کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5545308 | 1555320 | 2017 | 32 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Alpha/beta interferon receptor deficiency in mice significantly enhances susceptibility of the animals to pseudorabies virus infection
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم کشاورزی و بیولوژیک
علوم دامی و جانورشناسی
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چکیده انگلیسی
Pseudorabies virus, one of the neurotropic viruses, can infect numerous mammals. In particular, pseudorabies virus infection of swine occurs worldwide, and is a major threat to swine industry. However, the mechanism underlying the interaction between pseudorabies virus and host innate immune system is not fully understood. Here, we investigated the involvement of interferon α/β (IFN-α/β) receptor (IFNAR) in the pathogenesis of pseudorabies virus in a mouse model. The results showed that IFNAR-deficient (IFNARâ/â) mice were highly susceptible to the virus infection, as evidenced by markedly reduced survival rate of infected animals and increased viral replication. The expression of IFN-α/β and relevant interferon-stimulated genes in IFNARâ/â mice was significantly lower than that in wild-type (WT) littermates after the viral infection. Moreover, in response to the virus challenge, IFNARâ/â mice displayed elevated levels of inflammatory cytokines including interleukin 6 (IL-6) and IL-1β, and IFNARâ/â cells showed increased phosphorylation of STAT3. Collectively, these data reveal that the IFNARâ/â mice are more sensitive to pseudorabies virus infection than WT animals, and excessive IL-6/STAT3 response in IFNARâ/â mice may contribute to the pathogenesis. Our findings suggest that type I IFNs/IFNAR-dependent homeostatic control of the innate immunity is required for host defense against pseudorabies virus infection.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Veterinary Microbiology - Volume 203, May 2017, Pages 234-244
Journal: Veterinary Microbiology - Volume 203, May 2017, Pages 234-244
نویسندگان
Jingyun Wei, Yanmei Ma, Long Wang, Xiaojuan Chi, Ruoxiang Yan, Song Wang, Xinxin Li, Xiaoyong Chen, Wenhan Shao, Ji-Long Chen,