Quantum Biology

Close up of a virus brain?

I. Background

The better part of a decade ago Dredd Blog was complaining about a non-existent science called "Abiology" that should exist (Weekend Rebel Science Excursion - 27, quoting Dredd Blog posts from 2012).

About a year after that post I complained, along with other scientific researchers, about the scientists of the biology persuasion having loose lips:

"Since at least the 17th century (and mostly because of Newton), natural scientists have stopped using formal or final causes to explain natural phenomena ... except in biology. This was first pointed out by Colin Pittendrigh (Pittendrigh, C. S. Behavior and Evolution) (ed. by A. Rose and G. G. Simpson), Yale University Press, 1958), who coined the term "teleonomy" to refer to the kind of teleological phenomena observed in biological processes."

(On The Origin of Genieology - 2). "Abiology" still doesn't exist, and the elite among them still go on and on about possibly not knowing the difference between bio-(live) and abio-(not live), i.e. biology and abiology (Are Viruses Alive?).

And I am still pointing out that viruses are discussed in the science commentariat (media) without knowing what microbial host the viruses are replicated by:

"Seriously, it behooves researchers to closely examine the microbes that replicate the SARS-CoV-2 viruses (they haven't yet specified exactly which microbes those are)." (The Doll As Metaphor - 3; cf. On The Origin Of The Home Of COVID-19)

A microbiologist wrote: "Easy to see though, plaque as­says for counting phages [a type of virus] do not work if you have − or suspect you have − lots of phages in a sample but the host bacteria are difficult or impossible to culture on plates, or − even worse − not known." (Small Things Considered, emphasis added).

The virus commentariat's 'solution' all too often is to ignore "the host bacteria" of the virus ('home' of the virus), and to substitute that location/home with what is actually the "meta-host" or "epi-host".

That is, they substitute the host bacteria of that virus and tell us that the virus is "in a human host", "in an animal host", or in "a plant host".

That is a cover-up of their failure to locate the microbe host (including its characteristics and genome) from the public.

Thus, the worst case scenario of not knowing or saying what "the microbe host" of a virus (the single-celled microbe) really is happens to be a common practice:

"Previous outbreaks of human disease caused by coronaviruses, such as SARS and MERS, happened when a virus jumped from animals to humans. Investigations of virus genetics have shown that bats are host to a diverse range of coronaviruses, and the transfer of SARS and MERS viruses to humans involved intermediate hosts, camels in the case of MERS. On-going investigations of the new coronavirus, [SARS-CoV-2] the cause of COVID-19, also suggest that bats are the original host."

(Where did the new coronavirus come from?, emphasis added). Don't forget that the actual host of a virus is a single celled microbe located within a 'meta-host' or 'epi-host' (animal, human, plant).

When the single celled microbe host that replicates a virus is unknown, it is like asking a person for their address and receiving the answer "Earth".

Maybe morphology classes would be useful (What is Morphology?).

II. Why Are RNA Virus Mutation Rates So Damn High

One suspect is quantum mutation that takes place when a DNA or RNA virus is stable:

"At an extreme, an organism that’s “perfectly” adapted to its constant environment would do best to reduce its mutation rate to zero—there are no more beneficial mutations, so all mutations are likely worse than the current genotype. In a constant environment (one where the fitness landscape does not change), it would be best for the optimal genotype to not mutate at all."

(Why are RNA virus mutation rates so damn high). Quantum Biology has an answer to the question that historically has not been well received.

It has to do with "quantum tunneling" and other events of the science of quantum physics, i.e. quantum mechanics (The Doll As Metaphor - 4).

Ignoring the impact of protons (and photons?) on RNA takes place more often than it does with DNA.

So, the question is not being dealt with in a manner that includes all possible answers.

DNA quantum morphing was introduced decades ago, and was recently revisited by a research group at Cornell University (An Open Quantum Systems approach to proton tunneling in DNA, September 2021).

However, the RNA virus once again was not included in those Cornell University studies, even though there is a "double trouble" likelihood of such mutations.

III. Closing Comments

Thus, it is time to take the quantum hypothesis more seriously as I recently posted:

That Cornell University Paper uses the A-T ('T' = thymine) base pair of DNA in its work, whereas I will use the A-U ('U' = uracil) base pair of RNA in this post:

"Uracil is a pyrimidine type nitrogenous base that is found only in RNA molecules. It always pairs with adenine. Chemical difference of uracil and thymine is very small. Uracil has a hydrogen atom at C-5 carbon while thymine has a methyl group at the same [C-5]carbon."

(Difference Between Thymine and Uracil). My hypothesis is that the proton tunneling is less complicated in a single entity ("hydrogen atom [at C-5]") location than it is at "a methyl group [at C-5"] location (Uracil has a surprising new kind of proton transfer; cf. The Role of Reaction Force and Chemical Potential in Characterizing the Mechanism of Double Proton Transfer in the Adenine-Uracil Complex).

