New Analyses of Nearly 900,000 Genetic Sequences of Ebola Polymerase, VP35, and Glycoprotein Reveals Replikin Count Increase in 2012-13 — One Year in Advance of the Ebola Outbreak

LONDON, April 15, 2015 /PRNewswire-USNewswire/ — Replikins Ltd reported today that 886,277 automated analyses of Ebola gene sequences 1976-2015 show that significant Replikin Count increases occurred in virus polymerase, VP35 and glycoprotein in 2012 and 2013, in advance of the Ebola outbreak, which began in March 2014 (WHO). Such gene Replikin Count increases previously have been shown to be associated with rapid replication in advance of 41 outbreaks by 15 other viruses (1,2).  In the first 7 months of the Ebola outbreak in 2014, a sudden drop in gene Replikin Count of all three proteins occurred, followed 5 months later by the rapid decline of new cases (Figure); both the drop in Count and in new cases also occurred in three other high lethality H5N1 and SARS outbreaks. The Ebola Replikin Count has remained at 0.5+/-0.3 throughout 2014, but has risen again in 2015 (p<0.001) to 1.6+/-1.5.

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As the number of Ebola specimens published on Pubmed increased from 10,197 in September 2014 to 16,167 on April 10, 2015, Ebola gene analysis was repeated every few days, reaching a total of 886,277.  The increase in gene Replikin Counts in 2012 of the Ebola polymerase protein (p<0.05) and Ebola CV35 protein (p<0.001) preceded by 2 years, and the increase in the Ebola glycoprotein in 2013 (p<0.001) preceded by one year the clinical outbreak (see Figure).  Both the course of marked increase then sudden drop in gene Replikin Count, and the abrupt drop 5 months later in new clinical cases, are similar to those observed in three other high lethality viruses human outbreaks (1,2): H5N1 virus in Hong Kong 1997 (set. 33% mortality), SARS 2003 (est.10% mortality), H5N1 2007 Indonesia (est.90% mortality); Ebola 2014 (est.60-70% mortality)  (Figure 1). All four showed a precipitous drop in gene Replikin Count in the year of the outbreak and a similar decline in a few months in the number of new cases.

In contrast to the course of high lethality viruses above, low lethality (for example est. 1.3% in Canada), influenza H1N1 in the Pandemic of 2009 showed a more gradual decrease in gene Replikin Count and recurrent outbreaks from 2009 to 2015 (see Figure).

High human host mortality rate in a short period of time after infection, may severely limit the number and time of host sites available to the virus to replicate and spread, and thus contribute to an abrupt end of the epidemic.

Replikins are virus gene structures, peptides strictly defined by the length of the peptides, the number of lysine groups, the space between lysines, and the presence of histidine groups. These structures were first discovered and named as they increased in concentration with rapid replication of glioblastoma multiforme brain cancer cells growing in tissue culture. Replikins were then found in viruses associated with and preceding virus outbreaks. An algorithm was designed for automated analyses of Replikins in gene sequences. Increase in H1N1 gene Replikin Count (number of Replikins per 100 amino acids) in 2008 predicted the 2009 H1N1 influenza pandemic. Replikins increase and spread on the surface of H1N1 HA gene as the 2009 pandemic developed was also shown by 3D X-ray crystallography (1).

The finding of gene structures which provide one to two years of advance notice of coming virus outbreaks removes the previous advantage of viruses, that of surprise.  For the first time, software enables advance analysis of the structure of the emerging virus and allows testing in advance specific therapeutics, vaccines, and effective public health preemptive responses. Further, the finding of predictive specific Replikin gene structures provides the advance chemical possibility of interrupting and preventing the development of pandemics. The detailed genomic structural data obtained, in the case of Taura Syndrome Virus (1) and influenza H5N1 (3), has led to the solid phase synthesis in 7 days of efficacious completely synthetic Replikins vaccines. The same method is being applied to the development of a synthetic Ebola virus vaccine. All vaccine and public health efforts begun against Ebola should be maintained and strengthened as the Ebola Gene Replikin Count, at 0.5+/-0.3 throughout 2014, has begun in 2015 to increase again at p<0.001, having reached 1.6 +/-1.5 today.

Contact:  Samuel Bogoch; Email; Tel: 646-320-5910

References:

1. Nature Precedings. doi:10.1038/npre.2012.7144.1 and  Prediction of Specific Virus Outbreaks Made From the Increased Concentration of a New Class of Virus Genomic Peptides, Replikins. doi:10.1038/npre.2011.6279.1
2. Bogoch,S. and Bogoch E.S. Marked Increase in Ebola Gene Replikin Count in 2012 & 2013 Predicted Current Ebola Outbreak; Does Recent Sharp Drop in Replikin Count Signal Early End for the Current Ebola Outbreak? Reuters, October 4, 2014.
3. Jackwood,M.W., Bogoch, S., Bogoch ES, Hilt, D.,and Williams,S.M. Efficacy of aReplikin Peptide Vaccine against Low Pathogenicity Avian Influenza H5 Virus. Avian Diseases 53(4): 613617, 2009 Bogoch,S and Bogoch, E.S. Genome Replikin Count Predicts Increased Infectivity/Lethality of Viruses