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September 20th, 2021 
Awake Goy
“The effect of H2O2 on adenovirus types 3 and 6, adenoassociated virus type 4, rhinoviruses 1A, 1B, and type 7, myxoviruses, influenza A and B, respiratory syncytial virus, strain Long, and coronavirus strain 229E was studied in vitro, using different hydrogen peroxide (H2O2) concentration and times of exposure. Hydrogen peroxide in a 3 percent concentration inactivated all the viruses under study within 1-30 min. Coronavirus and influenza viruses were found to be most sensitive. Reoviruses, adenoviruses and adenoassociated virus were relatively stable. H2O2 is a convenient means for virus inactivation.” 1977 Europe PMC published study
Hydrogen peroxide works by increasing something already created by your body’s natural disease fighting response. When white blood cells attack an invader they create hydrogen peroxide to kill the invading organism. The human body is protected from the effects of hydrogen peroxide by the natural enzyme, catalase, which is found throughout the body and in the body’s own cells. Catalase protects the cells from harm by turning H2O2 into harmless oxygen and water. Viruses and bacteria do not have catalase and are therefore susceptible to the hydrogen peroxide.
Another study published in 2012 by Oregon Health & Science University working with colleagues at Najit Technologies confirmed that hydrogen peroxide was very effective at inactivating a number of viruses. The study used vaccines containing hydrogen peroxide to inactivate lymphocytic choriomeningitis virus (LCMV), smallpox virus, and West Nile virus (WNV).
To see whether H2O2 inactivation could generate a vaccine that elicits neutralizing antibody responses the researchers turned to smallpox vaccination. They gave mice subcutaneous injections of either a live attenuated smallpox vaccine (consisting of VV), a live modified vaccinia Ankara vaccine (which is replication deficient in humans and mice), or purified VV inactivated using either H2O2, formaldehyde, or ultraviolet (UV) irradiation. Antibody responses were measured 28 days after booster vaccination.
Again, not only did the H2O2-VV vaccination elicit much greater virus-specific neutralizing antibody responses than the vaccines generated using other inactivation approaches, but levels of antibody response induced by the H2O2-VV vaccine also more closely mirrored the immunity induced by live viral infection. And when immunized animals were subsequently challenged with a lethal dose of VV, 100% of the H2O2-VV-vaccinated animals survived.
Similarly, mice vaccinated with an H2O2-inactivated West Nile virus (WNV) vaccine generated 10-fold higher virus-specific antibody titers after booster vaccination than mice given Ft. Dodge Innovator, a formaldehyde-inactivated WNV vaccine used in horses. Encouragingly, in the experimental mice, antiviral antibody titers peaked at about 28 days after booster vaccination with the H2O2-WNV vaccine and showed no evidence of declining over the next six months of observation.
In fact, H2O2-WNV provided experimental animals with full protective immunity to a lethal dose of WNV administered more than 280 days after they were immunized. Of particular note was the finding that immune serum from H2O2-WNV-vaccinated animals was sufficient to completely protect naive mice against challenge with WNV,
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