(The Doll As Metaphor - 4). It is time to focus on the host microbe of a particular RNA virus in cases where the most stability is likely, while remembering the statement above:

"In a constant environment (one where the fitness landscape does not change), it would be best for the optimal genotype to not mutate at all."

(ibid @ Cornell University Paper quoted above). That is where the rubber meets the road, in terms of examining why mutations take place when they should not take place (because the fitness landscape has not changed).

Especially if they take place at the A-U ('U' = uracil) base pair of RNA in addition to the G-C location of RNA, as was studied in DNA viruses (double trouble).

The next post in this series is here.

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Yep, the sounds of silence Double Trouble:

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The Doll As Metaphor - 4

Proton induced RNA mutation

I. Background

I have tried to stimulate biologists/virologists into taking a look at the haphazard way RNA is depicted in major government databases (such as GenBank) to no avail (It's In The GenBank, 2, 3).

In the previous post of this series I set forth a wee bit of criticism based upon, among other things, the revolutionary work of Per-Olov Löwdin (see The Doll As Metaphor - 3).

In Löwdin's work he pointed out an abiological set of events, involving proton tunneling, that would engender mutations in microbe and virus genomes.

Long time Dredd Blog readers will remember that I also wrote about it several years ago (The Uncertain Gene; cf. If Cosmology Is "Off," How Can Biology Be "On?").

II. Proton Tunneling in DNA and its Biological Implications

Since Löwdin's hypothesis, others have addressed the subject (see eg. The Role of Proton Transfer on Mutations, An Open Quantum Systems approach to proton tunnelling in DNA, Comment on Masanari Asano et al.: A model of epigenetic evolution based on theory of open quantum systems).

Löwdin's concept is a revolutionary challenge to biologists, microbiologists, and virologists who want to play with their metaphorical dolls (microbes, viruses) by play pretending that they can do 'whatever evolution' (The Doll As Metaphor, 2, 3).

III. Proton Tunneling in RNA and its Biological Implications

So, let's take a look at the concept and specifically apply it to RNA rather than to DNA.

One of the papers took a deeper dive into the issue by addressing "where the rubber meets the road":

"One of the most important topics in molecular biology is the genetic stability of DNA. One threat to this stability is proton transfer along the hydrogen bonds of DNA that could lead to tautomerisation, hence creating point mutations. We present a theoretical analysis of the hydrogen bonds between the Guanine-Cytosine (G-C) nucleotide, which includes an accurate model of the structure of the base pairs, the quantum dynamics of the hydrogen bond proton, and the influence of the decoherent and dissipative cellular environment. We determine that the quantum tunnelling contribution to the process is several orders of magnitude larger than the contribution from classical over-the-barrier hopping. Due to this significant quantum contribution, we find that the canonical and tautomeric forms of G-C inter-convert over timescales far shorter than biological ones and hence thermal equilibrium is rapidly reached. Furthermore, we find a large tautomeric occupation probability of 1.73 × 10 −4 , suggesting that such proton transfer may well play a far more important role in DNA mutation than has hitherto been suggested. Our results could have far-reaching consequences for current models of genetic mutations."

(An Open Quantum Systems approach to proton tunneling in DNA, Cornell University, September 2021, emphasis added). This more recent Cornell University work is where I begin.

That Cornell University Paper uses the A-T ('T' = thymine) base pair of DNA in its work, whereas I will use the A-U ('U' = uracil) base pair of RNA in this post:

"Uracil is a pyrimidine type nitrogenous base that is found only in RNA molecules. It always pairs with adenine. Chemical difference of uracil and thymine is very small. Uracil has a hydrogen atom at C-5 carbon while thymine has a methyl group at the same [C-5]carbon."

(Difference Between Thymine and Uracil). My hypothesis is that the proton tunneling is less complicated in a single entity ("hydrogen atom") location than it is at "a methyl group" location (Uracil has a surprising new kind of proton transfer; cf. The Role of Reaction Force and Chemical Potential in Characterizing the Mechanism of Double Proton Transfer in the Adenine-Uracil Complex).

Furthermore, RNA mutation rates are orders of magnitude greater than DNA mutation, suggesting a closer look and further exploration is needed.

IV. Closing Comments

Thus, the Cornell University Paper's "probability of 1.73 × 10 −4" of proton tunneling at the A-T location in DNA is less probable than the even more likely probability at the A-U location in RNA.

In a future post I will "do the math", so stay tuned as we try to figure it out:

"Last January, a team of researchers searching for the coronavirus in New York City’s wastewater spotted something strange in their samples. The viral fragments they found had a unique constellation of mutations that had never been reported before in human patients — a potential sign of a new, previously undetected variant [a.k.a. dead bodies of microbes and viruses] ... because wastewater samples contain an amalgamation of lineages circulating in the sewer-shed, it is not possible to reconstruct individual genomes using standard methods."

(Mysto SARS-CoV-2 in NY , p. 2). We don't have much time before Halloween.

The next post in this series is here, the previous post in this series is here.