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Porcine reproductive and respiratory syndrome virus NADC 30‐like strain accelerates Streptococcus suis serotype 2 infection in vivo and in vitro
Author(s) -
Li Jianda,
Wang Jinbao,
Liu Yueyue,
Yang Jie,
Guo Lihui,
Ren Sufang,
Chen Zhi,
Liu Zhaoshan,
Zhang Yuyu,
Qiu Wenbin,
Li Yubao,
Zhang Shujin,
Yu Jiang,
Wu Jiaqiang
Publication year - 2019
Publication title -
transboundary and emerging diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.392
H-Index - 63
eISSN - 1865-1682
pISSN - 1865-1674
DOI - 10.1111/tbed.13072
Subject(s) - streptococcus suis , coinfection , biology , microbiology and biotechnology , serotype , porcine reproductive and respiratory syndrome virus , virology , innate immune system , immune system , in vitro , in vivo , virulence , virus , immunology , gene , biochemistry
Porcine reproductive and respiratory syndrome ( PRRS ), an economically significant pandemic disease, commonly results in increased impact of bacterial infections, including those by Streptococcus suis ( S. suis ). In recent years, PRRS virus ( PRRSV ) NADC 30‐like strain has emerged in different regions of China, and coinfected with S. suis and PRRSV has also gradually increased in clinical performance. However, the mechanisms involved in host innate responses towards S. suis and their implications of coinfection with NADC 30‐like strain remain unknown. Therefore, the pathogenicity of NADC 30‐like strain and S. suis serotype 2 ( SS 2) coinfection in vivo and in vitro was investigated in this study. The results showed that NADC 30‐like increased the invasion and proliferation of SS 2 in blood and tissues, resulting in more severe pneumonia, myocarditis, and peritonitisas well as higher mortality rate in pigs. In vitro, NADC 30‐like strain increased the invasion and survival of SS 2 in porcine alveolar macrophages ( PAM ) cells, causing more drastic expression of inflammatory cytokines and activation of NF ‐ ĸB signalling. These results pave the way for understanding the interaction of S. suis with the swine immune system and their modulation in a viral coinfection.