tetano
Editor, Senior Moderator
Viruses. 2019 Oct 29;11(11). pii: E994. doi: 10.3390/v11110994. [h=1]Contribution of Host Immune Responses Against Influenza D Virus Infection Toward Secondary Bacterial Infection in a Mouse Model.[/h]
Skelton RM[SUP]1[/SUP], Shepardson KM[SUP]2[/SUP], Hatton A[SUP]3[/SUP], Wilson PT[SUP]4[/SUP], Sreenivasan C[SUP]5[/SUP], Yu J[SUP]6[/SUP], Wang D[SUP]7[/SUP], Huber VC[SUP]8[/SUP], Rynda-Apple A[SUP]9[/SUP].
[h=3]Author information[/h] 1 Division of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD 57069, USA. raegan.nelson@coyotes.usd.edu. 2 Department of Microbiology and Immunology, Montana State University, Bozeman, MT 59717, USA. kelly.shepardson@montana.edu. 3 Department of Microbiology and Immunology, Montana State University, Bozeman, MT 59717, USA. alexishatton2222@gmail.com. 4 Division of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD 57069, USA. patrick.wilson@coyotes.usd.edu. 5 Department of Biology and Microbiology, South Dakota State University, Brookings, SD 57007, USA. Chithra.Sreenivasan@sdstate.edu. 6 Department of Biology and Microbiology, South Dakota State University, Brookings, SD 57007, USA. jieshi.yu@sdstate.edu. 7 Department of Biology and Microbiology, South Dakota State University, Brookings, SD 57007, USA. dan.wang@sdstate.edu. 8 Division of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD 57069, USA. victor.huber@usd.edu. 9 Department of Microbiology and Immunology, Montana State University, Bozeman, MT 59717, USA. agnieszka.rynda@montana.edu.
[h=3]Abstract[/h] Influenza D viruses (IDV) are known to co-circulate with viral and bacterial pathogens in cattle and other ruminants. Currently, there is limited knowledge regarding host responses to IDV infection and whether IDV infection affects host susceptibility to secondary bacterial infections. To begin to address this gap in knowledge, the current study utilized a combination of in vivo and in vitro approaches to evaluate host cellular responses against primary IDV infection and secondary bacterial infection with Staphylococcus aureus (S. aureus). Primary IDV infection in mice did not result in clinical signs of disease and it did not enhance the susceptibility to secondary S. aureus infection. Rather, IDV infection appeared to protect mice from the usual clinical features of secondary bacterial infection, as demonstrated by improved weight loss, survival, and recovery when compared to S. aureus infection alone. We found a notable increase in IFN-β expression following IDV infection while utilizing human alveolar epithelial A549 cells to analyze early anti-viral responses to IDV infection. These results demonstrate for the first time that IDV infection does not increase the susceptibility to secondary bacterial infection with S. aureus, with evidence that anti-viral immune responses during IDV infection might protect the host against these potentially deadly outcomes.
[h=4]KEYWORDS:[/h] influenza D virus; interferon; macrophages; secondary bacterial infection
PMID: 31671825 DOI: 10.3390/v11110994
Skelton RM[SUP]1[/SUP], Shepardson KM[SUP]2[/SUP], Hatton A[SUP]3[/SUP], Wilson PT[SUP]4[/SUP], Sreenivasan C[SUP]5[/SUP], Yu J[SUP]6[/SUP], Wang D[SUP]7[/SUP], Huber VC[SUP]8[/SUP], Rynda-Apple A[SUP]9[/SUP].
[h=3]Author information[/h] 1 Division of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD 57069, USA. raegan.nelson@coyotes.usd.edu. 2 Department of Microbiology and Immunology, Montana State University, Bozeman, MT 59717, USA. kelly.shepardson@montana.edu. 3 Department of Microbiology and Immunology, Montana State University, Bozeman, MT 59717, USA. alexishatton2222@gmail.com. 4 Division of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD 57069, USA. patrick.wilson@coyotes.usd.edu. 5 Department of Biology and Microbiology, South Dakota State University, Brookings, SD 57007, USA. Chithra.Sreenivasan@sdstate.edu. 6 Department of Biology and Microbiology, South Dakota State University, Brookings, SD 57007, USA. jieshi.yu@sdstate.edu. 7 Department of Biology and Microbiology, South Dakota State University, Brookings, SD 57007, USA. dan.wang@sdstate.edu. 8 Division of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD 57069, USA. victor.huber@usd.edu. 9 Department of Microbiology and Immunology, Montana State University, Bozeman, MT 59717, USA. agnieszka.rynda@montana.edu.
[h=3]Abstract[/h] Influenza D viruses (IDV) are known to co-circulate with viral and bacterial pathogens in cattle and other ruminants. Currently, there is limited knowledge regarding host responses to IDV infection and whether IDV infection affects host susceptibility to secondary bacterial infections. To begin to address this gap in knowledge, the current study utilized a combination of in vivo and in vitro approaches to evaluate host cellular responses against primary IDV infection and secondary bacterial infection with Staphylococcus aureus (S. aureus). Primary IDV infection in mice did not result in clinical signs of disease and it did not enhance the susceptibility to secondary S. aureus infection. Rather, IDV infection appeared to protect mice from the usual clinical features of secondary bacterial infection, as demonstrated by improved weight loss, survival, and recovery when compared to S. aureus infection alone. We found a notable increase in IFN-β expression following IDV infection while utilizing human alveolar epithelial A549 cells to analyze early anti-viral responses to IDV infection. These results demonstrate for the first time that IDV infection does not increase the susceptibility to secondary bacterial infection with S. aureus, with evidence that anti-viral immune responses during IDV infection might protect the host against these potentially deadly outcomes.
[h=4]KEYWORDS:[/h] influenza D virus; interferon; macrophages; secondary bacterial infection
PMID: 31671825 DOI: 10.3390/v11110994