Expression of porcine Mx1 with FMDV IRES enhances the antiviral activity against foot-and-mouth disease virus in PK-15 cells

Yuan, Bi-Feng; Fang, Hui; Shen, Chao; Zheng, Chengchao

doi:10.1007/s00705-015-2473-4

Cited by 12 publications

(7 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We also found a highly significant (P < 0.01) increase in OAS1a and PKR expression by infected macrophages from 4 to 18 h post-FMDV infection. In addition, Mx1 proteins inhibit the replication of FMDV in BHK-21 and PK-15 cells, supporting the antiviral activity against FMDV (Cai et al, 2013;Yuan et al, 2015). Up regulation of Mx1 transcripts from 4 to 12 hpi coincides with the decline in the copy number of FMDV after 12 hpi ( Fig.…”

Section: Discussionsupporting

confidence: 54%

Foot and mouth disease virus undergoes non-progressive replication in mice peritoneal macrophages and induces M1 polarization

et al. 2020

View full text Add to dashboard Cite

A B S T R A C TDespite the fact that macrophages link the innate and adaptive arms of immunity, it's role in the early infection of foot and mouth disease virus (FMDV) is largely unknown. Recently, depletion of macrophages in vivo after vaccination has shown to drastically diminish the protection against FMDV challenge in mouse model. Even the ability of macrophages to reduce or resist FMDV infection is not known hitherto. Therefore, we examined the replication ability of FMDV in mice peritoneal macrophages and the responsiveness in terms of macrophage polarization and cytokine production. Negative strand specific RT-PCR indicated replication of FMDV RNA in macrophages. Absolute quantitation of FMDV transcripts, immunofluorescence studies and titre of the infectious progeny virus revealed that replication peaked at 12 hpi and significantly declined by 18 hpi indicating nonprogressive replication in the infected macrophages. Further, significant up regulation of inducible nitric oxide synthase by 8 -12 hpi and increase of M1 specific CD11c + cells by 42.6 % after infection showed that FMDV induce M1 polarization. A significant up regulation of TNFα and IL12 transcripts at 8 hpi supported that M1 macrophages were functional. Further, we studied the expression of Type I to III interferons (IFN) and other antiviral molecules. The results indicate a marked up regulation of Type I IFNα and β by 9.2 and 11.2 fold, respectively at 8 hpi. Of the four IFN stimulated genes (ISG), viperin showed a significant up regulation by 286fold at 12 hpi in the mice macrophages. In conclusion, the results suggest that replication of FMDV in mice peritoneal macrophages is non-progressive with up regulation of Type I IFN and ISGs. Further, FMDV induces M1 polarization in murine peritoneal macrophages.

show abstract

Section: Discussionsupporting

confidence: 54%

Foot and mouth disease virus undergoes non-progressive replication in mice peritoneal macrophages and induces M1 polarization

et al. 2020

View full text Add to dashboard Cite

show abstract

“…5a, b ). IFN-stimulated genes (ISGs), such as MX1 (Interferon-induced GTP-binding protein), OASL (oligoadenylate synthetase-like protein), IFI6 (IFNα inducible protein 6), IFITs (The IFN-induced protein with tetratricopeptide repeats) and IFITMs (The interferon inducible transmembrane protein family members), were known as antiviral responder located downstream of the IFN-β and IFN-λ cascades in infected host [ 31 – 33 ]. They were found to be up-regulated to a different extent in cells infected with different subtypes of influenza A viruses (Fig.…”

Section: Resultsmentioning

confidence: 99%

Differential responses of innate immunity triggered by different subtypes of influenza a viruses in human and avian hosts

