Cytomegalovirus and Hypertension – Another Piece of the Herpesviridae Puzzle
Article Navigation: Previous article in this series
So I heard about this on the BBC World Service today:
“Based on a series of studies in mice, they said cytomegalovirus or CMV -- a herpes virus that affects some 60 to 99 percent of adults globally -- appears to increase inflammation in blood vessels, causing high blood pressure.
And when combined with a fatty diet, CMV may also cause hardening of the arteries, a major risk factor for heart attacks, strokes, and kidney disease, they said.” - (Reuters)
Which is AWESOME! And comes 17 years after this study in people:
Herpesvirus antibodies and vascular complications in essential hypertension.
Antibodies against herpes simplex virus (HSV) and cytomegalovirus (CMV) were examined in sera from 132 patients with essential hypertension and 54 normotensive healthy subjects of the same age and sex. Prevalences of HSV and CMV antibodies (titre greater than or equal to 4) were equal in patients and controls. A HSV antibody tire greater than or equal to 64 was found in 39.5% (17/53) of patients with WHO stage III hypertension, in 26.2% (22/85) of patients with stage I-II hypertension, and in only 9.4% (5/54) of normotensive subjects (p less than 0.0005). The HSV antibodies were mainly of type 1. No association between CMV antibodies and vascular complications could be demonstrated.
http://www.ncbi.nlm.nih.gov/pubmed/6297261
Which is great news – now we know that CMV AND HSV cause hypertension. Which should be no surprise – because other studies show connections between HSV and atherosclerosis/arteriosclerosis. And that’s in studies from 1982. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=442386
So let’s look at the mechanism behind this.
We know that herpesviridae require arginine to replicate.
We also know that they scavage lysine (because the replication mechanism mistakes lysine for arginine).
This paper: http://circ.ahajournals.org/cgi/content/full/95/2/311 – shows that arginine is required for NO pathway synthesis. Like most smooth tissue, arteries and veins require NO (nitric oxide) to relax.
Arterial and venous tissue is endothelial tissue, a specialized form of epithelial tissue.
Where does CMV like to hang out, and HSV like to replicate?
Yep, that’s right – epithelial tissue.
HSV, by the way, is known to promote blood clots too – as this paper shows: http://circ.ahajournals.org/cgi/content/full/95/2/311.
Ultimately, what we seem to be seeing here is that the herpesviridae strip-mine the arterial wall for arginine and lysine. Inflammation is promoted. Coagulation occurs. Adding arginine will help a little; but long term, the arginine is required for the viral replication to occur.
And this, by the way, is a repeating cycle. TNF-alpha is released by the body to signal that it is under attack in that area (by macrophages). The virus sees this as a signal to go from dormancy (latent infection, which in the case of HSV, the primary site is nerve tissue; whereas in CMV, it’s epithelial tissue, and epithelial tissue and endothelial tissue are very closely related), to full on replication. (http://www.springerlink.com/content/u6u8735318u7lw42).
Which scavenges more arginine. And causes more replication.
It’d be pretty simple at this point to come to the conclusion that a large preponderance of heart disease is caused by herpesviridae. Now, there’s other causes too – fungal infection, and bacterial infection – but I’d say that the most common cause are these viruses, which nearly everyone has.
(You’ve heard of the French Paradox, right? That drinking red wine, rich in resveratrol, reduces your risk of heart disease? Resveratrol inhibits herpes virus replication at a very early stage in its reproductive cycle. It also has other benefits – mainly by allowing sirtuins to spend more time switching off erroneously expressed genes, and less time fixing up damage, but that’s secondary to the heart disease issue).
So, going back to part 1 of this series, I stated that herpesviridae can cause the following:
- Alzheimer's Disease
- Type-II Diabetes
- High Cholesterol, including high HDL and high triglyceride levels
- Heart disease, including atherosclerosis (aka arteriosclerosis)
- Cancer of the gallbladder (cholangiocarcinoma)
- Colon cancer
- Crohn's disease
- Multiple sclerosis
- Rheumatoid arthritis
- Arthritis
- Osteoporosis
- Multiple myeloma
- Glioblastoma multiforme
- Bipolar disorder
- Schizophrenia
- Hodkin's Disease
- Lymphoma
- Breast Cancer
- Kaposi's Sarcoma
We can now add Hypertension to this list.
The common factor to all of these? Well, there’s actually two. We’re talking about diseases of epithelial tissue, and nerve tissue.
For example, take osteoporosis. Herpesviridae (specifically in this study, HSV-1), upregulates expression of Interleukin-6. Osteoblast and osteoclast differentiation are regulated by IL-6. Osteoclasts are also very similar in nature to epithelial cells.
A similar line of argument applies to arthritis.
Ultimately, we need more virion assay testing. Take tissue samples. Test for viruses. We have the technology. We should be able to generate lots of evidence FAST for the involvement of herpesviriade in these diseases.
We also need to start taking medical histories that include people who are in close contact with you. I’ll try to write about that next – it’s all about histocompatibility complexes, and how especially one spouse may have one disease, and the other spouse may have another, but it’s all the same root cause.
Simon Cooke is an occasional video game developer, ex-freelance journalist, screenwriter, film-maker, musician, and software engineer in Seattle, WA.
The views posted on this blog are his and his alone, and have no relation to anything he's working on, his employer, or anything else and are not an official statement of any kind by them (and barely even one by him most of the time).