Claudins in viral infection: from entry to spread

Colpitts, Che C.; Baumert, Thomas F.

doi:10.1007/s00424-016-1908-4

Cited by 19 publications

(13 citation statements)

References 107 publications

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“…Intriguingly, RSV infection induced marked upregulation of claudin-2 expression. 18 , 21 Claudin-2 belongs to a subset of TJ proteins called pore-forming TJ that prevent epithelial barrier formation, and claudin-2-deficient mice showed decreased permeability in renal proximal tubules. 68 Likewise, upregulation of claudin-2 by proinflammatory cytokines was shown to increase the permeability of epithelial barriers.…”

Section: Viral Disruption Of Tight Junctionsmentioning

confidence: 99%

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Airway tight junctions as targets of viral infections

et al. 2021

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The apical junctional complexes (AJCs) of airway epithelial cells are a key component of the innate immune system by creating barriers to pathogens, inhaled allergens, and environmental particles. AJCs form between adjacent cells and consist of tight junctions (TJs) and adherens junctions (AJs). Respiratory viruses have been shown to target various components of the AJCs, leading to airway epithelial barrier dysfunction by different mechanisms. Virus-induced epithelial permeability may allow for allergens and bacterial pathogens to subsequently invade. In this review, we discuss the pathophysiologic mechanisms leading to disruption of AJCs and the potential ensuing ramifications. We focus on the following viruses that affect the pulmonary system: respiratory syncytial virus, rhinovirus, influenza viruses, immunodeficiency virus, and other viruses such as coxsackievirus, adenovirus, coronaviruses, measles, parainfluenza virus, bocavirus, and vaccinia virus. Understanding the mechanisms by which viruses target the AJC and impair barrier function may help design therapeutic innovations to treat these infections.

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Section: Viral Disruption Of Tight Junctionsmentioning

confidence: 99%

“… 74 Similarly, in primary human nasal epithelial cells, HRV decreased ZO-1, occludin, claudin-1, and E-cadherin expression, thereby increasing permeability for viral entry. 21 , 24 …”

Section: Viral Disruption Of Tight Junctionsmentioning

confidence: 99%

Airway tight junctions as targets of viral infections

et al. 2021

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“…Viruses often need to cross epithelial barriers in order to infect a host or be transmitted. Human immunodeficiency virus 1 (HIV-1) alters claudin expression in genital epithelial cells, allowing for the virus to disseminate into the lumen of the genitourinary tract and be transmitted to a new host [ 12 ]. HIV-1 down-regulates TJ protein expression and induces increased permeability of the blood–brain barrier and the gastrointestinal tract, initiating neuropathogenesis and gastrointestinal distress, respectively [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Epithelial barrier function properties of the 16HBE14o- human bronchial epithelial cell culture model

et al. 2020

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The human bronchial epithelial cell line, 16HBE14o- (16HBE), is widely used as a model for respiratory epithelial diseases and barrier function. During differentiation, transepithelial electrical resistance (TER) increased to approximately 800 ohms x cm2 while 14C-D-mannitol flux rates (Jm) simultaneously decreased. Tight junctions were shown by diffusion potential studies to be anion selective with PC1/PNa = 1.9. Transepithelial leakiness could be induced by the phorbol ester, protein kinase C activator, 12-O-tetradecanoylphorbol-13-acetate (TPA), and the proinflammatory cytokine, Tumor Necrosis Factor-α (TNF-α). Basal barrier function could not be improved by the micronutrients, zinc or quercetin. Of methodological significance, TER was observed to be more variable and to spontaneously, significantly decrease after initial barrier formation, whereas Jm did not significantly fluctuate or increase. Unlike the strong inverse relationship between TER and Jm during differentiation, differentiated cell layers manifested no relationship between TER and Jm. There was also much greater variability for TER values compared to Jm. Investigating the dependence of 16HBE TER on transcellular ion conductance, inhibition of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) chloride channel with GlyH-101 produced a large decrease in short circuit current (Isc) and a slight increase in TER, but no significant change in Jm. A strong temperature dependence was observed not only for Isc, but also for TER. In summary, research utilizing 16HBE as a model in airway barrier function studies needs to be aware of the complexity of TER as a parameter of barrier function given the influence of CFTR-dependent transcellular conductance on TER.

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“…Claudin-1 interacts with CD81 to facilitate virus internalization during the HCV postbinding steps. It is a structural component of the hepatocyte tight junction and is highly expressed in liver tissue (6). By constituting the backbone of tight junction strands, claudins mediate cell adhesion and determine the permeability of epithelia.…”

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confidence: 99%

Sec24C-Dependent Transport of Claudin-1 Regulates Hepatitis C Virus Entry

Yin

Zhang

2017

J Virol

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Claudin-1 is a hepatitis C virus (HCV) coreceptor required for viral entry. Although extensive studies have focused on claudin-1 as an anti-HCV target, little is known about how the level of claudin-1 at the cell surface is regulated by host vesicular transport. Here, we identified an interaction between claudin-1 and Sec24C, a cargo-sorting component of the coat protein complex II (COPII) vesicular transport system. By interacting with Sec24C through its C-terminal YV, claudin-1 is transported from the endoplasmic reticulum (ER) and is eventually targeted to the cell surface. Blocking COPII transport inhibits HCV entry by reducing the level of claudin-1 at the cell surface. These findings provide mechanistic insight into the role of COPII vesicular transport in HCV entry. Tight junction protein claudin-1 is one of the cellular receptors for hepatitis C virus, which infects 185 million people globally. Its cellular distribution plays important role in HCV entry; however, it is unclear how the localization of claudin-1 to the cell surface is controlled by host transport pathways. In this paper, we not only identified Sec24C as a key host factor for HCV entry but also uncovered a novel mechanism by which the COPII machinery transports claudin-1 to the cell surface. This mechanism might be extended to other claudins that contain a C-terminal YV or V motif.

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Claudins in viral infection: from entry to spread

Cited by 19 publications

References 107 publications

Airway tight junctions as targets of viral infections

Airway tight junctions as targets of viral infections

Epithelial barrier function properties of the 16HBE14o- human bronchial epithelial cell culture model

Sec24C-Dependent Transport of Claudin-1 Regulates Hepatitis C Virus Entry

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