Doctorado en Ciencias Biológicas y de la Salud, Autonomous Metropolitan University (UAM), Calzada del Hueso 1100, Villa Quietud, C.P. 04960, Coyoacán, México City, México.
Department of Agricultural and Animal Production, Autonomous Metropolitan University, campus Xochimilco (UAM-X), Calzada del Hueso 1100, Villa Quietud, C.P. 04960, Coyoacán, México City, México.
Pol J Vet Sci. 2021 Sep;24(3):375-384. doi: 10.24425/pjvs.2021.138728.
Canine parvovirus (CPV) is a single-stranded DNA virus that causes severe and fatal gastrointestinal diseases in dogs. CPV has developed several strategies to evade innate immune response mediated by type I interferons (IFN-I) to achieve a successful infection. The aim of this work was to evaluate the capability of CVP-2c to evade the IFN-I mediated response in infected cells. To establish the role of this response, the gene expression of interferon β (IFNβ), IFIT1, IFIT3, MAVS, and STING were estimated in MDCK cells infected with CPV-2c. Viral replication and gene expression was evaluated by quantitative PCR, also, a treatment with IFN-I (interferon omega) was included to confirm the role of IFN-I during CPV infection. The results revealed that CPV-2c infection stimulates the expression of IFNβ moderately, in these cells. Due to low IFNβ induction, the IFIT1 and IFIT3 expression were also low, and therefore CPV-2c was able to replicate in these cells. However, when the cells were treated with exogenous IFN-I, the IFNβ expression was higher, leading to an increased gene expression of IFIT1 and IFIT3, responsible for antiviral control. The overexpression of these proteins reduced the expression of NS1 and VP2 viral genes and hence viral replication. MAVS and STING expression on infected cells showed a mild increase compared to IFNβ, suggesting that the viral infection could partially modify its expression. All results obtained in this study showed that during CPV-2c infection in MDCK cells, the IFNβ expression was altered since this cytokine is one of the most critical factors for the control and inhibition of viral replication.
犬细小病毒 (CPV) 是一种单链 DNA 病毒，可导致犬严重且致命的胃肠道疾病。CPV 已经开发了几种策略来逃避 I 型干扰素 (IFN-I) 介导的先天免疫反应，以实现成功感染。本工作旨在评估 CPV-2c 逃避感染细胞中 IFN-I 介导的反应的能力。为了确定这种反应的作用，我们估计了 CPV-2c 感染的 MDCK 细胞中干扰素 β (IFNβ)、IFIT1、IFIT3、MAVS 和 STING 的基因表达。通过定量 PCR 评估病毒复制和基因表达，还包括 IFN-I（干扰素 ω）处理以确认 IFN-I 在 CPV 感染过程中的作用。结果表明，CPV-2c 感染适度刺激这些细胞中 IFNβ 的表达。由于 IFNβ 的诱导较低，IFIT1 和 IFIT3 的表达也较低，因此 CPV-2c 能够在这些细胞中复制。然而，当用外源性 IFN-I 处理细胞时，IFNβ 的表达更高，导致 IFIT1 和 IFIT3 的基因表达增加，从而发挥抗病毒作用。这些蛋白的过表达降低了 NS1 和 VP2 病毒基因的表达，从而抑制了病毒复制。与 IFNβ 相比，感染细胞中 MAVS 和 STING 的表达略有增加，表明病毒感染可能部分改变其表达。本研究获得的所有结果表明，在 CPV-2c 感染 MDCK 细胞期间，IFNβ 的表达发生改变，因为这种细胞因子是控制和抑制病毒复制的最关键因素之一。
