What viral latency can tell us…
Viruses are a strange class of organism indeed. You spot one under a microscope and it almost always looks like a mine waiting to be stepped on; for activation purposes ofcourse.
You look at an influenza virus and you spot at least three (known) proteins; the M2, neuraminidase, and hemagglutinin responsible for host cell membrane penetration, uncoating, and viral RNA release which later replicates to form further viral copies.
But neither the human body nor the virus are as simple as that. The current pandemic situation is good enough an example. You see each month a new coronavirus breed is unleashed and an afflicted bunch finds its way to the hospital; some sadly even to the morgue.
It so happened that a good friend of mine after her second dose of the anti-COVID vaccine had a bad bout of Herpes. Peripheral neuropathy, mouth sores, and rashes were the general presentation. I was quick to postulate a connection between the timing of her vaccination and the onset of herpes infection. She proved an interesting case. I asked her and she answered, that she had suffered minor herpes symptoms when quite young.
A brief digression here…as I said earlier, viruses are not so simple. They are not a living thing; requirements being a nucleus which in turn requires some nutritional uptake and thereby generate energy. Viruses are non-living. Enclosed within a capsid is a single (or double) stranded piece of information (DNA or RNA) which encodes the viral genome. When introduced into the body, the virus requires cellular uptake by a host to thrive. The virus uncoats, undergoes certain changes, and injects its DNA/RNA into the host nuclear machinery which it then uses to produce multiple copies of itself. We then have conditions like viremia, when a viral population is detectable in blood.
No surprise that they are even used in the biotechnology sector as potent tools for cloning techniques (phage, adenovirus, retrovirus).
Herpes virus has a tendency to become dormant inside the anterior horn of spinal cord for later reactivation. It was therefore not very surprising when my friend’s dormant infection was reawakened by the second dose of the vaccine.
Neurological mechanisms can be at play here as to why vaccine response differs between individuals, here we tread into the realm of Pharmacogenomics 101; pro-oxidant products, reactive oxygen and nitrogen species can serve as potential gene switches in regulation of vaccine responsivity. The role of kelch like NrF2 is still under scrutiny, although its role in covid is something I believe should be studied. My own research involves the analysis of oxidative stress mechanisms on epileptic seizures.
Viruses work in an extensive and complicated manner. Their mechanism is deciphered on the protein level, but transcriptome studies are still not available. Taking a sample population (stratified according to factors such as race/geography/age) and performing quantitative studies would be costly but necessary. Otherwise, an absolute vaccine response seems unlikely at least in the near future. It is also possible that inoculation of pregnant and lactating mothers could potentially pass antibodies to the infant, but given that our encounter with COVID (in this dynamic) is relatively new, transplacental studies would require time.
In the end all I can say is that, all therapies for now are to be taken with a grain of salt. Being un-vaccinated is ill-advised, but not much research is being conducted in the way of ‘negative response’; that in favor of studying the effects we do not want, the panic attacks post recovery, the reactivation of childhood infection, potency of the virus inside the inoculum, full-scale coronavirus symptoms, even death. The vaccines, however many there are, are NOT the key to the life sciences. They are a mere attempt at preventing reinfection. Not a guarantee against it!