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Expression profile and histological distribution of IFITM1 and IFITM3 during H9N2 avian influenza virus infection in BALB/c mice

The H9N2 avian influenza virus is a pandemic threat which has repeatedly caused infection in humans and shows enhanced replication and transmission in mice. Previous reports showed that host factors, the interferon-inducible transmembrane (IFITM) protein, can block the replication of pathogens and a...

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Detalles Bibliográficos
Autores principales: Yu, Meng, Qi, Wenbao, Huang, Zhiqiang, Zhang, Kaizhao, Ye, Jinhui, Liu, Rongchang, Wang, Heng, Ma, Yongjiang, Liao, Ming, Ning, Zhangyong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7087031/
https://www.ncbi.nlm.nih.gov/pubmed/25265877
http://dx.doi.org/10.1007/s00430-014-0361-2
Descripción
Sumario:The H9N2 avian influenza virus is a pandemic threat which has repeatedly caused infection in humans and shows enhanced replication and transmission in mice. Previous reports showed that host factors, the interferon-inducible transmembrane (IFITM) protein, can block the replication of pathogens and affect their pathogenesis. BALB/c mice are routine laboratory animals used in influenza virus research, but the effects of H9N2 influenza virus on tissue distribution and expression pattern of IFITM in these mice are unknown. Here, we investigated the expression patterns and tissue distribution of IFITM1 and IFITM3 in BALB/c mice by infection with H9N2 AIV strains with only a PB2 residue 627 difference. The results showed that the expression patterns of ITITM1 and IFITM3 differ in various tissues of BALB/c mice at different time points after infection. IFITM1 and IFITM3 showed cell- and tissue-specific distribution in the lung, heart, liver, spleen, kidney and brain. Notably, the epithelial and neuronal cells all expressed the proteins of IFITM1 and IFITM3. Our results provide the first look at differences in IFITM1 and IFITM3 expression patterns in BALB/c mice infected by H9N2 influenza viruses. This will enhance research on the interaction between AIV and host and further will elucidate the pathogenesis of influenza virus infection based on the interferon-inducible transmembrane (IFITM) protein. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00430-014-0361-2) contains supplementary material, which is available to authorized users.