Eurosurveillancehttp://www.eurosurveillance.org/ViewArt ... leId=19760
Eurosurveillance, Volume 16, Issue 1, 06 January 2011
Virological analysis of fatal influenza cases in the United Kingdom during the early wave of influenza in winter 2010/11
Health Protection Agency, Centre for Infections, London, United Kingdom
The 2010/11 winter influenza season is underway in the United Kingdom, with co-circulation of influenza A(H1N1)2009 (antigenically similar to the current 2010/11 vaccine strain), influenza B (mainly B/Victoria/2/87 lineage, similar to the 2010/11 vaccine strain) and a few sporadic influenza A(H3N2) viruses. Clinical influenza activity has been increasing. Severe illness, resulting in hospitalisation and deaths, has occurred in children and young adults and has predominantly been associated with influenza A(H1N1)2009, but also influenza B viruses.
Influenza A(H1N1)2009 isolates characterised to date, in samples from the community, hospitalised patients and fatal cases, are antigenically homogeneous and similar to the A(H1N1)2009 virus included in the 2010/11 seasonal influenza vaccine, A/California/7/2009. Only minor genetic drift has been noted in influenza A(H1N1)2009 viruses circulating in 2010 compared with the earliest isolates in April 2009, and this observed genetic diversity has been consistent with expected patterns of virus evolution (Figure 3). Phylogenetic analysis shows that HA sequences from nine fatal and four severe cases in the UK in 2010 were interspersed with sequences from mild cases in 2010 from the UK and elsewhere. All UK 2010 viruses cluster in two main branches, characterised by either E374K with additional mutations in minor subclusters such as D97N, S185T, S451N and N125D, some of which have been recently described , or by A134T and S183P, with additional substitutions such as N441K, R509M and V527I. Almost all viruses from winter 2010 analysed to date from fatal and non-fatal cases had 222D in the HA gene (39/41).
Preliminary analyses from a limited number of whole genome sequences including some from fatal cases, indicate that these are consistent with observations from seasonal influenza and from the first and second waves of the recent pandemic: so far no unique mutations have been associated with severe or fatal cases of influenza A(H1N1)2009, but further comprehensive analysis is required.
some influenza B discussion:
Over 98% of influenza B viruses isolated in the UK since week 40 in 2010 have been from the B/Victoria/2/87 lineage, with most showing good reactivity to antisera raised against reference viruses from this lineage. The HA sequences group within the genetic clade represented by the current vaccine strain, B/Brisbane/60/2008, characterised by amino acid substitutions L58P N75K, N165K and S172P (Figure 4). A separate small cluster of three viruses from the antigenically distinct B/Yamagata/16/88 lineage have also been detected in one region of England: one fatal case and two hospitalised cases. The three known fatal influenza B cases were distributed across both lineages. The HA segment of the influenza B/Yamagata lineage virus isolated from a fatal case in week 46 belonged to a clade represented by influenza B/Bangladesh/3333/2007, with amino acid substitutions S150I, N165Y and S229D relative to a previous vaccine strain, B/Florida/4/06. This HA sequence contained two additional substitutions, G183R and M251V, which had been sporadically detected in influenza B viruses isolated in several countries in 2009/10.