Although we are going to be talking how our cells react to viral intrusions, you can consider that most of this is the same response to other sorts of cellular attacks.

Our immune system is called adaptive because it learns from previous attacks and how to react to similar threats.  The job of our immune system is to separate friend from foe.  The problem is that our bodies harbor all sorts of foreign cells. (Our body has 10X the number of microbes within it as to the human cells!)

The weapons of choice?  Macrophages, neutrophils, dendritic cells, and natural killer cells. Except when it comes to SARS-CoV-2, our bodies generally lack a clue- so there’s no clear method it has to eradicate the threat.  So, it tries lots of things.

(This is why we often resort to vaccinations for viral threats.  Consider our bodies response a Greek tragedy- and the vaccine serves as “deus ex machina”.)

The issue is that our weapons- those macrophages, killer cells, etc.- are pretty much specialized to fight only ONE foe.  Change the foe and the weapon is basically useless. But, when our body finds the right one- the body marshals its resources to produce tons of these active weapons.

Our immune system has two strategies.  Cell mediated immunity and antibody mediated immunity.

For starters, those macrophages, neutrophils, and dendritic cells attempt to encircle and engulf the invading viruses.  While the natural killer cells attempt to eradicate the viruses (and if they succeed, the body eliminates them.) But, the dendrites have portions of the virus on their surfaces, so that our T cells can more easily identify the invader, in case they failed to eradicate the invasion.

Our lymph nodes contain lymphocytes.  These can become either B or T cells.  They are the first components to come into the act;   B cells (emanate from the bone marrow) and T cells (also start in the marrow and but they migrate to the thymus).  The B cells can morph into plasma cells (these produce antibodies, Y shaped attackers that adhere to viruses and other invaders).  The antibody adheres to the pathogen via its binding site- if the pathogen is bound to the antibody, the binding site is no longer available to attack normal cells.  The antibodies can also bind together a bunch of the invading species, making them much easier to be identified and attacked by the macrophages and phagocytes. If our bodies were familiar (i.e., have been invaded by the virus or something similar) with the ‘enemy’ (this is a war, folks!), then these antibodies would preclude the coronavirus from binding to the ACE-2 receptors on our cells.

The T Cells can either kill pathogens or serve as helper cells.  (Both B and T cells retain the memory of past victories- so when attacked by similar pathogens, they are ready to join the battle.)

All that happens in the perfect world.

If our bodies get invaded by a brand new pathogen, say the SARS-CoV-2 virus, it lacks any knowledge of how to dispose or oppose the invasion.  It tries everything it can. Sometimes, this repulsive activity overstimulates the cytokines.  The small proteins (causing inflammation) can aid healing- but when they are overproduced, they actually attack and damage healthy cells.  This is the cytokine storm to which many a COVID-19 victim has succumbed.

Which brings us back to our research to deal with the pandemic.

Developing a vaccine would mean that our bodies would be able to recognize this brand new enemy.  And, marshal the immune system to repel the invasion.

Developing antibodies means we can add to our body’s arsenal to repel the invasion.

The first approach is active defense; the latter approach is offense after the fact.  Prevention of the invasion is the preferred avenue; but lacking a vaccine means we need to find a way to preclude serious infection and death.

Hope our battle plan is clearer now!