The Spikes which you saw on the surface of the virus have a high affinity with a receptor on the human cells (ACE2). The direct implications are a definite attachment and infection of the cell. Once it has latched on to the cell, it infests and starts replication (reproduction).

Keeping my promise of sharing ACTIONABLE  INFORMATION, let me start with why COVID is so infectious.

Airborne Dispersal

MOSTLY, if not ALWAYS INFECTION:  After exposure to COVID-19 (Highly Infective). The Spikes which you saw on the surface of the virus have a high affinity with a receptor on the human cells (ACE2). The direct implications are a definite attachment and infection of the cell. Once it has latched on to the cell, it infests and starts replication (reproduction). Visit this Youtube for learning the virus replication. https://www.youtube.com/watch?v=J4BN4dARpio

What do I do as a common man?

Isolation (lockdown), using masks and following all CDC, WHO, NIH, State, and Local guidelines. Build a staging area outside the home, do not get the virus inside the home. All essentials should be cleaned appropriately before those get ingress into your home. Presume everything from outside is contaminated until cleaned.

2) Lysogenic phase: Breaking the cells after making thousands of copies (lysogenic phase). Please visit https://www.youtube.com/watch?v=sQ0ShukSA5I. 

What do I do as a common man?

Clean after contamination. I follow the below steps – outer clothes removed in the Garage and set for laundry immediately, shower with soap/shampoo, nose blow, and peroxide gargles. The last two steps remove any adhered viruses from inside the nose and throat.

3) Early Symptoms: Step 1 follows in thousands of new normal respiratory cells. Fever, Nasal Congestion, loss of smell (because the olfactory cells are affected). Cells start producing exudate (copious secretions).

What do I do as a common man?

Get tested and isolate from other caregivers from the family and friends. Stay isolated (if mild symptoms and or test positive) until results are available or at the least 15 days after the lasts symptoms. If required, seek immediate help. DO NOT SELF MANAGE (explanation later).

4) Initial Phase of Lung Congestion: The virus travels inside to the Lungs and infects the respiratory lining cells. Visit the below video to learn more https://www.youtube.com/watch?v=4HPlSm94czk. Also, see https://www.youtube.com/watch?v=Xj1nUFFVK1E.

5) Cytokine Storm: Huge secretion of fluids (doctors call this as Cytokine Storm) blocking oxygen exchange. Ventilators are required to support oxygenation. However, I have had first-hand reports that it is painful to watch patients struggling to breathe even on ventilators.

What do I do as a common man?

Seek early help, Please do not self-treat? Why – You may have a sudden catastrophic fluid collection in the lungs. What else do I do? Of course isolation and other guidelines to be used as required)

6) Acute Respiratory Distress Syndrome and Mortality/Morbidity: This is the most dreaded step.

What do I do as a common man? Be careful at the initial steps (1-3) (Shashank Heda, MD).

COVID19 Local Statistics

Rule of Thumb

Folks, my neighbor taught me one simple rule of thumb – What is essential? Can I survive without this? If I can, then it is not essential.


  • SPREADING AWARENESS (ask questions if required)


Stay Safe!

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Based on the latest research from Nature and Cell BioSciences and analyzing the data (first hand) from Texas, I see it important to be all the stricter with isolation. Let me take a few issues individually.

Why SARS-CoV2 (COVID-19) is so dangerous?

Primarily because of the

1) Ridge on the S protein that allows it for tighter binding to the ACE2 receptor on the human cell
2) Suppression of antiviral immune response and
3) Concurrent activation of the pro-inflammatory response
Simply speaking – SARS-CoV2’s S protein (Spike protein) after binding with the ACE2 receptor on the human cell, changes its conformation to and goes into a tight affinity, primarily because of the ridge present on the S protein. That makes the SARS-CoV2 very infectious. Now, add to that, the florid inflammatory exudate (cytokine storm) and you get a double whammy. SARS-CoV is known to be exceedingly potent in the suppression of antiviral immunity and the activation of proinflammatory response.

Researchers are working to block the affinity of S protein or reduce the affinity. Another direction for research is controlling the cytokine storm. Our Milind is working on the Stellate Ganglion Block. You should bring him back here to ask more about them later.

Excerpt from Nature below (citations removed, reference link included) – A key to tackling this epidemic is to understand the virus’s receptor recognition mechanism, which regulates its infectivity, pathogenesis and host range. SARS-CoV-2 and SARS-CoV recognize the same receptor – human ACE2 (hACE2). SARS-CoV-2 receptor-binding domain (RBD) (engineered to facilitate crystallization) in complex with hACE2. Compared with the SARS-CoV RBD, a hACE2-binding ridge in SARS-CoV-2 RBD takes a more compact conformation; moreover, several residue changes in SARS-CoV-2 RBD stabilize two virus-binding hotspots at the RBD/hACE2 interface. These structural features of SARS-CoV-2 RBD enhance its hACE2-binding affinity. Additionally, we show that RaTG13, a bat coronavirus closely related to SARS-CoV-2, also uses hACE2 as its receptor. The differences among SARS-CoV-2, SARS-CoV, and RaTG13 in hACE2 recognition shed light on the potential animal-to-human transmission of SARS-CoV-2. This study provides guidance for intervention strategies targeting receptor recognition by SARS-CoV-2.

(Simplified – @ Shashank )


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The origins of SARS-CoV-2 and COVID-19. To make a long story short, two parental viruses of SARS-CoV-2 have now been identified. The first one is bat coronavirus RaTG13 found in Rhinolophus affinis from Yunnan Province and it shares 96.2% overall genome sequence identity with SARS-CoV-2 [3]. However, RaTG13 might not be the immediate ancestor of SARS-CoV-2 because it is not predicted to use the same ACE2 receptor used by SARS-CoV-2 due to sequence divergence in the receptor-binding domain sharing 89% identity in amino acid sequence with that of SARS-CoV-2. The second one is a group of betacoronaviruses found in the endangered species of small mammals known as pangolins [4], which are often consumed as a source of meat in southern China. They share about 90% overall nucleotide sequence identity with SARS-CoV-2 but carries a receptor-binding domain predicted to interact with ACE2 and sharing 97.4% identity in amino acid sequence with that of SARS-CoV-2. They are closely related to both SARS-CoV-2 and RaTG13, but apparently they are unlikely the immediate ancestor of SARS-CoV-2 in view of the sequence divergence over the whole genome. Many hypotheses involving recombination, convergence and adaptation have been put forward to suggest a probable evolutionary pathway for SARS-CoV-2, but none is supported by direct evidence. The jury is still out as to what animals might serve as reservoir and intermediate hosts of SARS-CoV-2. Although Huanan seafood wholesale market was suggested as the original source of SARS-CoV-2 and COVID-19, there is evidence for the involvement of other wild animal markets in Wuhan. In addition, the possibility for a human superspreader in the Huanan market has not been excluded. Further investigations are required to shed light on the origins of SARS-CoV-2 and COVID-19



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