PB2 E627K 或 D701N 取代不会改变犬流感病毒 H3N2 在小鼠和犬中的毒力。
PB2 E627K or D701N substitution does not change the virulence of canine influenza virus H3N2 in mice and dogs.
机构信息
College of Veterinary Medicine, South China Agricultural University, Guangzhou, 510642, China; Guangdong Provincial Key Laboratory of Prevention and Control for Severe Clinical Animal Diseases, Guangzhou, 510642, China; Guangdong Provincial Pet Engineering Technology Research Center, Guangzhou, 510642, China.
College of Veterinary Medicine, South China Agricultural University, Guangzhou, 510642, China.
出版信息
Vet Microbiol. 2018 Jul;220:67-72. doi: 10.1016/j.vetmic.2018.05.004. Epub 2018 May 9.
Recently, canine influenza virus H3N2 (CIV H3N2) has circulated continuously in the dog populations of Asia and the United States (US). As humans have close contact with pet dogs, the circulation of CIV H3N2 is a cause for concern. Previous studies have reported that the E627K and D701N substitutions in the PB2 subunit enhanced viral pathogenicity to mammals in various influenza viruses. However, how the E627K and D701N substitutions in the PB2 subunit might affect the virulence of CIV H3N2 is unclear. Here, we constructed recombinant viruses by introducing E627K or D701N into the PB2 gene in the genetic background of A/Canine/Guangdong/02/2011H3N2 using a reverse-genetic system. The results showed that the E627K or D701N substitutions in the PB2 subunit of CIV H3N2 enhanced polymerase activity, but these substitutions did not impact viral pathogenicity in mice or beagles.
最近，犬流感病毒 H3N2（CIV H3N2）一直在亚洲和美国的犬群中持续传播。由于人类与宠物狗密切接触，CIV H3N2 的传播令人担忧。先前的研究报告称，各种流感病毒中 PB2 亚基的 E627K 和 D701N 取代增强了病毒对哺乳动物的致病性。然而，PB2 亚基中的 E627K 和 D701N 取代如何影响 CIV H3N2 的毒力尚不清楚。在这里，我们使用反向遗传系统在 A/Canine/Guangdong/02/2011H3N2 的遗传背景下，通过在 PB2 基因中引入 E627K 或 D701N 构建了重组病毒。结果表明，CIV H3N2 的 PB2 亚基中的 E627K 或 D701N 取代增强了聚合酶活性，但这些取代并未影响病毒在小鼠或比格犬中的致病性。
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