytes within the jejunum and ileum .…”

Section: Introductionmentioning

confidence: 98%

Effects of porcine epidemic diarrhea virus on porcine monocyte-derived dendritic cells and intestinal dendritic cells

Gao

Zhao

Qin

et al. 2015

Veterinary Microbiology

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Section: Introductionmentioning

confidence: 98%

Effects of porcine epidemic diarrhea virus on porcine monocyte-derived dendritic cells and intestinal dendritic cells

Gao

Zhao

Qin

et al. 2015

Veterinary Microbiology

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“…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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“…While PEDV England-1-2000 was significantly different from the European prototype CV777 from the early 1980s (Ducatelle et al, 1981), current and established PCR tests in 2000 were able to detect the virus without modification, suggesting that similar strains were not simply missed due to lack of diagnostic potential. The virus also differs from the virulent North American/Asian and the INDEL variants such as OH851 currently circulating in Western Europe.…”

Section: Discussionmentioning

confidence: 96%

A retrospective study detects a novel variant of porcine epidemic diarrhea virus in England in archived material from the year 2000

Steinbach

Dastjerdi

Peake

et al. 2016

PeerJ

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Outbreaks of porcine epidemic diarrhea (PED) were first recorded in England in the 1970s and continued to be confirmed until 2002. Retrospective analysis of archived material from one of the last confirmed cases in England in the year 2000 demonstrates the previous existence of a very diverse PED virus strain. Following the outbreaks of PED in North America in 2013, there has been renewed interest in phylogenetic analysis of sequences from PEDV strains worldwide. There is a gap in the available sequence data between the mid 1980s and the mid 2000s. This work is an example of how this gap can be at least partially filled by the examination of archived material.

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In vivo morphogenesis of a new porcine enteric coronavirus, CV 777

Cited by 50 publications

References 12 publications

Effects of porcine epidemic diarrhea virus on porcine monocyte-derived dendritic cells and intestinal dendritic cells

Effects of porcine epidemic diarrhea virus on porcine monocyte-derived dendritic cells and intestinal dendritic cells

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

A retrospective study detects a novel variant of porcine epidemic diarrhea virus in England in archived material from the year 2000

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