Classical swine fever virus infection suppresses claudin-1 expression to facilitate its replication in PK-15 cells

Wang, Xiangmin; Yang, Yaqin; Yang, Xiaoying; Liu, Xiao; Wang, Xiaochun; Gao, Libo; Yang, Chao; Lan, Rui; Bi, Jianzhong; Zhao, Qian; Yang, Guliang; Wang, Jing; Lin, Yingbo; Liu, Jianping; Yin, Gefen

doi:10.1016/j.micpath.2021.105012

Cited by 3 publications

(4 citation statements)

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“…They participate in the formation of tight junctions and are therefore key components of physiological barriers. Upon flavividae infection, BBB and TJ are often disrupted: infection with West Nile virus and classic swine fever virus both lead to claudin-1 degradation (Medigeshi et al, 2009;Roe et al, 2012;Wang et al, 2021) and Japanese encephalitis virus infection induces the degradation of claudin-5 (Chang et al, 2015). Claudins can also directly participate in viral infection (Colpitts and Baumert, 2017).…”

Section: Introductionmentioning

confidence: 99%

Zika Virus Requires the Expression of Claudin-7 for Optimal Replication in Human Endothelial Cells

et al. 2021

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Zika virus (ZIKV) infection has been associated with a series of neurological pathologies. In patients with ZIKV-induced neurological disorders, the virus is detectable in the central nervous system. Thus, ZIKV is capable of neuroinvasion, presumably through infection of the endothelial cells that constitute the blood-brain barrier (BBB). We demonstrate that susceptibility of BBB endothelial cells to ZIKV infection is modulated by the expression of tight-junction protein claudin-7 (CLDN7). Downregulation of CLDN7 reduced viral RNA yield, viral protein production, and release of infectious viral particles in several endothelial cell types, but not in epithelial cells, indicating that CLDN7 implication in viral infection is cell-type specific. The proviral activity of CLDN7 in endothelial cells is ZIKV-specific since related flaviviruses were not affected by CLDN7 downregulation. Together, our data suggest that CLDN7 facilitates ZIKV infection in endothelial cells at a post-internalization stage and prior to RNA production. Our work contributes to a better understanding of the mechanisms exploited by ZIKV to efficiently infect and replicate in endothelial cells and thus of its ability to cross the BBB.

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Section: Introductionmentioning

confidence: 99%

Zika Virus Requires the Expression of Claudin-7 for Optimal Replication in Human Endothelial Cells

et al. 2021

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“…HAZV infection was found to induce cell surface expression of CLDN1 ( Figure 1C ), resulting in inhibition of HAZV growth ( Figures 2B , F ). CLDN1 also negatively regulates growth of other viruses including HSV-1 (the family Herpesviridae ) ( De Benedetto et al, 2011 ), hPIV-2 (the family Paramyxoviridae ) ( Yumine et al, 2019 ), and CSFV (the family Flaviviridae ) ( Wang et al, 2021 ). Furthermore, paracellular penetration of human papillomavirus 16 (the family Papillomaviridae ) was promoted in the presence of Tat and gp120 proteins of human immunodeficiency virus type 1 (HIV-1) that disrupt tight junction proteins including CLDN1 ( Tugizov et al, 2013 ).…”

Section: Discussionmentioning

confidence: 99%

“…CLDN1 was reported to undergo degradation by capsid proteins of West Nile virus and Japanese encephalitis virus through proteasome-mediated pathway ( Medigeshi et al, 2009 ; Agrawal et al, 2013 ). Infection of CSFV also causes degradation of CLDN1 ( Wang et al, 2021 ). Furthermore, gp120 of HIV-1 degrades other tight junction proteins, ZO-1 and ZO-2 ( Nakamuta et al, 2008 ).…”

Section: Discussionmentioning

confidence: 99%

“…CLDN1 reportedly inhibits growth of several viruses including herpes simplex virus type 1 (HSV-1) ( De Benedetto et al, 2011 ), human parainfluenza virus type 2 (hPIV-2) ( Yumine et al, 2019 ), and the classical swine fever virus (CSFV) ( Wang et al, 2021 ). In contrast, CLDN1 has been used as co-receptor of hepatitis C virus (HCV), and was shown to be involved in both cell-free and cell-to-cell transmission ( Evans et al, 2007 ; Brimacombe et al, 2011 ).…”

Section: Introductionmentioning

confidence: 99%

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Hazara orthonairovirus nucleoprotein facilitates viral cell-to-cell spread by modulating tight junction protein, claudin-1

et al. 2023

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BackgroundTight junctions act as a barrier that prevents invasion of pathogens through epithelial cells. This study aims to elucidate the correlation between tight junctions and nairoviruses using Hazara orthonairovirus (HAZV) as a surrogate model for Crimean-Congo hemorrhagic fever virus.MethodsmRNA, total protein, and cell surface protein levels of tight junction proteins were examined by quantitative real-time reverse transcription polymerase chain reaction, immunoblot and flow cytometry, respectively. HAZV growth was measured by plaque assay. Immunofluorescence assay was used to examine viral cell-to-cell spread. The interaction between HAZV nucleoprotein and claudin-1 was analyzed by immunoprecipitation.ResultsHAZV infection induced mRNA of several tight junction proteins, especially claudin-1. HAZV infection also induced cell surface expression of claudin-1 protein. Claudin-1 overexpression inhibited the growth of HAZV by blocking its cell-to-cell spread. In contrast, HAZV nucleoprotein completely inhibited HAZV-induced cell surface expression of claudin-1, and this inhibition required interaction between HAZV nucleoprotein and claudin-1.ConclusionHAZV nucleoprotein was shown to bind to claudin-1 to negatively regulate its cell surface expression, and so can promote cell-to-cell spread of HAZV. This is the first presentation of a possible mechanism behind how nairoviruses counteract tight junction barrier function.

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Long non-coding RNA LOC103222771 promotes infection of porcine reproductive and respiratory syndrome virus in Marc-145 cells by downregulating Claudin-4

Wang,

Bi,

Yang

et al. 2023

Veterinary Microbiology

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Classical swine fever virus infection suppresses claudin-1 expression to facilitate its replication in PK-15 cells

Cited by 3 publications

References 50 publications

Zika Virus Requires the Expression of Claudin-7 for Optimal Replication in Human Endothelial Cells

Zika Virus Requires the Expression of Claudin-7 for Optimal Replication in Human Endothelial Cells

Hazara orthonairovirus nucleoprotein facilitates viral cell-to-cell spread by modulating tight junction protein, claudin-1

Long non-coding RNA LOC103222771 promotes infection of porcine reproductive and respiratory syndrome virus in Marc-145 cells by downregulating Claudin-4

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