225G New to Norway and Ukraine; Worldwide Evaluation Concerning Range and Co-Circulation with 225E

“… viruses with a similar mutation had been detected in several other countries, including Brazil, China, Japan, Mexico, Ukraine and the United States. "No links between the small number of patients infected with the mutated virus have been found and the mutation does not appear to spread," ...”

If the official statement in today’s Washington Post is accurate concerning the circulating geography of the Norway polymorphism associated with several fatalities, then the only probable selection is 225G. Evaluating the meta-data of available published and partially public sequences, no other SNP of interest corresponds to the range stipulated.

The positive statement indicating low transmissibility of 225G, however, is not supportable at this time by solid evidence due to lack of surveillance using the proper tools and testing protocols.  The statement is perhaps intended to assuage rather than inform.

Countries with Probable * or Confirmed 225G

While 225G is probable or confirmed with very limited depth in 12 countries, our team is more concerned about the extensive range of 225E at the moment, documented with considerable penetration in at least 21 countries, including island nations and prominent international tourism hotspots.  At any measure, the 225E circulating range is wider and deeper than 225G though the two overlap geography in at least 6 countries.  Linked SNPs of interest appear to be more involved, as 225E demonstrates several clear acquisition paths that are not apparent with 225G.

Though the clinical attributions are not presently noted as a corollary to fatal cases like 225G, the accompanying changes and multiple backgrounds onto which the Glutamate at 225 (225E) is found may eventually provide a substantially more capable viral strain and most certainly is providing co-circulating sub-species of high interest alongside the 225G.

225G does, of course, merit scrutiny due to patterning with 230I on H1N1 Seasonal 2008 and 2009 sequences. If the range of 225G continues to smoulder, an attractant effect may draw 230I due to co-infection in areas that continue to have Seasonal H1N1 strains in circulation.  The very high level of bird involvement in transporting genetics across serotypes may provide proximity, attraction and opportunity for H5N1 as a donor candidate for 230I due to verified H5N1 ranges at geographic inflection points for PF11.  The world may not yet be seeing this permutation (225G & 230I) because the shortened infection to expiration timing also provides less time for viral recombination.

This 1918 and Avian SNP travels with H1N1 and H5N1 Avian polymorphisms indicating potential wild bird transport vectors.  In a human host, the Avian modifications may find advantage at certain tissue types due to body core proximity providing basal temperature increases and may drive replication behaviour.  The human lung may be precisely the correct temperature to promote rapid replication, more efficient binding or improved cleavage capability. 

Influenza Flux will eventually find the appropriate or optimal combination of genetics to achieve stasis, but until that stasis of PF11is achieved, these sub-species will continue to be quite dangerous, demonstrating varying levels of Cytokinic Dysregulation according the host-pathogen interplay and the viral strain's capacity for temporarily suspending early catalysts to the innate immune response, including suppression of RIG-I ubiquination as the viral NS1 protein binds TRIM25 ultimately leading to reduced intra-cellular synthesis of Type I IFN.  The timing and the level of RIG-I ubiquination suppression, thus interferon synthesis blocking, may eventually be found as the primary effector of host pathology from this IDRREAV, PF11.  We feel that the evidence is well structured toward timing as an effector equal in importance to the level of inactivation / suppression. 

225G gets the virus situated in the lung tissue and NS1 blocks the innate response.  Add back the rapid replication at a multiplier over the speed of a Seasonal Influenza strain and you find an overwhelming viral load before any cell has signalled for assistance.  When millions of viral particles erupt in a concentrated area from the lysed cells, the detritus alone drives an surging cascade of inflammatory cytokines.  A slow response creates deadly risk.  Then the body must take into account the travelling circus of sub-species that waste no time returning to their hard work of re-engineering the next cell for a viral production line.

As the data on 225G cases are released, including the sequences, presentation and progression, testing protocols, sampling protocols, prognoses, sequencing lab procedures and epidemiology, a higher level of interpretation may be made concerning these polymorphisms based on facts, rather than speculation.

A present 225G sequence set of less than 25 instances within ΣPF11 and those few having little to no associated clinicals does not provide a stable foundation at this time for determination of emergent characteristics such as rate of transmissibility, probability of co-infection with wildtype or spontaneous revision from wt due to tropism upon attaining deep lung infection.

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