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Online Discussion: Tracking new emerging diseases and the next pandemic since 2005; Coronavirus COVID-19 Pandemic Discussion Forum.

Great article reviewsCOV19 mechanisms

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Usk View Drop Down
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    Posted: April 24 2020 at 5:57pm

I am bringing this up again because some granted researchers are getting concerned that the number of people being asymptotic may mean something sinister may still be coming. Since there are now 3 different genetic variation of the original strain out of Wuhan  could another strain attack the asymptotic make a MERs or SARs more deadly to them?  Apparently one of them does not attack ACE receptors.   If you u get that one but had immunity to COV19 are you more likely to die ?  Or Am I off Base Here. Some Chinese virologist is checking this out  in mice

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CRS, DrPH View Drop Down
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Post Options Post Options   Thanks (0) Thanks(0)   Quote CRS, DrPH Quote  Post ReplyReply Direct Link To This Post Posted: April 26 2020 at 12:34am

Originally posted by Usk Usk wrote:

Thank you for this reference, which says:

For reasons that aren’t entirely clear, some people—especially the elderly and sick—may have dysfunctional immune systems that fail to keep the response to particular pathogens in check. This could cause an uncontrolled immune response, triggering an overproduction of immune cells and their signaling molecules and leading to a cytokine storm often associated with a flood of immune cells into the lung. “That’s when you end up with a lot of these really severe inflammatory disease conditions like pneumonia, shortness of breath, inflammation of the airway, and so forth,” says Rasmussen. 

Local inflammation can turn into widespread inflammation of the lungs, which then has ripple effects across all organs of the body. This could also happen if the virus replicates faster than the immune system can respond, so that it then has to play catch-up to contain the pathogen—a situation that could also cause the immune defense to spiral out of control. “With mice, we know that in some cases, particularly for SARS and MERS coronaviruses, virus replication is very rapid and in some cases overwhelming” to the immune system, says Perlman.  


One way to reduce mortality during fulminant infection would be to repress the cytokine storm, which involves release of immune chemicals such as Interluken-6 and Tumor Necrosis Factor from the patient's immune cells.  Very conventional biologic drugs such as Enbrel, Humira, etc. may possibly save thousands of lives if administered early.  Please see this key article in Lancet:

With more than 81 000 deaths worldwide from coronavirus disease 2019 (COVID-19) by April 8, 2020,

1it is incumbent on researchers to accelerate clinical trials of any readily available and potentially acceptably safe therapies that could reduce the rising death toll. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) gains access to host cells via angiotensin-converting enzyme 2, which is expressed in the type II surfactant-secreting alveolar cells of the lungs.
2Severe COVID-19 is associated with a major immune inflammatory response with abundant neutrophils, lymphocytes, macrophages, and immune mediators. Which mediators are most important in driving the immune pathology remains to be elucidated. Deaths from COVID-19 are chiefly due to diffuse alveolar damage with pulmonary oedema, hyaline membrane formation, and interstitial mononuclear inflammatory infiltrate compatible with early-phase adult respiratory distress syndrome (ARDS).
3 Prevention of ARDS and death in patients with COVID-19 is a pressing health emergency.

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