Understanding SARS-CoV-2: structure, mechanisim and medication

The nCoV-19 (SARS-CoV-2) is much like a warrior that mother nature has begotten to reclaim what her child has been plundering. She doesn't need to do it, but every now and then he forgets his place. He is mankind, her dearest child of all creation that is more brilliant and ferocious than any other. He realises that he has lost the battle, but its time to win the war. The war against the deadly virus and a cure to heal them all. 

Let's get down to the science. This virus comes armed with a lethal trimeric spike protein that interferes with porphyrin in RBCs. The membrane of this virus packs envelope proteins that aid in shielding the RNA within. The RNA codes for a protease that is involved in active replication within host cells. Thanks to leaps in technology we already have solved crystal and Cryo-EM structures of the protease and its spike protein. A detailed list of all their structures can be found here. Several researchers have studied the morphology of infected host cells and the virus itself. These have added interesting insights regarding the mechanism of viral infection that has not already been understood.

The spike protein attaches to the ACE2 (angiotensin-converting enzyme 2) receptors to bind host cells and triggers activation signals. Once bound the viral membrane fuses into the host and deposits the viral RNA into the cell. The viral RNA is translated to obtain protease and other machinery that the virus uses for making viral replicates. The virus incubates within the host for more than 14 days during which the host may not show any symptoms and also spread the virus to other hosts by droplet spreading.

After the incubation period, the spikes of the virus can be found in most parts of the body but more abundantly in blood. Their target within the blood is the oxygen carriers of the circulatory system, RBCs (red blood cells). RBCs carry oxygen using a protein called haemoglobin which is a tetrameric protein that cofactors a porphyrin molecule with a strong affinity to oxygen, carbon dioxide, carbon monoxide, and many others. The spike protein is one other candidate that the porphyrin binds to with even stronger affinity. This affinity with spike protein leaves the haemoglobin cofactor-less and hence the logistics of oxygen within the host is hampered. To add to the decline in oxygen, the porphyrin that shelters free iron radicals release them into the blood which then reacts with available oxygen entering the lungs to burden them with increased damage. Recovery is initiated by immune cells that respond to the damage marking susceptible cells with antibodies inhibiting their entry into the cells. Once the replication of the virus has been brought to a standstill the person can then fully recover and gain immunity to the virus. New RBC production needs to improve within good time if the host needs to survive. Any delay in the immune response can bring hosts much closer to death.

The cure for this disease is hidden in these protein structures and their mechanism of function. On one hand, vaccines like the mass-produced mAB (monoclonal antibodies), work on inhibiting the attachment between the virus and the host cells. This stops the virus from entering the host and also prevent its multiplication. Although trials for vaccines are underway there is an increasing need to find approved medications that target the viral machinery and stop its rapid replication. The other treatments include boosting immunity, selected FDA approved drugs that can target viral machinery, existing antiviral medications such as hydroxychloroquine and a few others.

Update: [1st May 2020]
SARS-CoV-2 productively infects human gut enterocytes [1]