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Mice with type 1 diabetes exhibit increased susceptibility to influenza A virus

tetano

Editor, Senior Moderator
Microb Pathog. 2017 Oct 21. pii: S0882-4010(17)30857-4. doi: 10.1016/j.micpath.2017.10.026. [Epub ahead of print]
[h=1]Mice with type 1 diabetes exhibit increased susceptibility to influenza A virus.[/h] Huo C[SUP]1[/SUP], Zhang S[SUP]2[/SUP], Zhang S[SUP]1[/SUP], Wang M[SUP]3[/SUP], Qi P[SUP]4[/SUP], Xiao J[SUP]4[/SUP], Hu Y[SUP]5[/SUP], Dong H[SUP]6[/SUP].
[h=3]Author information[/h]

[h=3]Abstract[/h] Type 1 diabetes (T1D) is a metabolic disease induced by abnormal insulin secretions from damaged islet B cells. Clinical observations have shown that T1D patients are more easily infected by influenza A virus (IAV) and suffer more serious symptoms than non-T1D patients. To investigate the susceptibility of T1D mice to IAV, a T1D mouse model was built by intraperitoneal injection of diluted streptozotocin (STZ) over 5 consecutive days, followed by infection with three subtypes of IAV (H1N1/H5N1/H7N2). The T1D-infected mice showed more serious clinical symptoms and lower survival rates than the non-T1D infected mice. The hematoxylin and eosin (H&E) staining results revealed an increase in serious pathological damage to the lung and pancreas in T1D-infected mice. Immunohistochemistry results indicated higher IAV loads and a more extensive distribution of positive signals in the lungs and pancreas of T1D-infected mice than in those of non-T1D infected mice. Furthermore, according to real-time quantitative polymerase chain reaction (PCR) results, viral replication appeared to occur more easily in the lungs of T1D-infected mice. Thus, T1D-infected mice exhibited higher susceptibility to IAV than did normal mice. This study contributes a mouse model suitable for T1D research as well as valuable information about the mechanism underlying T1D patients' increased susceptibility to IAV.
Copyright ? 2017. Published by Elsevier Ltd.


[h=4]KEYWORDS:[/h] Influenza A virus; Pancreas; Susceptibility; Type 1 diabetes

PMID: 29066377 DOI: 10.1016/j.micpath.2017.10.026
 
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