The vertebrates have co-evolved with a dark, infiltrating enemy over the past several hundred million years. Each vertebrate species has its own specialized enemy agent that evolved to infect that particular species. It stealthily infects us by the time we are infants, mostly hides in shadows during our lives, occasionally reactivates and inflames our immune system into a frenzied, futile battle to eradicate it, but eventually kills every single one of us if we live long enough.
I am talking about the herpesvirus family of neurotropic viruses. One of the most significant findings of my research is that these viruses appear to be at the root cause of a wide variety of mysterious diseases whose causes are still considered unknown to science. In particular, these include autoimmune diseases and degenerative syndromes where the conventional medical narrative vaguely implicates "the immune system turning upon the body for some unknown reason". Experts in many disease specialty fields have made this observation in isolation, but in this article I bring together the many theatres of battle in which we can catch a glimpse of our relentless herpesvirus sappers in action.
HSV-1
HSV-1 is a ubiquitous herpesvirus that infects virtually all humans worldwide. It is transmitted through the mouth, nose, and eyes, and from there makes its way to its impenetrable stronghold in the trigeminal ganglion, a three-pronged nerve cluster that innervates the mouth, nose and eyes. From the trigeminal ganglion, HSV-1 keeps the immune system chronically provoked.
HSV-1 uses a sophisticated repertoire of tricks to evade the immune system. It packs itself deeply into the chromatin (DNA) of our cells, inextricable from our own DNA. It actively tries to switch the immune system from Th1 (antimicrobial) to Th2 (anti-parasite) mode, to try to throw off the threat. It interacts with host cell genome and proteins to try to mask itself. It prevents the host cell from surfacing antigens that would ordinarily signal neighboring immune cells that it has been infected.
HSV-1 infects a very particular and dispersed set of brain areas. It appears to me from the targeted brain areas that the "strategy" of the neurotropic HSV-1 virus is:
- Replicate during daylight, hide at night (when the immune system is on the prowl)
- Induce stress in the host organism (to dampen immune system response)
- Disrupt sleep of the host organism (to reduce the immune system effectiveness)
- Preferentially infect neural stem cells--especially the dentate gyrus and indusium griseum--to ensure that new neurons generated to replace ones terminated by the immune system are pre-infected
HSV-2
HSV-2 is the sexually-transmitted virus that most people associate 'herpes' with. HSV-2 tends to infect the pelvic region and the lower regions of the spinal cord, rather than the central nervous system as with HSV-1. Like HSV-1, HSV-2 infection lasts a lifetime and cannot be fully cured. Unlike HSV-1, HSV-2 is generally only transmitted through sexual contact or other direct exchanges of bodily fluids.
Viral encephalitis
Alzheimer's Disease
Alzheimer's disease is characterized by the accumulation of amyloid plaques in the brain. It appears that this is detritus from a lifetime of battling HSV-1. The plaques are the immune system's attempt to wall off the invaders.
https://pubmed.ncbi.nlm.nih.gov/18973185/
Parkinson's Disease
Fibromyalgia
Multiple Sclerosis
The herpesvirus HHV-6 appears to cause MS.
https://pubmed.ncbi.nlm.nih.gov/13129768/
Guillain-Barre syndrome
https://pubmed.ncbi.nlm.nih.gov/22136568/
https://jnnp.bmj.com/content/jnnp/52/6/788.full.pdf
Bell's Palsy
Celiac disease
Wheat gluten can be mistaken by the immune system for viral antigens, causing an immune reaction to gluten.
https://science.sciencemag.org/content/356/6333/44
Irritable Bowel Syndrome
Periodontal disease
It appears that herpesvirus and gingivitis-causing bacteria synergistically promote infection of the gums.
https://www.ncbi.nlm.nih.gov/books/NBK2484/
https://pubmed.ncbi.nlm.nih.gov/10368051/
Hashimoto's thyroiditis
Rheumatoid arthritis
Lupus
Dermatitis herpetiformis: Gluten Mimics Viral Capsid Envelopes
Herpesvirus Prevent Bubonic Plague
By constantly provoking the immune system, herpesvirus keeps the immune system on alert to overwhelm a nasty bacterium that causes bubonic plague (Yersinia pestis), and prevent it from gaining a foothold. Yersinia has a very nasty strategy of trying to shut down the immune response immediately after infection. Because herpesvirus keeps the immune system active, it immediately eradicates Yersinia if it shows up. Mice who had their herpesvirus removed succumbed to the plague.
This causes one to contemplate what the definition of a 'pathogen' is in the context of such competitive evolutionary pressures. It is interesting to speculate that those humans alive today are those that keep herpesvirus in check, but not so much that their immune systems were not chronically inflamed, as only those with this low-grade herpesvirus infection survived the bubonic plague.
MicroRNA-138 Mediates a Truce With Herpesvirus
The cell has a special messenger--a microRNA called miRNA-138--that downregulates HSV-1 expression inside of cells.
