Why Is COVID-19 Different Than Other Coronaviruses?

March 23, 2020

From Ahvie Herskowitz, MD and Devin Wilson, ND

Pneumonia, Acute Respiratory Distress Syndrome and Acute Lung Injury due to COVID-19

Coronaviruses such as the current SARS-CoV-2 as well as the SARS-CoV of 2003 and MERS-CoV of 2012 are known to cause respiratory disease with symptoms ranging from those of a common cold to severe pneumonia.

According to a review done between 1.12.2020 and 2.6.2020, patients with COVID-19 pneumonia experienced greatest severity of lung disease roughly 10 days after initial onset of symptoms.

  • 86% of patients with non-severe pneumonia showed lesions in both lungs by day 9 to day 13 after onset of symptoms.
  • 81% of critically ill type COVID-19 would progress to life threatening acute respirator distress syndrome (ARDS) which requires mechanical ventilation to assist in breathing and sustain blood oxygen levels.

Although SARS-CoV-2, SARS-CoV and MERS-CoV are all coronaviruses and SARS-CoV-2 is approximately 79% similar to SARS-CoV the infectious rates are significantly different.

COVID-19 is not your typical coronavirus. It is highly infectious and estimated to be 1,000 times more infectious than SARS-CoV of 2003.

In 2003, SARS-CoV, a viral cousin to the current SARS-CoV-2, infected approximately 8,000 people worldwide in roughly 3 months. As of March 28, 2020, SARS-CoV-2 has already infected over 200,000 with over 8,000 deaths worldwide since the outbreak began in late December 2019.

It is estimated that SARS-Cov-2 is 1,000 times more infectious than SARS-CoV. This is thought to be due to number of different factors including high mutation rate, early active viral replication and method used to invade human cells.

It took 7 to 10 days after onset of symptoms for the SARS-CoV to reach peak viral concentrations compared to the 5 days it takes for SARS-CoV-2. In addition, active viral replication of SARS-CoV-2 not only occurs in the lower respiratory tract but also in the throat during the first 5 days after the onset of symptoms.

The way SARS-CoV-2 invades human cells is more effective than SARS-CoV and dramatically adds to the high degree of infectiousness. Scientists propose that unlike SARS-CoV, SARS-CoV-2 has a special site called a furin cleavage site on its outer surface proteins. Since almost all cell surfaces in the human body have furin enzymes on them, the furin cleavage site of SARS-CoV-2 significantly increases its ability to invade almost all human cells and become activated. Activation of SARS-CoV-2 allows it to effectively bind to ACE2 receptors primary found in the lung and cardiovascular system infecting more cells and causing additional damage. Interestingly, the presence of furin cleavage sites allows SARS-CoV-2 to invade human cells regardless of whether cells have low expression of the ACE2 receptor.

Exaggerated immune response due to NLRP3 inflammasomes of SARS-CoV-2 causes lung damage and cardiovascular complications

Once SARS-CoV-2 is activated inside a human cell it releases NLRP3 inflammasomes which quickly initiates a cascade of largely uncontrolled immune reactions.

Inflammaomses are an important part of our innate immune system as they sense pathogens and other threats and respond by releasing a controlled amount of pro-inflammatory cytokines to defend host cells. Cytokines are a double edged sword. When controlled they can support an appropriate immune response to defend host cells. When uncontrolled they can lead to a cytokine storm and wreak havoc on the body. Cytokine storms can result in death due to severe organ damage and organ failure.

In regards to COVID-19, the lungs are the organ most affected and many patients develop pneumonia, acute respiratory distress syndrome (ARDS) and or acute lung injury (ALI).

Recently, NLRP3 inflammasomes and the inflammatory cytokines it releases including IL-1beta and IL-18 have been implicated with the development of ARDS and ALI.

Cardiovascular complications are also seen in COVID-19 patients. Reports from China show that a significant portion of COVID-19 patients with severe symptoms had underlying high blood pressure, heart disease and arrhythmia. 35% of patients who died from COVID-19 had a history of high blood pressure and 17% had a history of coronary heart disease.

SARS-CoV-2’s negative effect on cardiovascular health is also due to NLRP3 inflammasomes increasing pro-inflammatory cytokines. Inflammasomes are definitely associated with the progression of atherosclerosis, heart attack and heart failure. This effect on cardiovascular health was also seen in SARS-Cov infection of 2003.

SARS-CoV-2 is more pathogenic than other coronaviruses

All viruses have proteins that can interfere with the host’s immune system in some way or another. Some viruses work to evade the immune system while others directly disrupt the immune response.

SARS-CoV from 2003 used special ion channel proteins called viroporins (Viroporin ORF3a and E protein), which have essential roles in viral replication, virulence and pathogenicity. They are so essential that without them a virus would not be able to invade cells and replicate.

The activity of the viroporins from SARS-CoV triggers the activation of the NLRP3 inflammasome. As discussed above, NLRP3 causes an over production of inflammatory cytokines which can lead to severe inflammation, a cytokine storm, and the development of ARDS and ALI.

Recently, SARS-CoV-2 has been shown to have these same viroporins, which contributes to its high degree of virulence and pathogenicity.

Sources:

Get More COVID-19 Information

  

Follow us for updates

About Ahvie Herskowitz, MD

Dr. Herskowitz’s extensive training includes a medical degree from The Albert Einstein College of Medicine, residencies in Anatomic Pathology and Internal Medicine, and Fellowship training in Cardiology at The Johns Hopkins Medical Center. During his 12 years at Johns Hopkins, he became Associate Professor of Medicine and Immunology and Molecular Microbiology and led a research team in the study of molecular and immunological mechanisms of inflammation, autoimmunity, ischemia, heart transplantation rejection and congestive heart failure.

Dr. Herskowitz’s latest academic appointment was as Clinical Professor of Medicine at UC San Francisco. To learn more about Dr. Herskowitz, you can read it bio here.

      

About Devin Wilson, ND

Dr. Devin Wilson is a licensed Naturopathic Doctor in the state of California. He treats an array of acute and chronic diseases using a holistic and integrative approach to health. Dr. Wilson is also a health consultant, researcher and writer focusing on anti-aging and longevity medicine including stem cell therapy and exosome therapy.

Contact Us

If you would like to learn more about our treatments or want to schedule an appointment, you can either fill out our form here, or you can call us at 1 (888) 453-6825.

If you have questions about a bill or other information, then please call us directly at 1 (888) 453-6825.

Useful Links

HIPAA Privacy Policy

Contact Form

Any and all statements and opinions are provided for educational information and are not intended for medical diagnosis. As with all medical treatments and procedures, results may vary on an individual basis.

Follow Us

      

Office Hours


We are closed on Federal Holidays.

Where we are


Anatara Medicine & San Francisco Stem Cell Treatment Center  |  1700 California Street, Suite 520  |  San Francisco, CA 94109  |  P: 1 (888) 453-6825  |  F: (415) 345-0059