Dataset Information

Characterization of a Feline Influenza A(H7N2) Virus.

ABSTRACT: During December 2016-February 2017, influenza A viruses of the H7N2 subtype infected ≈500 cats in animal shelters in New York, NY, USA, indicating virus transmission among cats. A veterinarian who treated the animals also became infected with feline influenza A(H7N2) virus and experienced respiratory symptoms. To understand the pathogenicity and transmissibility of these feline H7N2 viruses in mammals, we characterized them in vitro and in vivo. Feline H7N2 subtype viruses replicated in the respiratory organs of mice, ferrets, and cats without causing severe lesions. Direct contact transmission of feline H7N2 subtype viruses was detected in ferrets and cats; in cats, exposed animals were also infected via respiratory droplet transmission. These results suggest that the feline H7N2 subtype viruses could spread among cats and also infect humans. Outbreaks of the feline H7N2 viruses could, therefore, pose a risk to public health.

SUBMITTER: Hatta M

PROVIDER: S-EPMC5749472 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature

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Characterization of a Feline Influenza A(H7N2) Virus.

Hatta Masato M Zhong Gongxun G Gao Yuwei Y Nakajima Noriko N Fan Shufang S Chiba Shiho S Deering Kathleen M KM Ito Mutsumi M Imai Masaki M Kiso Maki M Nakatsu Sumiho S Lopes Tiago J TJ Thompson Andrew J AJ McBride Ryan R Suarez David L DL Macken Catherine A CA Sugita Shigeo S Neumann Gabriele G Hasegawa Hideki H Paulson James C JC Toohey-Kurth Kathy L KL Kawaoka Yoshihiro Y

Emerging infectious diseases 20180101 1

During December 2016-February 2017, influenza A viruses of the H7N2 subtype infected ≈500 cats in animal shelters in New York, NY, USA, indicating virus transmission among cats. A veterinarian who treated the animals also became infected with feline influenza A(H7N2) virus and experienced respiratory symptoms. To understand the pathogenicity and transmissibility of these feline H7N2 viruses in mammals, we characterized them in vitro and in vivo. Feline H7N2 subtype viruses replicated in the resp ...[more]

PMID: 29260686

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Project description:Influenza A virus (IAV) is a segmented negative-stranded RNA virus that brings a potentially serious threat to public health and animal husbandry. Mast cells play an important role in both the inherent and adaptive immune response. Previous studies have indicated that mast cells support the productive replication of H1N1, H5N1, and H7N2. To date, the distinct molecular mechanism behind the pathogenesis in mast cells among the three different viruses has been poorly understood. In this study, we investigated the genomic profiles in detail and the dynamic change of genomes regulated by different subtypes of IAV in mouse mast cells using microassays. Compared with any two of the three IAV-infected groups, many more differentially expressed genes (DEGs), cellular functions, and signaling pathways were confirmed in H1N1 or H7N2 group, with the H7N2 group showing the highest levels. However, few DEGs were detected and various cellular functions and signaling pathways were dramatically suppressed in the H5N1 group. With an in-depth study on the H1N1 and H7N2 groups, we demonstrated the essential role of the 5-HT signaling pathway and the cyclic guanosine monophosphate (cGMP)/protein kinase G (PKG) signaling pathway, which were preferentially activated in P815 cells infected by H1N1, and the crucial role of the HIF-1 signaling pathway that was preferentially activated in P815 cells infected by the H7N2 virus. Furthermore, real-time quantitative polymerase chain reaction (RT-qPCR) results showed significantly increased mRNA levels of 5-HT and PKG in H1N1-infected P815 cells and increased HIF-1 in H7N2-infected P815 cells. In addition, exosomes were preferentially secreted from H1N1-infected or H7N2-infected P815 cells and are potentially pivotal in innate immunity to fight IAV infection. This study provides novel information and insight into the distinct molecular mechanism of H1N1, H5N1, and H7N2 viruses in mast cells from the perspective of genomic profiles.

Project description:Background: Influenza A virus (IAV) is a segmented negative-stranded RNA virus that brings a potentially serious threat to public health and animal husbandry. Mast cells play an important role in both the inherent and adaptive immune response. Previous studies have indicated that mast cells support the productive replication of H1N1, H5N1, and H7N2. To date, the distinct molecular mechanism behind the pathogenesis in mast cells among the three different viruses has been poorly understood. Methods: We investigated the genomic profiles in detail and the dynamic change of genomes regulated by different subtypes of IAV in mouse mast cells using microassays in order to the distinct molecular mechanism behind the pathogenesis in mast cells among the three different viruses. Mouse mast cells (P815) were infected at a multiplicity of infection of 1 (infectious viruses/cell) and incubated for 12 hr before collection of total RNA and microarray anlaysis using the Affymetrix platforms. Any two of the three IAV-infected groups were compared to detect genomic distinct. Based on the results of microassays, the further verification was performed by real-time PCR and western blotting. Here, the mRNA levels of 5-HT, PKG and HIF-1 in P815 cells following H1N1, H5N1 and H7N2 infection were determined by real-time PCR. The protein levels of exosomes in P815 cells following H1N1, H5N1 and H7N2 infection were detected by western blotting. Results: Compared with any two of the three IAV-infected groups, much more diﬀerentially expressed genes (DEGs), cellular functions and signaling pathways were confirmd in H1N1 or H7N2 group, and H7N2 group showed the highest levels. However, few DEGs were detected as well as various cellular functions and signaling pathways were dramatically suppressed in H5N1 group. With an in-depth study on H1N1 and H7N2 group, we demonstrated the 5-HT signaling pathway and cGMP/PKG signaling pathway terms were enriched in P815 cells infected by H1N1 while HIF-1 signaling pathway terms were enriched in P815 cells infected by H7N2 virus. Furthermore, RT-qPCR results also showed significantly increased mRNA of 5-HT and PKG in H1N1-infected P815 cells as well as HIF-1 in H7N2-infected P815 cells. Besides, exosomes were highly secreted from H1N1-infected or H7N2-infected P815 cells. Conclusions: H1N1 and H7N2 viruses could result in a variety of DEGs in mast cells and activate various cellular functions and signaling pathways while H5N1 virus cause the few DEGs in mast cells as well as suppression of cellular functions and signaling pathways. Furthermore, 5-HT signaling pathway and cGMP/PKG signaling pathway were preferentially activated in P815 cells infected by H1N1 while HIF-1 signaling pathway were preferentially activated in P815 cells infected by H7N2 virus. In addition, exosomes were also preferentially secreted from H1N1-infected or H7N2-infected P815 cells that are potentially pivotal in innate immunity to fight IAV infection. The study provides novel information and insight into the distinct of molecular mechanism of H1N1, H5N1 and H7N2 viruses in mast cells from the perspective of genomic profiles.

Dataset Information

Characterization of a Feline Influenza A(H7N2) Virus.

Publications

Characterization of a Feline Influenza A(H7N2) Virus.

Similar Datasets

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