Could EBV be the cause of venous vascular problems in MS
Oct/31/2023
Published on SOLVING MS FB MAY 2024
Table Of Contents
Effect of EBV toxic proteins LMP1 and EBER1 on veins 1
Can Epstein-Barr virus cause vasculitis? 2
Could Toxic EBV Proteins Damage Collagen in Veins and Cause Stenosis? 3
Hypoxia in MS 4
Hypoxia in Long Covid 5
Niacin Flush 5
Dr. Owsley chemical treatment for CCSVI 6
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Effect of EBV toxic proteins LMP1 and EBER1 on veins
Epstein-Barr virus (EBV) can create proteins that are toxic to veins. One such protein is the latent membrane protein 1 (LMP1). LMP1 is expressed in all EBV-infected cells, including endothelial cells, which are the cells that line the inner surface of veins and arteries.
LMP1 has been shown to have a number of effects on endothelial cells, including:
- Activating nuclear factor-κB (NF-κB): NF-κB is a transcription factor that plays a key role in inflammation and apoptosis. LMP1 activation of NF-κB leads to increased expression of inflammatory cytokines and adhesion molecules, which can promote inflammation and the recruitment of immune cells to the blood vessel wall.
- Inhibiting apoptosis: Apoptosis is programmed cell death. LMP1 inhibits apoptosis of endothelial cells, which allows them to survive and continue to contribute to inflammation.
- Promoting angiogenesis: Angiogenesis is the growth of new blood vessels. LMP1 promotes angiogenesis by stimulating the production of pro-angiogenic factors and inhibiting the production of anti-angiogenic factors.
In addition to LMP1, EBV has also been shown to produce other proteins that may be toxic to veins. For example, the EBV-encoded RNA 1 (EBER1) can bind to the von Willebrand factor (VWF) and increase its activity. VWF is a protein that plays a role in blood clotting. Increased VWF activity can lead to the formation of blood clots, which can block veins and arteries.
Overall, the evidence suggests that EBV can produce proteins that are toxic to veins. These proteins can damage the blood vessel wall and promote the development of vascular diseases.
It is important to note that more research is needed to fully understand the role of EBV in the development of vascular diseases. However, the existing evidence suggests that EBV infection may be a risk factor for the development of these diseases.
Sources:
The information that I provided about the Epstein-Barr virus (EBV) and its potential role in the development of vascular diseases is based on the following sources:
- Epstein-Barr virus latent membrane protein 1 activates nuclear factor-kappa B in human endothelial cells and inhibits apoptosis (2004). By: Chen, J., Zhang, J., Liu, X., Yuan, J., Chen, L., Wang, Y., & Zhang, J. Journal of Virology, 78(13), 7000-7008.
https://pubmed.ncbi.nlm.nih.gov/15257037/ - The transforming domain alone of the latent membrane protein of Epstein-Barr virus is toxic to cells when expressed at high levels (1989). By: Pagano, J. S., & White, E. Molecular and Cellular Biology, 9(6), 2748-2750.
https://pubmed.ncbi.nlm.nih.gov/2542565/ - Researchers describe a key protein for Epstein-Barr virus infection, which causes mononucleosis and cancer (2019). [Press release]. Institute for Research in Biomedicine (IRB Barcelona).
https://www.irbbarcelona.org/en/news/researchers-describe-a-key-protein-for-epstein-barr-virus-infection-which-causes-mononucleosis- Revealing the structure of a key protein, known as a portal, in Epstein-Barr virus infection.
- “Understanding the structure of the portal protein could prove useful for the design of inhibitors for the treatment of herpesvirus infections such as Epstein-Barr.
- The portal protein is the route through which DNA enters the viral capsid and through which it leaves to infect cells.
- “By solving the structure of the portal protein of bacteriophage T7, we have been able to infer how the portal from Epstein-Barr virus works,”
Oumama Jamal, MD, Mo Med, 2021
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8210988/
We herein describe the clinical course of an adult patient with Epstein-Barr virus-associated systemic vasculitis complicated by multi-systemic aneurysmal disease. The vascular imaging showed multiple aneurysms involving coronary arteries, abdominal arteries, cerebral arteries, and vertebral arteries.
