Abstract
Goose parvovirus (GPV) and avian influenza virus subtype H9N2 are single-stranded DNA (ssDNA) and single-stranded RNA (ssRNA) viruses, respectively, both of which can spread in goslings and cause a significant economic loss. To explore the comprehensive transcriptome of GPV- or H9N2-infected goose spleens and to understand the immune responses induced by a DNA virus (GPV) or a RNA virus (H9N2), RNA-seq was performed on the spleens of goslings at the fifth day post infection. In the present study, 2604 and 2409 differentially expressed unigenes were identified in the GPV- and H9N2-infected groups, respectively. Through KEGG pathway enrichment analyses, the up-regulated transcripts in the two virus-infected groups were mainly involved in immune-related pathways. In addition, the two virus-infected groups displayed similar expression patterns in the immune response pathways, including pattern-recognition receptor signaling pathways, the antigen processing and presentation pathway, the NF-κB signaling pathway and the JAK-STAT signaling pathway, as well as cytokines. Furthermore, most of the immune-related genes, particularly TLR7, TRAF3, Mx, TRIM25, CD4, and CD8α, increased in response to GPV and H9N2 infection. However, the depression of NF-κB signaling may be a mechanism by which the viruses evade the host immune system or a strategy to achieve immune homeostasis.
Highlights
Over the past years, the H5N1 influenza virus, originating from geese (Anser cygnoides), has been regarded as the proposed contributor to the human influenza-like illness that broke out in Hong Kong in 1997 [1] and continued to circulate in geese in Southeastern China, indicating that the goose is essential in the zoonotic transmission of the H5N1 influenza virus and is a potential transmitter of influenza viruses [2]
It was reported recently that goose parvovirus (GPV) might be a contributor to the novel GPV (N-GPV), which causes beak atrophy and dwarfism syndrome (BADS) of commercial Cherry Valley duck flocks, with a morbidity rate between 10% and 30%, and even up to 50% in Northern China, since March 2015 [5]
The body weight of the goslings infected with GPV maintained the increase from one day post infection to 4 dpi, a significant loss of body weight was observed at 5 dpi when the GPV-infected goslings were extremely significantly slim compared with mock-infected goslings
Summary
The H5N1 influenza virus, originating from geese (Anser cygnoides), has been regarded as the proposed contributor to the human influenza-like illness that broke out in Hong Kong in 1997 [1] and continued to circulate in geese in Southeastern China, indicating that the goose is essential in the zoonotic transmission of the H5N1 influenza virus and is a potential transmitter of influenza viruses [2]. The goose is an important transmitter and natural reservoir for many avian viruses, such as goose parvovirus (GPV) and the H9N2 influenza virus (H9N2). The IFN-mediated immune response of the host cell during viral infections was partially described [8], much less is known about the antiviral response of the goose against infection at the molecular level, as well as the effects of infection with different pathogens on the expression patterns of host genes
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