Clathrin- and serine proteases-dependent uptake of porcine epidemic diarrhea virus into Vero cells

Park, Jung Eun; Cruz, Deu John M.; Shin, Hyun‐Jin

doi:10.1016/j.virusres.2014.07.022

Cited by 46 publications

(40 citation statements)

References 36 publications

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“…Our previous published research found that TGEV can be internalized into IPEC-J2 cells, however the mechanism of TGEV entry is still not known. It has been confirmed that PEDV invades via clathrin-mediated endocytosis independent of caveolin-mediated endocytosis (Park et al, 2014). Our results suggest that TGEV infection reduces in clathrin or caveolin targeting shRNAs cells.…”

Section: Discussionsupporting

confidence: 77%

Epidermal growth factor receptor is a co-factor for transmissible gastroenteritis virus entry

2018

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Transmissible gastroenteritis virus (TGEV) causes severe diarrhea and high mortality in newborn piglets. It is well established that porcine intestinal epithelium is the target of the TGEV infection, however the mechanism that TGEV invades the host epithelium remains largely unknown. Aminopeptidase N (APN) is a known receptor of TGEV. This study discovered that the extracellular receptor binding domain 1 pertaining to epidermal growth receptor (EGFR) interact with TGEV spike protein. APN and EGFR synergistically promote TGEV invasion. TGEV promotes APN and EGFR clustering early in infection. Furthermore APN and EGFR synergistically stimulate PI3K/AKT as well as MEK/ERK1/2 endocytosis signaling pathways. TGEV entry is via clathrin and caveolin mediated endocytosis in IPEC-J2 cells. TGEV binds with EGFR, and subsequently promotes EGFR internalization by a clathrin-mediated endocytosis pathway. These results show that EGFR is a co-factor of TGEV, and that it plays a synergistic role with APN early in TGEV infection.

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Section: Discussionsupporting

confidence: 77%

Epidermal growth factor receptor is a co-factor for transmissible gastroenteritis virus entry

2018

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“…5). It was previously reported that PEDV enters Vero cells through an initial endocytic uptake, followed by the viral fusion between the PEDV S and host endosomal membrane (Park et al, 2014;Liu et al, 2016). This is consistent with the results that the cellassociated PEDV was significantly higher at 37°C than 4°C regardless of the presence of PC10, PEDV-negative IgG, or DMEM alone, indicating that PEDV is taken up by cells through endocytosis more efficiently at 37°C than at 4°C.…”

Section: Discussionsupporting

confidence: 92%

A spike-specific whole-porcine antibody isolated from a porcine B cell that neutralizes both genogroup 1 and 2 PEDV strains

Shan

et al. 2017

Veterinary Microbiology

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Porcine epidemic diarrhea (PED), caused by an alpha coronavirus, is a highly contagious disease and causes high morbidity and mortality in suckling piglets. Isolating PEDV neutralizing antibodies from porcine B cells is critical to elucidate the development of PEDV neutralizing antibodies and the protective mechanism of PEDV infection. Here, we described the isolation of a PEDV-neutralizing antibody from the B cell of a vaccinated pig. The antibody, named PC10, was demonstrated to target the conformational epitope of PEDV spike protein, specifically bind to the infected cells of PEDV genogroup 1 and 2 strains, and potently neutralize PEDV infection. PC10 neutralized PEDV infection through interfering with the viral life stages after cellular attachment instead of blocking the attachment of PEDV to cells. These results suggest that PC10 could be a promising candidate for passive protection and inform PEDV vaccine design because of its specificity and substantial neutralization potency.

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“…Many viruses, including PEDV, utilize receptor-mediated endocytosis to gain entry into the host cells (Park et al, 2014). During the endocytic entry processes, viruses or viral genome translocate to cytoplasm (endosomal escapes) and initiate virus replication.…”

Section: Discussionmentioning

confidence: 99%

Proteases facilitate the endosomal escape of porcine epidemic diarrhea virus during entry into host cells

Kim

Chang

2019

Virus Research

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A B S T R A C TExogenous and endogenous proteases play important roles in porcine epidemic diarrhea virus (PEDV) entry and replication. The roles of proteases in the viral endosomal escape and replication using trypsin (KD) or elastase (AA)-adapted US PEDV strains were studied. While PEDV KD and AA require different exogenous protease for efficient replication in cells, PEDV KD was more dependent on the protease than PEDV AA. There was no marked difference in viral trafficking between them during the entry events. Both PEDV were observed in the endosomes with or without protease at 1 h after virus inoculation. With protease, viral signals in the endosomes disappeared after 4 h, and newly synthesized viral proteins were detected in the ER after 6 h. However, without protease, viruses remained in the endosomes up to 24 h, which correlated with limited virus replication. Inhibitors of cathepsins, endogenous proteases, significantly reduced the replication of both PEDV by interfering with the viral endosomal escape.

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Clathrin- and serine proteases-dependent uptake of porcine epidemic diarrhea virus into Vero cells

Cited by 46 publications

References 36 publications

Epidermal growth factor receptor is a co-factor for transmissible gastroenteritis virus entry

Epidermal growth factor receptor is a co-factor for transmissible gastroenteritis virus entry

A spike-specific whole-porcine antibody isolated from a porcine B cell that neutralizes both genogroup 1 and 2 PEDV strains

Proteases facilitate the endosomal escape of porcine epidemic diarrhea virus during entry into host cells

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