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Age-specific incidence of influenza A responds to change in virus subtype dominance

tetano

tetano

Editor, Senior Moderator
Clin Infect Dis. 2020 Jan 27. pii: ciaa075. doi: 10.1093/cid/ciaa075. [Epub ahead of print] [h=1]Age-specific incidence of influenza A responds to change in virus subtype dominance.[/h]
Gagnon A[SUP]1,[/SUP][SUP]2[/SUP], Acosta E[SUP]1,[/SUP][SUP]3[/SUP], Miller MS[SUP]4[/SUP].
[h=3]Author information[/h]

[h=3]Abstract[/h] When H3N2 replaced H1N1 as the dominant influenza subtype during the 2018-19 season, the pattern of age-specific influenza incidence shifted due to the lingering effects of antigenic imprinting. The characteristic shape that imprinting leaves on influenza susceptibility could foster important advances in understanding and predicting the epidemiology of influenza.
? The Author(s) 2020. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.


[h=4]KEYWORDS:[/h] Influenza incidence; age-specific analysis; antigenic imprinting; cohort effect

PMID: 31985006 DOI: 10.1093/cid/ciaa075
 
Very interesting - had to do some background reading. https://en.wikipedia.org/wiki/Original_antigenic_sin Is the wikipedia page accurate? Very interesting references to T-cells, HIV and ensuing cytokine activity " It has been demonstrated that during the secondary infection by a different strain of dengue virus, the CTLs prefer to release cytokines instead of causing lysis of cell. As a result, the production of these cytokines are thought to increase vascular permeability and exacerbate the damage of endothelial cells"

I read here https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6153324/ that viral sepsis could be exacerbated by the presence of a second virus and even a coinfection with bacteria. Undoubtedly no one will be able to test this with the overwhelming situation. Extra info - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6546210/ this also references secondary viral coinfection leading to severe respiratory disease.

Could this be the reason they are using the anti viral for HIV that is being tested? Could the anti virals actually be dampening down our memory B cells?

Thank you Tetano. Very interesting information as always.
 
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