Update on COVID therapy for cytokine storm

One of our members asked if I would provide an update on the use of advanced biotechnologies for COVID therapies, so here goes! 

1.  The challenge:  SARS-CoV2 corona virus is a "novel" virus, formerly unknown to humanity, and so we are undergoing a "natural experiment."  It appears likely that this coronavirus spilled over from a bat host into humans, perhaps through an intermediary host (pangolin, civet cat etc.).  This is how the original SARS virus came to infect humanity in 2003, and we are very lucky that this was stamped out quickly. 

2.  The pathogen:  The SARS-CoV2 virus causes a great deal of damage to the human body during infection, primarily through instigation of the famous "cytokine storm."  Cytokines are chemicals generated by our immune systems to help destroy invading pathogens, but if the immune response is exaggerated, the storm can cause a great deal of damage to healthy human tissue and organ systems such as lungs, heart and circulatory systems.  

3.  Treating the storm:  Dating back to the original SARS outbreak in 2003, it was postulated that certain approved drugs, used to treat autoimmune diseases such as psoriasis, could be used to counteract the cytokine storm caused by novel coronaviruses.   A key cytokine in the storm is TNF (Tumor Necrosis Factor), a chemical that is particularly lethal against human tissue and, as the name implies, meant to help kill cancerous cells that have gone awry. 

I postulated that anti-TNF drugs might be life-saving for treating severe COVID-19 patients and so began to research this, using my resources from the University of Illinois College of Medicine.  Interestingly, I found a reference from 2008, long before the COVID-19 outbreak began!   The article is a bit heavy-lifting, but many of you will find it interesting!  

Please see:  https://www.tandfonline.com/doi/pdf/10.1185/030079903125002757?needAccess=true

TNF-α inhibition for potential therapeutic modulation of SARS coronavirus infection

Summary: Clinical and experimental evidence implicate TNF as a possible mediator of the severe immune-based pulmonary injury which can follow infection with H5N1 influenza and SARS coronavirus.  Compared with the use of corticosteroids, the use of biologic TNF inhibitors, including etanercept, has the potential to be a more specific and more effective

method of ameliorating the severe alveolar damage which can occur following infection with these agents.  Further study is indicated.

Big thanks, Chuck!

Thanks Chuck. That's good to know. I've had 4 elderly relatives in Europe who've had the vaccines and no side effects yet except 2 of them had a sore arm. But 2 of them have been joking that they're not even sure they were injected because their arms feel fine. 2 of them had the Pfizer and 2 had the Oxford. The sore arms were with the Oxford. The Pfizer has been fine.

CRS, DrPH wrote:  I highly recommend these vaccines, they are some of the safest I've ever studied.  Be safe!

That is wonderful news.  Thanks

I saw this in the CIDRAP newsletter today. 

Tocilizumab associated with less death in moderate-to-severe COVID-19

Tocilizumab was associated with a lower risk of death 90 days after treatment in COVID-19 patients with moderate-to-severe infection or pneumonia at the time of enrollment, particularly those with high C-reactive protein (CRP) levels, according to a JAMA Internal Medicine research letter yesterday. CRP is a marker of inflammation.

In the continuation of a previous JAMA Internal Medicine study that found an association between tocilizumab and reduced ventilation or death by day 14 (but not mortality by day 28), the researchers followed up with the 63 patients who received tocilizumab and the 67 in the control group. By day 90, 7 in the intervention group (11.1%) and 11 in the control group (16.4%) died (adjusted hazard ratio [aHR], 0.64; 95% confidence interval [CI], 0.25 to 0.65).

In the original study, researchers stratified data by CRP levels and found that patients most benefited from tocilizumab when they had CRP levels higher than 15.0 milligrams per deciliter. Of these patients, 18% who received tocilizumab needed ventilation or died versus 57% in the control group by day 14. Now by day 90, the researchers found that those with high CRP levels had a lower likelihood of mortality if they received tocilizumab compared with those who didn't (aHR, 0.18; 95% CI, 0.04 to 0.89).

"This follow-up analysis suggests that tocilizumab may be considered for treating patients with moderate-to-severe COVID-19–associated pneumonia and high CRP levels," write the researchers. "Further studies will help determine which patients with COVID-19–associated pneumonia would benefit the most from a combination of tocilizumab and dexamethasone."
May 24 JAMA Intern Med study