We will be touching on the mechanism of H7N9 for this post. In an article posted on Journal of Virology, [A(H7N9) virus results in early induction of proinflammatory cytokine responses in both human lung epithelial and endothelial cells and shows increased human adaption compared with avian H5N1 virus.]. This article shows the comparison of the mechanism of H7N9 and H5N1 through a series of tests. This is so the pathogenic mechanism of H7N9 is not fully known yet.

This article states that in epithelial cells, it replicates efficiently while in pulmonary endothelial cells it efficiently initiated infection. The H7N9 virus is able to bud off from both kind of cells( ciliated and mucin-secretory cells).The fact that it is able to load itself on lung cells and “induction of host responses in endothelial cells”  these factors might be the reason for causing severe pulmonary disease. With the possibility of H7N9 accessing and damaging the lungs endothelial cells, this might be the cause of pneuomia once being infected.

In another article published in PLOS|ONE, titled  “Novel Avian Influenza A (H7N9) Virus Induces Impaired Interferon Responses in Human Dendritic Cells” has shown that since H7N9 was not able to efficiently induce antiviral Interferon, this results in the lack response that the body will have in the presence of the virus. The lack of regulation of interferon responses might also have been caused by  NS1. NS1 protein can block IRF3 and this affects the expression of again antiviral Interferon. These factors  lead to the virus being able to spread around the body easily and thus explaining the high level of virus present in the airway tissue. This being said, the low levels of interferon being demonstrated can also induce antiviral state in the human cells and H7N9 is also very sensitive to the low levels of IFN and thus sometimes IFN can be used as a kind of treatment.

In conclusion, with the ability to attach to both kinds of cells and the ability of blocking the production of IFN due to different kind of factors, these pathogenic factors are what make H7N9 a possible pandemic disease especially so with the easy spreading of the virus within the host body.

References

  1. Zeng.H, Belser.J et.al (2015). A(H7N9) virus results in early induction of proinflammatory cytokine responses in both human lung epithelial and endothelial cells and shows increased human adaption compared with avian H5N1 virus. Journal of Virology11th February, retrieved 4th February from <http://jvi.asm.org/content/early/2015/02/05/JVI.03095-14
  2. Arilahti. V, Mäkelä. Sanna.M, Tynell.J, Julkunen. I,   Österlund.P          (2014). Novel Avian Influenza A (H7N9) Virus Induces Impaired Interferon Responses in Human Dendritic Cells. PLOS, 7th May, retrieved 4th February from <http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0096350&gt;
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2 thoughts on “Mechanism of H7N9

  1. Thank you for this post. It educated me briefly on the pathogenesis of H7N9. Hopefully, with this information, researchers can develop a vaccine or at least a method of controlling the spread of H7N9, if there isn’t already such a method of course.

    Like

  2. Hi, I wasn’t notice about this virus until I saw ur post. Was thinking the is it the virus like the environment with high oxygen, that’s why it replicates more often at lung tissue?

    Like

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