#11,872
Once a month during the winter, and a little less regularly during the summer and fall, the ECDC releases a report on the influenza viruses collected and submitted by their member nations to the Francis Crick Worldwide Influenza Centre (WIC).
Seasonal flu viruses (H1N1, H3N2, and both the Victoria & Yamagata B Viruses) are continually evolving and each can have multiple variants or strains in circulation at the same time.Some of these strains will be more `biologically fit' than others, and are therefore likely to be more successful. As populations gain immunity against existing strains, new strains evolve to take their place.
And - as we saw with the emergence of a `drifted' H3N2 virus in the fall of 2014 - those emerging strains can sometimes spread rapidly and play havoc with the flu vaccine's effectiveness.We've the first virus characterization report of the fall from the ECDC today which shows most of the viruses tested still appear to be a decent match for this year's flu vaccine which contains:
• A/California/7/2009 (H1N1)pdm09-like virus,
• A/Hong Kong/4801/2014 (H3N2)-like virus and a
• B/Brisbane/60/2008-like virus (B/Victoria lineage)
• Quadrivalent vaccines contain the above strains plus B/Phuket/3073/2013-like virus (B/Yamagata lineage)
This summary from the ECDC. Follow the link to read the full report.
Influenza virus characterisation, Summary Europe, September 2016
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04 Nov 2016
Abstract
In the course of the 2015–2016 influenza season, over 139 000 influenza detections across the Region have been reported. Influenza type A viruses have prevailed over type B with A(H1N1)pdm09 viruses, greatly outnumbering A(H3N2) and B/Victoria-lineage detections representing two-thirds of the type B viruses assigned to a lineage.
Since 1 January 2016, EU/EEA countries have shared 596 influenza-positive specimens with the Francis Crick Institute, London, for detailed characterisation. Since the July report, 47 viruses have been characterised antigenically and genetically.
Of the 21 A(H1N1)pdm09 viruses characterised antigenically all (100%) were similar to the vaccine virus A/California/7/2009. Worldwide new genetic subclusters of viruses within the 6B clade have emerged, with two being designated as subclades: 6B.1 defined by HA1 amino acid substitutions S162N and I216T and 6B.2 defined by HA1 amino acid substitutions V152T and V173I. Of the 493 viruses characterised genetically for the 2015–2016 season, 29 (6%) were clade 6B, 453 (92%) were subclade 6B.1, and 11 (2%) were subclade 6B.2.
The two A(H3N2) test viruses characterised by haemagglutination inhibition (HI) assay were poorly recognised by reference antiserum raised against the recommended 2015–2016 vaccine virus, egg-propagated A/Switzerland/9715293/2013. The test viruses were recognised somewhat better by antisera raised against egg-propagated A/Hong Kong/4801/2014, the virus recommended for use in 2016–2017 northern hemisphere and both 2016 and 2017 southern hemisphere influenza vaccines. Of 127 A(H3N2) viruses characterised genetically for the 2015–2016 season, two (2%) were clade 3C.3, 90 (71%) were subclade 3C.2a, and 35 (27%) were subclade 3C.3a.
The 20 B/Victoria-lineage viruses were antigenically similar to tissue culture-propagated surrogates of B/Brisbane/60/2008. All 184 viruses characterised genetically for the 2015–2016 season fell in genetic clade 1A, as do recently collected viruses worldwide.
Four B/Yamagata viruses have been characterised since the previous report. They reacted well with post-infection ferret antiserum raised against egg-propagated B/Phuket/3073/2013, the recommended vaccine virus for the northern hemisphere 2015-16 influenza season and for quadrivalent vaccines in the 2016–17 northern hemisphere and both 2016 and 2017 southern hemisphere seasons. Of the 29 viruses characterised genetically for the 2015–2016 season, 28 fell in genetic clade 3 and one in clade 2.
