Report on influenza viruses received and tested by the Melbourne WHO Collaborating Centre for Reference and Research on Influenza in 2018
Author
Price, OH; Spirason, N; Rynehart, C; Brown, SK; Todd, A; Peck, H; Patel, M; Soppe, S; Barr, IG; Chow, MKDate
2020-03-16Source Title
Communicable Diseases Intelligence Quarterly ReportPublisher
AUSTRALIAN GOVERNMENT, DEPT HEALTH & AGEINGAffiliation
Microbiology and ImmunologyDoherty Institute
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Journal ArticleCitations
Price, O. H., Spirason, N., Rynehart, C., Brown, S. K., Todd, A., Peck, H., Patel, M., Soppe, S., Barr, I. G. & Chow, M. K. (2020). Report on influenza viruses received and tested by the Melbourne WHO Collaborating Centre for Reference and Research on Influenza in 2018. COMMUNICABLE DISEASES INTELLIGENCE, 44, https://doi.org/10.33321/cdi.2020.44.16.Access Status
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http://doi.org/10.33321/cdi.2020.44.16Abstract
As part of its role in the World Health Organization's (WHO) Global Influenza Surveillance and Response System (GISRS), the WHO Collaborating Centre for Reference and Research on Influenza in Melbourne received a total of 3993 human influenza-positive samples during 2018. Viruses were analysed for their antigenic, genetic and antiviral susceptibility properties. Selected viruses were propagated in qualified cells or hens' eggs for use as potential seasonal influenza vaccine virus candidates. In 2018, influenza A(H1)pdm09 viruses predominated over influenza A(H3) and B viruses, accounting for a total of 53% of all viruses analysed. The majority of A(H1)pdm09, A(H3) and influenza B viruses analysed at the Centre were found to be antigenically similar to the respective WHO-recommended vaccine strains for the Southern Hemisphere in 2018. However, phylogenetic analysis indicated that a significant proportion of circulating A(H3) viruses had undergone genetic drift relative to the WHO-recommended vaccine strain for 2018. Of 2864 samples tested for susceptibility to the neuraminidase inhibitors oseltamivir and zanamivir, three A(H1)pdm09 viruses showed highly reduced inhibition by oseltamivir, while one B/Victoria virus showed highly reduced inhibition by both oseltamivir and zanamivir.
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