Pathology of US Porcine Epidemic Diarrhea Virus Strain PC21A in Gnotobiotic Pigs

Jung, Kwonil; Wang, Qiuhong; Scheuer, Kelly; Lu, Zhongyan; Zhang, Yan; Saif, Linda J.

doi:10.3201/eid2004.131685

Cited by 196 publications

(277 citation statements)

References 15 publications

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“…19 PEDV replication in mature enterocytes is rapid, with previous investigations demonstrating antigen or detecting nucleic acid 24 hpi. 2,7,11 In the current study, PEDV antigen and RNA were detected at 12 hpi. It is possible that PEDV RNA detected by fecal swab collection at 12 hpi represented the inoculum as it passed through the intestine.…”

Section: Discussionmentioning

confidence: 99%

“…The finding could be a consequence of gut permeability in 1-day-old piglets; however, it was recently reported that PEDV viremia can occur in the acute stage of infection of young inoculated gnotobiotic pigs and naturally infected 3-to 5-month-old commercial swine, thus suggesting that the young age of piglets in this study was not the reason for the high prevalence of viremia. 7 Detection of PEDV RNA in nonenteric tissue samples has not been reported and may well be a function of viremia. Although the identification of PEDV in extraintestinal tissues suggests the potential for avenues of virus transmission other than the fecal-oral route, this has yet to be demonstrated.…”

Section: Discussionmentioning

confidence: 99%

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Characterization of Porcine Epidemic Diarrhea Virus Isolate US/Iowa/18984/2013 Infection in 1-Day-Old Cesarean-Derived Colostrum-Deprived Piglets

et al. 2015

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Porcine epidemic diarrhea virus (PEDV) was first recognized in North America in April 2013 and has since caused devastating disease. The objective of this study was to characterize disease and viral detection associated with an original North American PEDV isolate inoculated in neonatal piglets. Thirty-six 1-day-old cesarean-derived and colostrum-deprived piglets were randomly assigned to the control (n ¼ 16) or challenged group (n ¼ 20); the latter were orogastrically inoculated with 1 ml of US/Iowa/ 18984/2013 PEDV isolate titered at 1 Â 10 3 plaque-forming units per milliliter. Rectal swabs were collected from all piglets prior to inoculation and every 12 hours postinoculation (hpi) thereafter, with 4 control and 5 challenged piglets euthanized at 12, 24, 48, and 72 hpi. One piglet had a positive real-time quantitative polymerase chain reaction test on rectal swab at 12 hpi, and all remaining piglets were positive thereafter, with highest viral quantities detected at 24 and 36 hpi. Diarrhea was evident in 30% and 100% of challenged piglets at 18 and 24 hpi, respectively. Viral antigen was detected in enterocytes by immunohistochemistry in the duodenum and ileum of piglets euthanized at 12 hpi and was apparent throughout the small intestine of all piglets thereafter, with villus height:crypt depth ratios consistently below 4:1. Viremia was confirmed in 18 of 20 pigs at euthanasia. Clinical disease was severe and developed rapidly following infection with an original North American PEDV isolate, with lesions, viremia, and antigen detection possible by 12 hpi.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Characterization of Porcine Epidemic Diarrhea Virus Isolate US/Iowa/18984/2013 Infection in 1-Day-Old Cesarean-Derived Colostrum-Deprived Piglets

et al. 2015

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“…As noted earlier, epidemic PEDV strains are highly enteropathogenic and mainly infect villous epithelial cells of the small intestine before disseminating (11,12). It is well known that the intestinal epithelium has two important functions: absorbing helpful substances and providing a physical fence against harmful substances.…”

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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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“…The extent of intestinal villi shortening was associated with the stage of the infection or disease process. 101 Massive loss of absorptive enterocytes by PEDV infection results in a consequence of malabsorption, followed by watery diarrhea and dehydration in piglets.…”

Section: Gross and Histological Lesionsmentioning

confidence: 99%

“…12,101 Histological lesions of PEDV infection include cytoplasmic vacuolation and exfoliation of small-intestinal enterocytes in superficial villous, necrosis of scattered enterocytes followed by sloughing, and contraction of the subjacent villous lamina propria containing apoptotic cells. The extent of intestinal villi shortening was associated with the stage of the infection or disease process.…”

Section: Gross and Histological Lesionsmentioning

confidence: 99%

Porcine epidemic diarrhea virus: current insights

Lv¹,

Xiao²,

Li³

et al. 2016

VAAT

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Pathology of US Porcine Epidemic Diarrhea Virus Strain PC21A in Gnotobiotic Pigs

Cited by 196 publications

References 15 publications

Characterization of Porcine Epidemic Diarrhea Virus Isolate US/Iowa/18984/2013 Infection in 1-Day-Old Cesarean-Derived Colostrum-Deprived Piglets

Characterization of Porcine Epidemic Diarrhea Virus Isolate US/Iowa/18984/2013 Infection in 1-Day-Old Cesarean-Derived Colostrum-Deprived Piglets

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

Porcine epidemic diarrhea virus: current insights

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