RNA virus luck

Observations about a fairly straight forward explanation of how RNA viruses work at https://www.youtube.com/watch?v=Eeh054-Hx1U

Observation 1.   There are many viruses that operate this way, each one with a unique genetic code and coding for different externally presenting proteins that happen to be very compatible with healthy cell receptor proteins yet different enough so that existing immune systems can not recognize them.  What luck.

Observation 2.  Once the virus binds to the cell, the two lipid-bilayers naturally merge because they are just a chemical arrangement of two layers with one side seeking water and the other side seeking lipids.   Of course, this kind of merging should occur anytime two cells come in contact to each other but this does not happen with normal cells.  It only happens with viruses encountering cells.   The cell membrane is selective enough not to merge with other healthy cells but it completely submissive to viruses and not just this one virus but any virus of numerous genetics that is able to find a binding site.   What luck.

Observation 3.  Because the lipid bilayer of the virus merges with the normal cell, the externally presenting proteins of the virus continue to present themselves to on the cell’s membrane.   This gives the immune system an opportunity to recognize the defect and begin mounting a defense against it.  While this is ultimately bad for the virus, the immune response will take a long time to be effective, and the virus has the good luck of having plenty of time to do its deed.

Observation 4. The virus contains an RNA strand.   Once it is present in the cell’s cytoplasm, the cell’s biology cannot distinguish it from an RNA strand coming from the cell’s nucleus and proceeds to build a protein coded by the virus RNA.   Good luck for the virus that the cell’s protein-building machinery is so indiscriminate.   Again, there are a multitude of infectious RNA viruses.  Apparently all of them give instructions for the cell to build a very specific kind of protein: one whose purpose is to make a negative copy of the RNA.  What luck that so many RNA sequences can build such a RNA copier.

Observation 5.  While the cell’s protein-building biology is indiscriminate about building proteins from any RNA strand floating around, the protein that makes negative copies of the virus RNA apparently has some affinity to the virus RNA or else it would waste time and energy on building copies of all the other RNA floating around in the cell.  Maybe it is making copies of all the RNA, but I get the impression that the virus-encoded protein spends most of its time only on the RNA from the virus.   The cell’s biology does not distinguish between normal RNA and virus RNA, but the virus RNA-copying protein is selective for just virus RNA.   If that is so, what luck for the virus to come up with this.

Observation 6. The same protein that makes a negative copy of the virus RNA is also able to make a negative copy of that negative copy, thus resulting in a positive copy of the RNA.   The protein is able to work with two different copies of the RNA that happen to be mirror images of each other, but presumably able to avoid wasting time with non-virus RNA.   What luck for a virus to do this.   What extraordinary luck for all RNA viruses to do this with different genetic codes.

Observation 7.  RNA-copying protein is made by reading the entire RNA.   However, different proteins are made by reading just parts of the same RNA.   These proteins just happen to be the proteins needed on the virus membrane.   Despite these proteins being foreign to the cell, the cell obediently delivers these proteins to the cell’s membrane.

Observation 8.  As this proceeds, the cell produces more and more copies of just the virus RNA leading to exponentially increasing numbers of both negative and positive copies of virus RNA.   Meanwhile the cell’s membrane accumulates more of the externally presenting proteins needed by the virus.   Note that the cell’s membrane also continues to have normal externally presented proteins for receptors and channels.   Eventually, the cell buds off a new virus.  This budded version has a lipid bilayer that just has a positive copy of the RNA strand.  Somehow the mechanism leaves the negative copy behind.    In addition, the budded membrane contains the necessary virus proteins on the membrane and leaves behind the regular cell’s externally-presenting proteins.   What luck for this selectivity.   The new virus particle is a copy of what originally infected the cell, permitting it to infect other cells in the same body or eventually getting expelled to infect a different body.  What luck for this to happen.

Observation 9.  The virus is constantly mutating.   It can be presumed that a lot of these mutations are unsuccessful, but enough are successful enough to infect different populations and yet continue to operate the same way.   Some of the variants may be different enough that the immunity to an earlier strain would be ineffective for the new strain.  What luck for the virus to mutate this successfully while the body’s immunity is so selective to allow the virus to get away with this.

And, as noted already, many other viruses have the exact same luck and have been getting away with this sequence of lucky moves for eons.   It just makes me wonder whether viral accommodation by cells is a part of normal biology of a species for some greater goal that outweighs even the survival of the individual.

Given that the virus RNA instructs the cell to create a protein to make a copy of the virus RNA, and that the same RNA instructs the cell to create the necessary proteins to permit future viruses to invade new cells, I wonder whether may be yet more proteins secretly migrating back to the nucleus to rewrite the DNA.

After all, a lot of the human DNA contains contents from viruses, they got there somehow.

This means there is a path allowing a new protein to somehow copy the instructions for building that protein into the host’s DNA.

It is possible for DNA to learn from the environment.   What is it learning?

Addendum 3/9/2020:

Observation 10.  An initial infection may affect the upper respiratory system (throat or nose).   Luckily for the virus, the body cooperatively induces sneezes and coughs that thrust the new viruses deeper into the lungs where they can find more room to multiply and cause even more severe coughing to propel new viruses into the environment.  It seems that the body is doing as much to accommodate the virus as it is to fight it off.

One thought on “RNA virus luck

  1. Pingback: Governing time-constant diversity | Hypothesis Discovery

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