If mRNA vaccination is sufficient to launch an immune response which
includes somatic hypermutation in immunoglobulin genes with B lymphocytes
coding for certain portions of antibodies increasing their stickiness due
to weak forces(???):
“The binding between antigen and antibody is not covalent but depends on
many relatively weak forces, such as hydrogen bonds, van der Waals forces,
and hydrophobic interactions. Since these forces are weak, successful
binding between antigen and antibody depends on a very close fit over a
sizeable area, much like the contacts between a lock and a key.”
From _Immunology_ by Richard Coico
> You are shoving everything I wrote about the bait down a memory hole, and
> putting everything
> you've got into the switch issues. Well, even there
> I had something very relevant to say.
The switches are the most intriguing parts.
>>> You seem
>>> to be unable to reason properly wrt the biology about which you wrote below.
>> You haven’t even touched any of that,
> Yes, I have, liar.
Not that I’ve seen.
You didn’t pick up on the relevance. That the older group had less SHM
activity resulting from mRNA vaccination than younger leads me to the
perhaps erroneous conclusion that mRNA vaccination can result in SHM
(somatic hypermutation) then by inference. Perhaps putting all my eggs in
one basket. But it pushes toward my point in the OP that SHM is a
>> I guess you’re still avoiding the topic of somatic hypermutation.
> So much for “That’s the part I’m focused on...affinity maturation..." Is
> this another bait and switch scam?
Switching between terms affinity maturation and SHM is a bait and switch
scam? Really? Are you stalling to play catsup?
> I'll give you the benefit of the doubt, and keep talking about the real life implications
> of antibody affinity maturation, and the question you asked Ron O,
> [who is, btw, an expert in bait and switch scams, in his own mind and probably yours]
> for a while longer.
Well I’m plugging along in a book that will introduce another bait and
switch scam about molecular evolution bridging innate and adaptive
The authors discussing strategies of innate immune defense against
“If large amounts of DNA suddenly appear free in the cytosol, then that is
a clear indication that something has gone badly wrong. ” From
_Evolutionary Concepts in Immunology
Robert Jack & Louis Du Pasquier_
And something utilized has interesting family members. They continue:
“APOBEC3G deaminase has evolved in mammals as an innate system effector
that deals with this particular situation.”
They eventually cite: https://www.mdpi.com/1999-4915/7/6/2757
Willems L, Gillet NA. APOBEC3 Interference during Replication of Viral
Genomes. Viruses. 2015; 7(6):2999-3018. https://doi.org/10.3390/v7062757
“Co-evolution of viruses and their hosts has reached a fragile and dynamic
equilibrium that allows viral persistence, replication and transmission. In
response, infected hosts have developed strategies of defense that
counteract the deleterious effects of viral infections. In particular,
single-strand DNA editing by Apolipoprotein B Editing Catalytic subunits
proteins 3 (APOBEC3s) is a well-conserved mechanism of mammalian innate
immunity that mutates and inactivates viral genomes. In this review, we
describe the mechanisms of APOBEC3 editing during viral replication, the
viral strategies that prevent APOBEC3 activity and the consequences of
APOBEC3 modulation on viral fitness and host genome integrity.
Understanding the mechanisms involved reveals new prospects for therapeutic
The book authors go on to talk about this APOBEC3 as a cytidine deaminase
attacking retroviral invaders and its relative “Activation-Induced
Deaminase” which is quite relevant to adaptive immunity (another bait and
switch I am pulling here obviously). They cite:
Silvestro G. Conticello, Cornelia J. F. Thomas, Svend K. Petersen-Mahrt,
Michael S. Neuberger, Evolution of the AID/APOBEC Family of Polynucleotide
(Deoxy)cytidine Deaminases, Molecular Biology and Evolution, Volume 22,
Issue 2, February 2005, Pages 367–377,
“The AID/APOBEC family (comprising AID, APOBEC1, APOBEC2, and APOBEC3
subgroups) contains members that can deaminate cytidine in RNA and/or DNA
and exhibit diverse physiological functions (AID and APOBEC3 deaminating
DNA to trigger pathways in adaptive and innate immunity; APOBEC1 mediating
apolipoprotein B RNA editing). The founder member APOBEC1, which has been
used as a paradigm, is an RNA-editing enzyme with proposed antecedents in
yeast. Here, we have undertaken phylogenetic analysis to glean insight into
the primary physiological function of the AID/APOBEC family. We find that
although the family forms part of a larger superfamily of deaminases
distributed throughout the biological world, the AID/APOBEC family itself
is restricted to vertebrates with homologs of AID (a DNA deaminase that
triggers antibody gene diversification) and of APOBEC2 (unknown function)
identifiable in sequence databases from bony fish, birds, amphibians, and
mammals. The cloning of an AID homolog from dogfish reveals that AID
extends at least as far back as cartilaginous fish. Like mammalian AID, the
pufferfish AID homolog can trigger deoxycytidine deamination in DNA but,
consistent with its cold-blooded origin, is thermolabile. The fine
specificity of its mutator activity and the biased codon usage in
pufferfish IgV genes appear broadly similar to that of their mammalian
counterparts, consistent with a coevolution of the antibody mutator and its
substrate for the optimal targeting of somatic mutation during antibody
maturation. By contrast, APOBEC1 and APOBEC3 are later evolutionary
arrivals with orthologs not found in pufferfish (although synteny with
mammals is maintained in respect of the flanking loci). We conclude that
AID and APOBEC2 are likely to be the ancestral members of the AID/APOBEC
family (going back to the beginning of vertebrate speciation) with both
APOBEC1 and APOBEC3 being mammal-specific derivatives of AID and a complex
set of domain shuffling underpinning the expansion and evolution of the
So even if vaccination against COVID is insufficient to launch SHM, this
deeper evolutionary aspect tying components of innate and adaptive immunity
is very intriguing (as a bait and switch of course).
I apologize for the total lack of scientific content.