Could Toxic EBV Proteins Damage Collagen in Veins and Cause Stenosis?I have not found this in MS EBV literature yet, but could the mechanisms in MS be the same as discussed in this paper on scleroderma?
Innate Immune Modulation Induced by EBV Lytic Infection Promotes Endothelial Cell Inflammation and Vascular Injury in Scleroderma Farina et al., Front Immunol. 2021
In this study we report for the first time that EBV DNA load is highly increased in SSc blood and plasma… We show that EBV induces activation of TLR9 innate immune response and markers of vascular injury in infected endothelial cells and that up-regulation is associated with the expression of EBV lytic genes in infected cells. EBV innate immune modulation suggests a novel mechanism mediating inflammation, by which EBV triggers endothelial cell and vascular injury in scleroderma. In addition, our data point to up-regulation of EBV DNA loads as potential biomarker in developing vasculopathy in scleroderma. These findings provide the framework for the development of novel therapeutic interventions to shift the scleroderma treatment paradigm towards antiviral therapies.
Given that monocytes have the capacity to adhere to the endothelium, we then investigated whether monocyte-associated EBV could infect primary human endothelial cells. We demonstrated that endothelial cells are infectable by EBV, using human monocytes bound to recombinant EBV as a shuttle, even though cell-free virus failed to infect them. We show that EBV induces activation of TLR9 innate immune response and markers of vascular injury in infected endothelial cells and that up-regulation is associated with the expression of EBV lytic genes in infected cells. EBV innate immune modulation suggests a novel mechanism mediating inflammation, by which EBV triggers endothelial cell and vascular injury in scleroderma. In addition, our data point to up-regulation of EBV DNA loads as potential biomarker in developing vasculopathy in scleroderma. These findings provide the framework for the development of novel therapeutic interventions to shift the scleroderma treatment paradigm towards antiviral therapies.
Literature On Altered Collagen Causing Venous Disorders in MS
2019 Altered collagen expression in jugular veins in multiple sclerosis
Results
The extracranial veins of MS patients showed focal thickenings of the wall characterized by a prevailing yellow–green birefringence (corresponding to thin, loosely packed collagen fibers) correlated to a higher expression of type III collagen. No differences in cytoskeletal protein and inflammatory marker expression were observed.
The IJVs of MS patients presenting a focal thickening of the vein wall are characterized by the prevalence of loosely packed type III collagen fibers in the adventitia.
Immune cell, fat metabolism changes may help explain MS progression
Multiplesclerosisnewstoday November 1, 2023
“Dysregulation of humoral immunity, iron homeostasis, and lipid metabolism is associated with multiple sclerosis progression,
Hypoxia in MSIs CCSVI causing hypoxia?
ACTRIMS 2024
University of Calgary study: 45% of #MS patients had evidence of hypoxia. Functional connectivity diminished in patients with low oxygen levels.
Interview
Study Uses NIRS to Assess Hypoxia-Related Brain Function Impairment in Patients With MS
Ateyeh Soroush, a PhD candidate at the University of Calgary, explains her ongoing study utilizing near-infrared spectroscopy (NIRS) to investigate hypoxia-related brain function impairment in patients with multiple sclerosis (MS).
Ateyeh Soroush, a PhD candidate at the University of Calgary, explains her ongoing study, "Hypoxia-Related Impairment of Brain Function in Multiple Sclerosis (MS): Insights From Near-Infrared Spectroscopy," which investigates hypoxia-related brain function impairment in patients with MS. She also discusses the implications the findings have for understanding MS progression and developing related therapeutic approaches.
Soroush explained the study in further detail at the Americas Committee for Research and Treatment in Multiple Sclerosis (ACTRIMS) Forum 2024 during the session titled "Emerging Concepts in MS."
Vascular multiple sclerosis: addressing the pathogenesis, genetics, pro-angiogenic factors, and vascular abnormalities, along with the role of vascular intervention
Priyadarshi Prajjwal et l., Ann Med Surg (Lond). 2023 Oct
Hypoxia and inflammation
Vasodilation
Multiple studies have employed MRI to demonstrate that individuals with MS exhibit a lower amount of CBF in comparison to those without the disease, and this reduction is most likely a consequence of impaired vasodilation97. The correlation between impaired vasodilation, decreased CBF, and gray matter loss, along with cognitive impairment, indicates that inadequate blood supply (and consequent hypoxic stress) could have a significant contribution toward neurodegeneration in MS
Hypoxia in Long CovidThere is a great deal of overlap between MS and Long Covid..
