After Ebola patients declared free of Ebola in the blood, many probably developed a symptomless Ebola Mutation in the central nervous system and separated genetic reproduction center. This Symptomless Ebola can relapse into contagious Ebola at any time, implicating that potentially ten thousand ticking time bombs walking around in the Mano River Region.
Also, it is not impossible that this new form of Ebola could be contagious without exterior body fluids or even become aerosol in further mutations. If that happens the prediction from W.H.O. and CDC in 2014, that millions of people will die of Ebola in the Mano River Region will become a self-prophesying reality.
WHY THESE MEDICINES WORK? Atorvastatin and Irbesartan can treat the dysfunction of the endothelial cells that line the blood vessels, preventing the leakage of fluid from the blood into tissues.
This maintains blood volume and cuts down on fluid loss from diarrhea. By maintaining fluid balance, treatment allows patients to live long enough to develop their own immune response to EBOV and other diseases, and they use that response to get rid of the virus.
SELECTIVE ESTROGEN RECEPTOR MODULATORS (SERMs) Before the Ebola virus enters the cytoplasm in the blood it can be blocked with a specific Selective Estrogen Receptor Modulator drug (SERM) even before it enters the cell.
According to the US Army Medical Research Institute of Infectious Diseases, and the University of Virginia, SERM inhibits multiplication of the Ebola virus within the cell lessening the burden of infection.
On 19 June 2013, the FDA approved their application to inhibit Ebola Virus Infection through cell-based mechanisms unrelated to the classical estrogen signaling pathing with Selective Estrogen Receptor Modulators specifically the antiviral activity against the type species Zaire Ebolavirus (EBOV).
The inhabitation occurs after viral binding and internalization. STATINS. When the Ebola virus already entered a cell, STATINS can block the transport of viruses to the cytoplasm of cell volume so they cannot multiply and prevents vascular leakage. One specific substance the Ebola virus requires to move around is the cholesterol transporter Niemann-Pick C1. Researchers discovered that patients without Nieman-Pick C1 (NPC1) survived Ebola because there were no means to transport the virus any longer. susceptibility.
Apoptosis of lymphocytes It is justifiable to conclude that extrapolating NPC1 with STATINS blocks the action of NPC1 and has the possibility of thwarting the Ebola infection while enabling the body to recover. ANGIOTENSIN RECEPTOR BLOCKERS (ARBs) The Angiotensin enzyme is a devastating blood vessel narrower (vasoconstrictor) while reducing vasodilator (widening) responses in arteries.
Like with severe sepsis, Angiotensin causes intestinal bleeding caused by an overreaction of the immune system, resulting in organ failure which is a complication that in most cases kills Ebola patients. Angiotensin Receptor Blockers (ARB) interrupt the renin-angiotensin hormone system’s over-activity by blocking a specific receptor that mediates the pathogenic (inflammatory) activity of Angiotensin which deregulates blood pressure and water fluid balance leading to hypertension, heart failure, and kidney & liver failure.
It reduces the amount of harmful cytokine release. ARBs modify or reverse abnormalities in blood vessel walls’ function and blood coagulation in patients with sepsis and Ebola, reducing the incidence of organ failure which is one of the complications that often kills Ebola patients.
According to a meeting of international ethics experts convened by WHO on the 8 August 2014, if experimental drugs – i.e. those that have not been tested and licensed for use in humans to help them fight Ebola infection – are given to patients in the outbreak, “there is a moral obligation to collect and share all data generated.”
“Unfortunately this is not always taking place. Several interventions, including amiodarone, statins, antihypertensives and even intravenous ozone, have been tried by various medical teams,” Friede says.
“Even where some data have been collected, they have not always been sufficient for a full assessment of the safety and efficacy of these approaches by WHO.” “Reports on these ad-hoc tests, which have not gone through formal approval processes, have led to a debate in social media about whether Africans were being used as human guinea pigs,” he says. There are also other concerns. All trials of Ebola therapeutics must be conducted under rigorous biosafety conditions, which means using full protective gear.
The trials put researchers providing experimental 136 blood transfusions and intravenous medicines at a risk of infection. PROPOSED MEDICINES EFFECTIVE FOR EBOLA, MARBURG, LASSA, INFLUENZA & DIABETES. According to a publication in Clinical Infectious Diseases 2012:1466–73 published by Oxford University Press on behalf of the Infectious Diseases Society of America 2012.(DOI: 10.1093/cid/cis733), pneumonia and influenza together are the eighth leading cause of death and the leading causes of infectious death in the United States [COUNTS THE SAME IN AFRICA].
Only a few new classes of antibiotics have been added to the armamentarium for treating pneumonia in the last 20 years. Recent studies have demonstrated that HMG-CoA reductase inhibitors (“STATINS”) and angiotensin-converting enzyme (ACE) inhibitors have significant immunomodulatory effects and reduce systemic cytokine levels. Cytokines play an important role in host defense mechanisms for patients with pneumonia [AND EBOLA & LASSA & MARBURG] but under certain conditions may lead to septic shock or acute respiratory distress syndrome.
Studies evaluating the impact of these medications on outcomes for those with clinical infections have given connecting results. Several studies have demonstrated that for patients hospitalized with bacteremia, diabetic lower extremity infections, or community-acquired pneumonia, statin or ACE inhibitor use was associated with decreased odds of death or decreased rates of severe sepsis.
Approved drugs inhibiting Ebola virus entry into host cells. A second group comprises the estrogen receptor modulators Toremifene (IC5050.56 mM), Tamoxifen (IC5050.73 mM), and Raloxifene (IC5051.8 mM). A 2013 report indicated that Toremifene and another estrogen receptor modulator, Clomiphene, effectively block Ebola virus infection independent of the estrogen receptor and were effective in a mouse infection model.
As previously reported, HeLa cells are estrogen receptor-negative,17–19 and the effect of estrogen receptor modulators in blocking Ebola virus entry is believed to be unrelated to the classical estrogen receptors. The identification of estrogen receptor modulators and microtubule inhibitors in our screen validates the BSL-2 Ebola virus entry assay for the identification of virus entry inhibitors.
13 NOVEMBER 2014
(1) Internal Medicine, Morningside MediClinic, Johannesburg, South Africa,
(2) Department of Medicine, University of the Witwatersrand, Johannesburg, South Africa,
(3) Department of Medicine, University of Pretoria, Pretoria, South Africa,
(4) National Institute of Communicable Disease, Sandringham, South Africa,
(5) Centers for Disease Control and Prevention, Atlanta, Georgia, United States of America,
(6) Tulane School of Public Health and Tropical Medicine, New Orleans, Louisiana, United States of America.
In 2008, a nosocomial outbreak of five cases of viral hemorrhagic fever due to a novel arenavirus, Lujo virus, occurred in Johannesburg, South Africa. Animal models of sepsis have suggested that statin drugs may improve outcomes in septic shock.
Furthermore, a large, population-based cohort analysis in Canada showed a reduced risk of sepsis in patients with cardiovascular disease who were treated with statins. Shock and multi-organ system failure, often with evidence of disseminated intravascular coagulopathy, ensued in the second week, with death in four of the five cases.
Distinctive treatment components of the one surviving patient included rapid commencement of the antiviral drug ribavirin and administration of HMG-CoA reductase inhibitors (statins), N-acetylcysteine, and recombinant factor VIIa.
Johan van Dongen