US bioweapons scientists working at Kenema Government Hospital yesterday published an article, saying the Zaire Ebola virus strain has been in circulation in West Africa since 2006.
http://www.sciencecodex.com/sierra_leone_samples_ebola_evidence_in_west_africa_in_2006-137467
This raises the question: what made the Zaire Ebola virus so deadly all of a sudden? How come hundreds of People have died from it in West Africa the space of a few weeks when there was not a single death from it in all the preceding eight years? Where did this deadly variation suddenly come from?
Did the “novel” variant of the Zaire Ebola virus come, in fact, from a US bioweapons laboratory? Did US bioweapons scientists working at Kenema Hospital give a particularly lethal, bioengineered, weaponized strain of the Ebola virus to local people as part of the Tekmira clinical trials, which started in January, involve a Zaire Ebola virus, which seem to have a missing cohort of healthy humans and which were funded by the Department of Defense?
http://biotechnologyfocus.ca/tekmira-doses-first-subject-in-human-clinical-trial-of-tkm-ebola/
Read the US bioweapon scientist’s new report here:
http://wwwnc.cdc.gov/eid/article/20/7/13-1265_article
“These serologic results provide evidence that ebolaviruses are circulating and infecting humans in West Africa. All of the ebolavirus-reactive samples demonstrated only IgM and no evidence of IgG, suggesting acute infection. PRNT results indicated that the infecting virus was most closely related to EBOV, except for 1 SUDV-reactive patient sample. This finding was unexpected because our assumption was that any ebolavirus would more likely be TAFV, the only species described in West Africa. Although the serum samples were able to neutralize EBOV only at a low level (1:40 dilution), it is possible that the virus is an EBOV genetic variant. This presumptive diagnosis of EBOV infection extends the ebolavirus geographic region to Sierra Leone and the surrounding region. The MBGV-reactive samples, similar to the ebolavirus samples, had evidence only of IgM, suggesting acute infection. Unfortunately, we were unable to determine whether the samples could neutralize any MBGV because we were unable to acquire a known neutralizing serum to use as a positive control.
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