Below is some ideas that I have been working on base on
my medical test results (angiogram-MRI, VZV, CMV, HHV-6) and the test results of
others.
Betaherpesvirinae dependent POIS"Furthermore, angioplasty-induced injury to the vessel wall and reperfusion after balloon angioplasty produce ROS8 and cytokines. The resulting activation of NF-kB can in turn stimulate the MIEP present in latently infected cells and thereby contribute to reactivation of latent CMV...Recent studies have shown that CMV infection of human cells leads to stimulation of arachidonic acid (AA) release." -Aspirin Attenuates Cytomegalovirus Infectivity and Gene Expression Mediated by Cyclooxygenase-2 in Coronary Artery Smooth Muscle Cells (1998)
Cytomegalovirus (CMV, HHV-5) and HHV-6 are
Betaherpesvirinae that primarily latently infect endothelial cells such as blood vessels and epithelial mucosa such as intestinal epithelia (
Ref). This is unlike alpha-herpes viruses (HSV-1, HSV-2, VZV) which primarily latently infect neurons. Within minutes of infecting endothelial cells CMV upregulates reactive oxygen species (H
2O
2), NF-kB, COX-2 and cytokines (
RefSE). These
Betaherpesvirinae maintain this inflammatory environment while latent.
"These results suggest that infection by CMV or HHV-6 causes vascular endothelial injury, with HHV-6 having a stronger effect than CMV, and combined infection having a stronger effect than either virus alone."
-Endothelial damage caused by cytomegalovirus and human herpesvirus-6 (2003)
CMV (and HHV-6) latency within endothelial cells leads to injury of vascular and smooth muscle tissue (
Ref,
Ref). Stretching this injured tissue causes a stress response of free radical production (
RefGR) leading to reactivation and replication of the virus (
RefSE).
The reponse of the immune system to this virus replication is POIS."Enhancement of promoter activity by endogenous catecholamines is essential for high-level transgene expression from MIECMV within the vasculature." -Beta-Adrenoceptor Blockade Markedly Attenuates Transgene Expression From Cytomegalovirus Promoters Within the Cardiovascular System
During orgasm there is a sudden rise in norepinephrine (noradrenaline) and epinephrine (adrenaline).
This norepinephrine (and epinephrine) causes vasodilation via the beta2-adrenergic receptor of the arteries in the brain and through out the body. This vasodilation is a ballooning stress on the arteries that is normal under certain temporary conditions such as orgasm or exercise where increased blood flow is needed in certain areas of the body. However, any arteries that have been injured by latent infection of CMV (or HHV-6) will be triggered by this stretching stress to reactivate the virus (
Ref) causing an immune response. Norepinephrine levels may fall shortly after orgasm. However, because of the immune response to reactivated CMV, histamine and nitric oxide levels rise causing a secondary vasodilation (stretching) of the arteries.
Eating induced POIS-related/POIS-like symptoms: This is of course just a hypothesis. Betaherpesvirae like CMV can infect and establish latency in intestinal epithelia (
Ref). If the intestinal epithelia are infected by CMV (and/or HHV-6) at a certain location, food passing through the stomach can stretch the intestines at the location of the infection and causing stress-reactivation of the virus. This passing food would, by stretching that part of the intestine induce an immune response leading to either local irritable bowel syndrome or systemic inflammation. This effect may lead people to think that specific foods are causing their IBS when it is just over eating. If there is a food that you really like or has MSG in it, you may be more inclined to over-eat. The MSG has nothing to do with the IBS. It is the inability to know when to stop eating that is causing the IBS/inflammation. Again, this is a hypothesis.
With all that said, I found out this about varicella zoster virus:
"Upon reactivation, varicella zoster virus (VZV) spreads transaxonally, infects cerebral arteries and causes ischemic or hemorrhagic stroke, as well as aneurysms. The mechanism(s) of VZV-induced aneurysm formation is unknown. However, matrix metalloproteinases (MMPs), which digest extracellular structural proteins in the artery wall, play a role in cerebral and aortic artery aneurysm formation and rupture." -Differential regulation of matrix metalloproteinases in varicella zoster virus-infected human brain vascular adventitial fibroblasts
In general, the alphaherpesvirusae (HSV-1, HSV-2, VZV) upregulate matrix metalloproteinases and cause collagen break down. So the line for which viruses infect the vasculature is very blurry.
Also, there is also another thread discussing vasculature related issues at
Ideas on Endothelial Dysfunction. There they discuss alternative explanations for endothelial and collagen abnormalities that may explain POIS and general inflammation. I think this diversity of ideas is good for the POIS community. But there is a need for more people to be virus tested to be able to rule out or statistically correlate viruses as a cause of POIS.