The methods have been detailed in references 1-4. All 4,588 HA gene sequences and 3,163 p B1 gene sequences reported in the Pubmed data base from 2003 to 2011 were analyzed for Replikin peptides.
The Figure shows that in 2001, bird and human H5N1 virus HA genes, had a high concentration or Replikin Count (greater than 4.0 Replikins per 100 amino acids) (Replikin Count=number of Replikins per 100 amino acids) which comprised 60% of the Replikins of the total H5N1 population. Low Counts (4.0 and below) are associated with 'resting' non-outbreak states of the virus (4). This concentration decreased after 2001 to only 20% in 2009. Then in 2010, more H5N1 HA genes had higher Replikin Counts. By 2011, H5N1 HA genes with Replikin Counts greater than 4.0 now have been found to comprise 82% of the total H5N1 population, the highest such concentration ever found.
p B1 Gene
Similarly, the Figure shows that the p B1 gene 'high' Replikin Count increased almost four-fold from 2001 to 2010, two-fold from 2009 to 2010, and peaked one year before outbreaks in Cambodia and Vietnam. In influenza, increasing Replikin Counts at p<0.001 have been followed by an outbreak in seven of seven previous Replikins prediction trials, including two for H5N1 (4).
In addition, not shown separately in the Figure, in 2011, human H5N1 Mean Replikin Counts also peaked; HA Mean Counts were 4.9(+/-0.8), and p B1 Mean Counts 12.7(+/-15.1).
The following pattern has now repeatedly been observed: genomic Replikin Counts increase to high levels, accompanied by sporadic lethal human cases, as recently seen in Cambodia (1), followed by an outbreak of rapidly replicating spreading lethal human d
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