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PP2A-B56

Turn off a cancer supressing gene and the virus can't replicate

1) Kruse 2017: The Ebola Virus Nucleoprotein Recruits the Host PP2A-B56 Phosphatase to Activate
2) Ruvolo 2016: The broken “Off” switch in cancer signaling: PP2A as a regulator of tumorigenesis, drug resistance, and immune surveillance



https://www.chemistryworld.com/feature/nicotine-rehab/3004707.article
"Nicotine has amazing powers as an anti-inflammatory. Now researchers are hunting for a nicotine surrogate that bypasses its nasty side effects"

Infection causes only part of the damage. What makes patients critically ill is their fiercely aggressive immune response, the so-called ’cytokine storm’. This exaggerated inflammatory response becomes even more dangerous than the original infection, causing multiple organ failure.

During sepsis, macrophages (white blood cells that surround and kill microorganisms), cells and other immune cells churn out huge quantities of molecules called inflammatory cytokines that raise a physiological alarm. If the production of these pro-inflammatory molecules is overwhelming, it can lead to capillary leakage, tissue damage and, eventually, death from cardiovascular dysfunction and multiple organ failure.

Ulloa and collaborators have found that nicotine can temper this overshooting inflammatory response, to the point of reversing sepsis in mice. As far as anti-inflammatory treatments go, this is tremendously powerful.

Acetylcholine is the parasympathetic nervous system’s principal neurotransmitter. This subconscious division of the nervous system is sometimes called the ’rest and digest’ system because it slows the heart rate and increases intestinal activity during digesting.

Through acetylcholine, the parasympathetic system also modulates the production of inflammatory cytokines in macrophages and other immune cells. In a normally functioning body, acetylcholine production ensures that the minor inflammatory fires that constantly crop up are quenched.

At every opportunity, nicotine is more effective than acetylcholine. In fact, the clamp-down on inflammation by nicotine is powerful enough not only to prevent sepsis in mice and improve their survival but also to rescue mice from sepsis, even when the treatment is started after the onset of the disease - a feat accomplished by no other drug.
(Emph mine - rjs. "No other drug" other than" NAC, Ascorbate, thiamine and niacin. Niacin does what nicotine does.)


https://www.usnews.com/news/articles/2014/10/27/how-we-are-treating-ebola

US Ebola care, Oct 27, 2014

This is the day the Ebola crisis peaked.

"The treatments raise ethical dilemmas. Experimental drugs are being used in the U.S. and in Europe, where the number of patients can be counted on two hands. Meanwhile, the disease is ravaging West Africa, killing 4,922 to date, with no sign of slowing."

"ZMapp, which has shown successful testing in monkeys, is a cocktail of three genetically engineered antibodies that boosts a patients' ability to fight off Ebola by latching onto the virus and neutralizing it. ZMapp is a combination of two different serums made by two companies – Leaf Biopharmaceutical, an arm of Mapp Biopharmaceutical, Inc.; and Defyrus Inc.

Dr. Kent Brantly, American missionary Nancy Writebol and British nurse William Pooley were cured after taking it; but Miguel Pajares, a 75-year-old Spanish priest, did not survive.

There are no additional doses of ZMapp left, and the drug can take six months to produce per dose. Health officials expect there will be no more than hundreds or thousands next year, which is not nearly enough to combat the virus in West Africa. To make it, scientists take a genetically engineered virus and inject it into a tobacco plant, which then produces antibodies. "

US News and World Report


http://www.who.int/medicines/ebola-treatment/2015_0703TablesofEbolaDrugs.pdf

Categorization and prioritization of drugs for consideration for testing or use in patients infected with Ebola

This table, which is updated on a continuous basis, summarizes the data on drugs that are either being tested or considered for testing in patients with Ebola virus disease (EVD) or have already been used in patients with EVD, as well as those which had been considered but which have been deemed to not be appropriate for further investigation.


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4893094

Chinese military medical teams in the Ebola outbreak of Sierra Leone

The most deadly pathophysiological change caused by EVD was hypovolemic shock caused by severe vomiting and diarrhoea or internal bleeding; thus, the primary principle of our therapeutic strategy was to provide adequate fluid resuscitation and to correct electrolyte abnormalities. This was generally achieved by the administration of rehydration fluid orally in mild and medium category patients or intravenously in severe ill patients.

In addition, treatment aimed to protect or restore the function of vital organs such as the brain, kidney and liver, and to provide adequate energy and nutrition as well as any other appropriate symptom-relief treatments.2

Approximately 15% of our patients were children under the age of 12, and in addition to the regular treatments, additional supportive treatments were also introduced to paediatric EVD cases—zinc supplementation was given to children who had suffered from diarrhoea for more than 10 days and vitamins A and K were provided to all children under five and children with haemorrhage, respectively.2