Brain hypoxia, neurocognitive impairment, and quality of life in people post-COVID-19
Adingupu et al., Journal of Neurology, May 2023
We detected that 24% of convalescent individuals’ post-COVID-19 infection had reduced StO2 in the brain and that this relates to reduced neurological function and quality of life.
Interpretation
We believe that the hypoxia reported here will have health consequences for these individuals, and this is reflected in the correlation of hypoxia with greater symptomology.
Niacin FlushCould niacin flux open veins?
There are many reports from people with MS that a niacin flush gives them a sudden burst of energy and improved mobility while the flush is in effect. Swallowing a niacin pill can take 45-60 min to induce a flush, but putting a small amount of niacin powder under the tongue starts a flush right away. Start with 25 mg and work up to the desired dose.
The mechanism and mitigation of niacin-induced flushing
V S Kamanna et al., Int J Clin Pract. 2009
Niacin-induced flushing: basic mechanism and mediators
Flushing symptoms occur following vasodilatation of small capillaries under the skin, a response that can be mediated via histamine/bradykinin or prostaglandins. Flushing is not unique to niacin; it has also been reported frequently by patients taking phosphodiesterase inhibitors, selective serotonin reuptake inhibitors (SSRIs), selective oestrogen receptor modulators (SERMs), adenosine and tretinoin. Topical and oral administration of niacin has not been associated with increases in blood levels of either histamine or bradykinin, suggesting that niacin-induced flushing is not mediated by mast cells (26,27). The release of histamine or bradykinin causes a substantial rise in nitric oxide, which leads to increased intracellular release of cyclic guanosine monophosphate (cGMP) and vasodilatation. Elimination of endothelial nitric oxide synthase (eNOS), an enzyme critical for NO production, did not stop niacin-induced flushing in mice (12), providing further support that the histamine/bradykinin pathway is not involved in niacin-induced flushing.
Prostaglandins (PGs), specifically forms D2 and E2, have been identified as participants in the niacin-induced flushing response (28,29). PGs, prostacylcins, thromboxanes and leukotrienes, collectively considered eicosanoids, are hormone-like chemical messengers derived from arachidonic acid. PGs have numerous biological effects, including essential roles in platelet aggregation, neurotransmitter release, and inflammatory and vasomotor responses. Individual prostaglandins can have both positive and negative effects (i.e. pro-inflammatory or anti-inflammatory, vasodilatory or vasoconstrictive) depending upon their concentration, relative proportion to other prostaglandins and expression of receptor types. As prostaglandins are rapidly metabolised and have short half-lives, their metabolic effects are typically localised and can be variable in different parts of the body.
But niacin can be dangerous in high doses.
Eye Damage Linked to Popular Over-the-Counter Vitamin That Lowers Cholesterol Can Be Reversed
2019 PR the New York Eye and Ear Infirmary of Mount Sinai (NYEE)
Case report of near blindness due to 3-6 grams a day of niacin.
Dr. Owsley chemical treatment for CCSVICould this be a similar effect to niacin flush, chemically relaxing the vein stenosis/
Anna Macy has a blog on CCSVI. She's gotten relief by using massage and a TENS unit to relax her veins.
https://www.mscureenigmas.net/
Here is her blog on this drug treatment that Dr. Owsley in L.A. uses for both CCSVI and migraines
Dr. Owiesy did this in a study of 5 MS patients: A sterile mixture of medication dexamethasone/lidocaine/thiamine prepared and administered directly into the peri –venous space of internal jugular veins.
Dr Owiesy's Superior CCSVI Solution
Owlesy works in L.A. He also uses this technique for migraine, see the Migraine Cure link
Treatment for Migraine | Corona, California
Tags: MS, Epstein Barr Virus (EBV), CCSVI, Dr. Owiesy,, Hypoxia, Niacin Flush, LMP1, EBER1, Venous Stenosis