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Commentary
The above comment on the jump in severe H1N1 in young patients in England is cause for concern. Last season the acquisition of D225G was linked to severe and fatal cases, but the level of D225G in circulation was relatively low. However, the report by Mill Hill that A/Lviv/N6/2009 with D225G was a “low reactor” raised concerns that the level of D225G could increase substantially in a variant that emerged after immunity to wild type had been established. The likelihood of such an emergence is highest between seasons, when the earlier clade loses effectiveness because of immunity in the target population, and variants arise and become dominant. Recent sequences from Australia are largely a variant that arose during the summer, and appears to have spread into the northern hemsphere. Recent sequences from Australia have several changes previously found in low reactors (D225G, G158E, N159K) as well as S188T which is in the flanking region of position 190, which played a role in the establishment of H274Y in seasonal H1N1 (clade 2B – Brisbane/59-like). An increase in the levels of D225G in circulation could have a dramatic effect on the availability of ICU beds and ECMO machines leading to a significant limitation of treatment options for severe cases in young adults. The situation is beginning to appear in England at the start of the flu season, raising concerns that such variants could quickly spread throughout the northern hemisphere and severely tax health care delivery. Clustering of severe and/or fatal cases has been a concern, and the rapid increase of such cases in England demands a rapid analysis of genetic changes associated with this increase. Therefore, the release of H1N1 sequences associated with the cases in England should receive a very high priority and be made public immediately. Media link Recombinomics
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