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. 2022 May 31:12:874936.
doi: 10.3389/fcimb.2022.874936. eCollection 2022.

Peste des Petits Ruminants Virus Exhibits Cell-Dependent Interferon Active Response

Jingyu Tang  1 , Aoxing Tang  1 , Hanyu Du  1 , Nannan Jia  1 , Jie Zhu  1 , Chuanfeng Li  1 , Chunchun Meng  1 , Guangqing Liu  1
Affiliations

Peste des Petits Ruminants Virus Exhibits Cell-Dependent Interferon Active Response

Jingyu Tang et al. Front Cell Infect Microbiol. .

Abstract

Peste des petits ruminants (PPR) is an acute and highly pathogenic infectious disease caused by peste des petits ruminants virus (PPRV), which can infect goats and sheep and poses a major threat to the small ruminants industry. The innate immune response plays an important role as a line of defense against the virus. The effect of PPRV on the active innate immune response has been described in several studies, with different conclusions. We infected three goat-derived cell lines with PPRV and tested their innate immune response. PPRV proliferated in caprine endometrial epithelial cells (EECs), caprine skin fibroblasts cells (GSFs), and goat fibroblast cells (GFs), and all cells expressed interferon (IFN) by poly (I: C) stimulation. PPRV infection stimulated expression of type I and type III IFN on EECs, and expression of the latter was significantly stronger, but IFN was not stimulated in fibroblasts (GSFs and GFs). Our results suggested that the effect of PPRV on IFN was cell-type specific. Nine IFN-stimulated genes (ISGs) were detected in EECs, but only ISG15 and RSAD2 were significantly upregulated. The effects of PPRV on IFN and IFN-induced ISGs were cell-type specific, which advances our understanding of the innate immune response induced by PPRV and creates new possibilities for the control of PPRV infection.

Keywords: Peste des petits ruminants virus; caprine endometrial epithelial cells; caprine skin fibroblasts cells; goat fibroblast cells; interferon; interferon-stimulated genes.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
PPRV proliferated in three types of goat cells. (A–C) Nucleoprotein mRNA, protein levels and viral titers in PPRV-infected CSFs were determined. (D–F) Nucleoprotein mRNA, protein levels, and viral titers in PPRV-infected GFs GFs were determined. (G, H) Nucleoprotein mRNA and protein levels and viral titers in PPRV-Infected EECs were determined. ****P < 0.0001.
Figure 2
Figure 2
Poly (I: C) induced expression of type I and type III IFNs in epithelial cells and fibroblasts. (A–C) CSFs were stimulated with poly (I: C) for 12 and 24 h, and expression of IFN-α, IFN-β, and IFN-λ3 was measured by RT-PCR. (D–F) GFs were stimulated with poly (I: C) for 12 and 24 h, and IFN-α, IFN-β, and IFN-λ3 expression was measured by RT-PCR. (G–I) EECs were stimulated with poly (I: C) for 12 and 24 h, and expression of IFN-α, IFN-β, and IFN-λ3 was measured by RT-PCR.
Figure 3
Figure 3
PPRV induces innate immunity in EECs, but not CSFs and GFs. (A–C) CSFs were infected with PPRV for 12-48 h, and expression of IFN-α, IFN-β, and IFN-λ3 was measured by RT-PCR. (D–F) GFs were infected with PPRV for 12-48 h, and expression of IFN-α, IFN-β, and IFN-λ3 was measured by RT-PCR. (G–I) EECs were infected with PPRV for 12-48 h, and expression of IFN-α, IFN-β, and IFN-λ3 was measured by RT-PCR. Comparisons between groups were calculated using two-way ANOVA in GraphPad Prism 8. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001; ns, no significant difference.
Figure 4
Figure 4
PPRV induced upregulation of RSAD2 and ISG15 on EEC cells. (A–I) EECs were infected with PPRV for 12-48 h, and expression of ISG15, RSAD2, GBP2, TRIM25, IFIT1, IFIT5, ISG20, MX1 and OASL was measured by RT-PCR. Comparisons between groups were calculated using two-way ANOVA in GraphPad Prism 8. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001; ns, no significant difference..
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