Cao

Huang

et al. 2017

BMC Med Genomics

View full text Add to dashboard Cite

BackgroundInnate immunity provides first line of defense against viral infections. The interactions between hosts and influenza A virus and the response of host innate immunity to viral infection are critical determinants for the pathogenicity or virulence of influenza A viruses. This study was designed to investigate global changes of gene expression and detailed responses of innate immune systems in human and avian hosts during the course of infection with various subtypes of influenza A viruses, using collected and self-generated transcriptome sequencing data from human bronchial epithelial (HBE), human tracheobronchial epithelial (HTBE), and A549 cells infected with influenza A virus subtypes, namely H1N1, H3N2, H5N1 HALo mutant, and H7N9, and from ileum and lung of chicken and quail infected with H5N1, or H5N2.ResultsWe examined the induction of various cytokines and chemokines in human hosts infected with different subtypes of influenza A viruses. Type I and III interferons were found to be differentially induced with each subtype. H3N2 caused abrupt and the strongest response of IFN-β and IFN-λ, followed by H1N1 (though much weaker), whereas H5N1 HALo mutant and H7N9 induced very minor change in expression of type I and III interferons. Similarly, differential responses of other innate immunity-related genes were observed, including TMEM173, MX1, OASL, IFI6, IFITs, IFITMs, and various chemokine genes like CCL5, CX3CL1, and chemokine (C-X-C motif) ligands, SOCS (suppressors of cytokine signaling) genes. Third, the replication kinetics of H1N1, H3N2, H5N1 HALo mutant and H7N9 subtypes were analyzed, H5N1 HALo mutant was found to have the highest viral replication rate, followed by H3N2, and H1N1, while H7N9 had a rate similar to that of H1N1 or H3N2 though in different host cell type.ConclusionOur study illustrated the differential responses of innate immunity to infections of different subtypes of influenza A viruses. We found the influenza viruses which induced stronger innate immune responses replicate slower than those induces weaker innate immune responses. Our study provides important insight into links between the differential innate immune responses from hosts and the pathogenicity/ virulence of different subtypes of influenza A viruses.Electronic supplementary materialThe online version of this article (10.1186/s12920-017-0304-z) contains supplementary material, which is available to authorized users.

show abstract

“…The cells were then analyzed by flow cytometry using FACS (CyAn ADP; Beckman Coulter). The anti-3D polymerase of FMDV polyclonal antibody was provided by B. Yuan (44). The anti-calnexin (endoplasmic reticulum marker) antibody, anti-GM130 (Golgi matrix protein) antibody, anti-integrin polyclonal antibodies against ␤1, ␤3, and ␤6, and monoclonal antibodies against GAPDH and ␤-actin were purchased from Proteintech.…”

Section: Cells and Viruses Fmdv Serotype O Viral Strains (Akesu/58/2mentioning

confidence: 99%

Single-Cell Analysis of the Impact of Host Cell Heterogeneity on Infection with Foot-and-Mouth Disease Virus

Xin

Wang

Han

et al. 2018

J Virol

Self Cite

View full text Add to dashboard Cite

Viral infection and replication are affected by host cell heterogeneity, but the mechanisms underlying the effects remain unclear. Using single-cell analysis, we investigated the effects of host cell heterogeneity, including cell size, inclusion, and cell cycle, on foot-and-mouth disease virus (FMDV) infection (acute and persistent infections) and replication. We detected various viral genome replication levels in FMDV-infected cells. Large cells and cells with a high number of inclusions generated more viral RNA copies and viral protein and a higher proportion of infectious cells than other cells. Additionally, we found that the viral titer was 10- to 100-fold higher in cells in G/M than those in other cell cycle phases and identified a strong correlation between cell size, inclusion, and cell cycle heterogeneity, which all affected the infection and replication of FMDV. Furthermore, we demonstrated that host cell heterogeneity influenced the adsorption of FMDV due to differences in the levels of FMDV integrin receptors expression. Collectively, these results further our understanding of the evolution of a virus in a single host cell. It is important to understand how host cell heterogeneity affects viral infection and replication. Using single-cell analysis, we found that viral genome replication levels exhibited dramatic variability in foot-and-mouth disease virus (FMDV)-infected cells. We also found a strong correlation between heterogeneity in cell size, inclusion number, and cell cycle status and that all of these characteristics affect the infection and replication of FMDV. Moreover, we found that host cell heterogeneity influenced the viral adsorption as differences in the levels of FMDV integrin receptors' expression. This study provided new ideas for the studies of correlation between FMDV infection mechanisms and host cells.

show abstract

Expression of porcine Mx1 with FMDV IRES enhances the antiviral activity against foot-and-mouth disease virus in PK-15 cells

Cited by 12 publications

References 29 publications

Foot and mouth disease virus undergoes non-progressive replication in mice peritoneal macrophages and induces M1 polarization

Foot and mouth disease virus undergoes non-progressive replication in mice peritoneal macrophages and induces M1 polarization

Differential responses of innate immunity triggered by different subtypes of influenza a viruses in human and avian hosts

Single-Cell Analysis of the Impact of Host Cell Heterogeneity on Infection with Foot-and-Mouth Disease Virus

Contact Info

Product

Resources

About