Monthly Archives: May 2026

Ebola, Hantavirus, Influenza, and Friends

You may wish to read:

While dogma that life has a single ancestor has softened somewhat, the manifest presence of Darwin’s evolution implies that species radiate from a common ancestor in a branching pattern sometimes referred to as the Tree of Life. Before the advent of tools for DNA analysis, the  relationship of complex organisms on that tree was educated guess based upon comparison of  body plan and other traits, together called phenotype.

This was never an option for viruses. Though they became visible with the advent of the electron microscope in the late 1930’s. the images revealed little of functional significance.  Some viruses are pleomorphic, with the same species exhibiting a variety of forms.

A virus resembles a computer program that hijacks a computer. A computer program does not depend upon how it is displayed; it is pure information. Except for a few recently discovered exceptions, which bring some of their own tools to the job, a virus analogizes very well with a program, with the cell as the infected computer.

So how can we get a meaningful classification? These criteria don’t work:

  • How a virus infects a cell.
  • Mechanism by which it produces disease.
  • Severity.
  • Incubation period.
  • Infectivity.
  • Symptoms.
  • species infected, et al.

They don’t work because, no matter how many traits are considered,  they don’t reduce to a small number of classes. Reduction is the basis of modern science, and this idea, based on apparent observation, is not reductive. David Baltimore’s scheme solves this.  Most viruses fit cleanly into seven categories, defined by the carrier of the genetic material, and how it reproduces.

Ebola, Hantavirus, and Influenza are Baltimore Class 5, with a negative-sense, single-stranded RNA (–ssRNA) genome. Virus evolution is too messy  to assert one ancestor from which these viruses descended, but it is likely that many or most viruses of a single Baltimore class evolved by a combination of radiation and recombination of genetic material. The Tree of Virus Life has branches that swap parts.

This is  particularly likely with Class 5 viruses, because  single strand RNA is unstable, with repair procedures that are usually  faulty. The genome is constantly changing. In the case of influenza, only a small percentage of replicated  virions are actually  capable of reproduction. See (NIH) Biological activities of ‘noninfectious’ influenza A virus particles.

I wasn’t able  to find a figure for total number of virions in a flu patient (as opposed to just the nose), but for a very rough idea, we might use the estimate for COVID of  1 to 100 billion; see (NIH) The total number and mass of SARS-CoV-2 virions. How does all this replication work, when it does?  The virus must first copy its genome, producing messenger RNA that will direct the cell ribosomes to make more virus. The enzyme RdRp is the agent. It works in haste, with no proofreading. If the original strand of RNA which served as a template breaks, RdRp bounces around the cell looking for another. The chance that it finds a proper replacement is not good. This is like doing brain surgery in a dive bar.

This Frankenstein process, template switching, is routine for Baltimore Class 5. If the resulting substitution is large enough, it is called reassortment. If the cell is simultaneously infected with another strain, or conceivably, species of virus, there is a very tiny chance that the resulting virions are viable, and an even smaller chance that the switch confers an advantage. But the number of virions per infection, and the number of infections, are so huge, that occasionally, the resulting virus is something truly monstrous.

Template switching is a  documented way for this to happen. Spontaneous mutation at a point in the genome, genetic drift, is another. But there are also instances when genetic material has been transplanted by no known mechanism.  It is almost as if a bomb went off in the cell, the exploded pieces came raining down, and reassembled into something viable.

The most likely result is a fitness defect; the virion is nonviable, or can’t compete. What are the chances that something monstrously novel will result, something not recognized by the adaptive immune system, perhaps a virus that would kill everybody? These stand in the way:

  • The innate immune system possessed by all healthy humans . Requiring no training to recognize novel pathogens, this has been honed to a pitch since the dawn of life.
  • Small size of most viruses. This  limits the size of the viral genome. Virtually all viruses are one-trick ponies, with one way to attack a cell, one way to reproduce, and one way to propagate.
  • Fitness defect. A virus which is very good at one thing might be at a competitive disadvantage in some other way. This could explain the  so-far failure of bird flu to adapt to humans. Or it could be simply a matter of time.
  • Genetic diversity of the host, in this case,  human. The pathological machinery of a virus specializes to a host with a narrow range of genomes. Genetic diversity within a species obstructs the ability of a virus to kill everybody.

For the most important reason, see this series: COVID Resurgent: Of Hares and Foxes; Primer for Policy Makers, Parts 1 to 4. In short, a virus which exterminates all possible hosts has nothing to live on.

Nevertheless, there is no hard boundary on how lethal a virus can be. Suppose a cell is simultaneously infected with Hantavirus, Influenza, and Ebola, all of which belong to Baltimore Class 5.  Do this a trillion trillion times. The worst that can result is unknown.

In Let Us be Thankful for Vaccines, I wrote

What is the limit of virulence? Without the need to preserve some hosts for future infection,  is there a limitation to all viral machinery? Is it Ebola or a rabies virus, packaged for airborne delivery? Can stealth aspects be added, as observed with COVID-19 ? What of a constellation of virusoids that co-infect and extend the virulence of the engineered virus?

As a universal killer of all life, the Satan bug is almost impossible. Fiction takes dramatic license.  Life fights back with genetic diversity. But the border of reality is unknown. Vaccine technology has made great strides. The methods of trialing a vaccine have not; they do not reflect knowledge at molecular level that was unknown in the whole-virus live-or-killed vaccine era.

This time, the cost in lives of the prolonged vaccine trials will be in the low millions, or tens of millions. It could have been much worse.  (Atlantic) Hic sunt dracones. There be dragons.

Quoting from (CNN) Fauci’s new 2022 timeline for Covid fight,

A decade ago, there were DARPA programs for rapid vaccine production to defend against biological warfare. The  programs were successful in rapid production of vaccines of variable quality, for deployment against dire threat. But the loop was never closed; identification  of dire need was never pursued. The process infrastructure for identification of dire need remains vacant.

***Hic sunt dracones***