Abstract
Astrovirus infections pose a significant problem in the poultry industry, leading to multiple adverse effects such as a decreased egg production, breeding disorders, poor weight gain, and even increased mortality. The commonly observed chicken astrovirus (CAstV) was recently reported to be responsible for the “white chicks syndrome” associated with an increased embryo/chick mortality. CAstV-mediated pathogenesis in chickens occurs due to complex interactions between the infectious pathogen and the immune system. Many aspects of CAstV–chicken interactions remain unclear, and there is no information available regarding possible changes in gene expression in the chicken spleen in response to CAstV infection. We aim to investigate changes in gene expression triggered by CAstV infection. Ten 21-day-old SPF White Leghorn chickens were divided into two groups of five birds each. One group was inoculated with CAstV, and the other used as the negative control. At 4 days post infection, spleen samples were collected and immediately frozen at −70 °C for RNA isolation. We analyzed the isolated RNA, using RNA-seq to generate transcriptional profiles of the chickens’ spleens and identify differentially expressed genes (DEGs). The RNA-seq findings were verified by quantitative reverse-transcription PCR (qRT-PCR). A total of 31,959 genes was identified in response to CAstV infection. Eventually, 45 DEGs (p-value < 0.05; log2 fold change > 1) were recognized in the spleen after CAstV infection (26 upregulated DEGs and 19 downregulated DEGs). qRT-PCR performed on four genes (IFIT5, OASL, RASD1, and DDX60) confirmed the RNA-seq results. The most differentially expressed genes encode putative IFN-induced CAstV restriction factors. Most DEGs were associated with the RIG-I-like signaling pathway or more generally with an innate antiviral response (upregulated: BLEC3, CMPK2, IFIT5, OASL, DDX60, and IFI6; downregulated: SPIK5, SELENOP, HSPA2, TMEM158, RASD1, and YWHAB). The study provides a global analysis of host transcriptional changes that occur during CAstV infection in vivo and proves that, in the spleen, CAstV infection in chickens predominantly affects the cell cycle and immune signaling.
Highlights
Astroviruses cause enteritis in humans and other animals such as chickens, turkeys, sheep, cattle, swine, dogs, cats, and mice
We found that chicken astrovirus (CAstV) significantly suppressed the mRNA levels of several genes (SPIK5, SELENOP2, HSPA2 (HSP70), TMEM158, RASD1, and 14-3-3β (YWHAB))
Our results demonstrated that CAstV infection triggered innate responses in the chicken spleen and revealed a series of IFN-stimulated gene (ISG) that interact during viral infection
Summary
Astroviruses cause enteritis in humans and other animals such as chickens, turkeys, sheep, cattle, swine, dogs, cats, and mice. In poultry, they cause enteritis combined with growth depression and a higher mortality, but their presence has been described in healthy flocks [1]. They cause enteritis combined with growth depression and a higher mortality, but their presence has been described in healthy flocks [1] The cause of such a phenomenon may be the existence of astroviruses of various virulence, and the possibility of inducing a disease through the synergistic effect of several viruses simultaneously, e.g., astroviruses with rotaviruses or parvoviruses [2]. Other enteric pathogens such as avian nephritis virus (ANV), avian orthoreoviruses, and fowl adenoviruses are often detected in co-infections with CAstV. CAstV infections spread mainly horizontally via the fecal–oral route. CAstV strains transmit vertically from naive parent birds to chicks [3]
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