The interaction between claudin-1 and dengue viral prM/M protein for its entry

Che, Pulin; Tang, Hengli; Li, Qianjun

doi:10.1016/j.virol.2013.08.009

Cited by 51 publications

(41 citation statements)

References 74 publications

(91 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This result, which needs to be investigated further, corroborates the presence of interplay between gypsy and Wolbachia during maternal transmission. Our hypothesis is that Wolbachia could modify gypsy localization at junctions between follicle cells and at the apical domain, as it has previously been shown that bacteria and viruses can interact with junctions between epithelial cells (28–30). We therefore propose a model which takes into account previously proposed gypsy and Wolbachia transmission models (8, 9, 13).…”

Section: Discussionmentioning

confidence: 98%

Wolbachia Influences the Maternal Transmission of the gypsy Endogenous Retrovirus in Drosophila melanogaster

Touret

Guiguen

Terzian

2014

mBio

View full text Add to dashboard Cite

The endosymbiotic bacteria of the genus Wolbachia are present in most insects and are maternally transmitted through the germline. Moreover, these intracellular bacteria exert antiviral activity against insect RNA viruses, as in Drosophila melanogaster, which could explain the prevalence of Wolbachia bacteria in natural populations. Wolbachia is maternally transmitted in D. melanogaster through a mechanism that involves distribution at the posterior pole of mature oocytes and then incorporation into the pole cells of the embryos. In parallel, maternal transmission of several endogenous retroviruses is well documented in D. melanogaster. Notably, gypsy retrovirus is expressed in permissive follicle cells and transferred to the oocyte and then to the offspring by integrating into their genomes. Here, we show that the presence of Wolbachia wMel reduces the rate of gypsy insertion into the ovo gene. However, the presence of Wolbachia does not modify the expression levels of gypsy RNA and envelope glycoprotein from either permissive or restrictive ovaries. Moreover, Wolbachia affects the pattern of distribution of the retroviral particles and the gypsy envelope protein in permissive follicle cells. Altogether, our results enlarge the knowledge of the antiviral activity of Wolbachia to include reducing the maternal transmission of endogenous retroviruses in D. melanogaster.

show abstract

Section: Discussionmentioning

confidence: 98%

Wolbachia Influences the Maternal Transmission of the gypsy Endogenous Retrovirus in Drosophila melanogaster

Touret

Guiguen

Terzian

2014

mBio

View full text Add to dashboard Cite

show abstract

“…Claudin-1 expression is upregulated in early stages of DENV infection, which would facilitate virus entry into host cells (Gao et al, 2010;Che, Tang and Li 2013). Some pathogens use tight junction proteins to enter host cells; for instance, it has already been demonstrated that claudin-1 is a co-receptor for HCV entry (Meertens et al, 2008;Liu et al, 2009;Harris et al, 2010).…”

Section: Putative Receptors and Attachment Factors In Mammalian Cellsmentioning

confidence: 99%

“…Some pathogens use tight junction proteins to enter host cells; for instance, it has already been demonstrated that claudin-1 is a co-receptor for HCV entry (Meertens et al, 2008;Liu et al, 2009;Harris et al, 2010). In this context, claudin-1 could function as a co-receptor/receptor for DENV entry, interacting with prMcontaining DENV particles (immature or partially mature particles) and facilitating host cell entry (Gao et al, 2010;Che et al, 2013). Interestingly, claudin-1 expression is decreased in the late stages of infection, which would prevent the entry of a second wave of incoming virus particles, reducing the risk of super-infection.…”

Section: Putative Receptors and Attachment Factors In Mammalian Cellsmentioning

confidence: 99%

Receptors and routes of dengue virus entry into the host cells

Cruz-Oliveira

Freire

Conceição

et al. 2015

FEMS Microbiology Reviews

238

204

View full text Add to dashboard Cite

One-sentence summary: This review addresses the structural rearrangements of dengue virus proteins and their functions during virus entry into the host cells, exploring (a) the cellular elements involved in virus binding to mammalian and mosquito cells, (b) the internalization routes that ultimately lead to virus entry into the cell and (c) the mechanisms by which viral genome gain access to the cytoplasm, including original insights from our recent work that supports the hypothesis that the capsid protein has a role in this process. Editor: Urs Greber ABSTRACTDengue is the most prevalent arthropod-borne viral disease, caused by dengue virus, a member of the Flaviviridae family. Its worldwide incidence is now a major health problem, with 2.5 billion people living in risk areas. In this review, we integrate the structural rearrangements of each viral protein and their functions in all the steps of virus entry into the host cells. We describe in detail the putative receptors and attachment factors in mammalian and mosquito cells, and the recognition of viral immunocomplexes via Fcγ receptor in immune cells. We also discuss that virus internalization might occur through distinct entry pathways, including clathrin-mediated or non-classical clathrin-independent endocytosis, depending on the host cell and virus serotype or strain. The implications of viral maturation in virus entry are also explored. Finally, we discuss the mechanisms of viral genome access to the cytoplasm. This includes the role of low pH-induced conformational changes in the envelope protein that mediate membrane fusion, and original insights raised by our recent work that supports the hypothesis that capsid protein would also be an active player in this process, acting on viral genome translocation into the cytoplasm.

show abstract

“…For example, the tight junction protein occludin has been identified as an essential host factor for entry of several viruses, such as coxsackie B virus (CBV), rotavirus, human hepatitis C virus (HCV), West Nile virus, and others (21,(23)(24)(25). In addition to occludin, the tight junction protein claudin-1 is tightly related to the infection of dengue virus, HCV, West Nile virus, and others (25)(26)(27)(28). During PEDV infection, it has been demonstrated that structural destruction and disorganization of tight junctions are observed (12,29).…”

mentioning

confidence: 99%

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

Luo

Guo

Zhang

et al. 2017

J Virol

View full text Add to dashboard Cite

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

show abstract

The interaction between claudin-1 and dengue viral prM/M protein for its entry

Cited by 51 publications

References 74 publications

Wolbachia Influences the Maternal Transmission of the gypsy Endogenous Retrovirus in Drosophila melanogaster

Wolbachia Influences the Maternal Transmission of the gypsy Endogenous Retrovirus in Drosophila melanogaster

Receptors and routes of dengue virus entry into the host cells

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

Contact Info

Product

Resources

About