Epstein Barr Virus has been a topic of conversation for many decades. Both in medical literature and average discussion, this creature has received a great deal of attention.
It has been called The Yuppie Flu, Chronic Fatigue Syndrome, Mono, and an insignificant bug that everyone has been exposed to. There is a lot of misinformation being passed around by both lay persons and the medical community.
In looking at peer review, legitimate medical research this creature is anything but insignificant.
It has been linked with almost a dozen different CANCERS, ATHEROSCLEROSIS, MS, LUPUS, MENINGITIS, MYELITIS AND SEVERE FATIGUE.
The following articles support this.
This is not a creature to be taken lightly.
Yes it is common to be exposed to it, and most of the population has been. But if it lingers, and exists in combination with a weakened or damaged immune response, then risk for disaster is far greater.
It is a member of the Herpesvirus family, yet rarely causes a skin outbreak or rash. Sometimes when EBV is active and people take antibiotics a viral exanthem (rash) will occur.
Because its life cycle is generally asymptomatic, and can lay dormant in the body for years and the fact that it is difficult for the average person to understand or realize, it is a major threat to our good health.
For almost 20 years, I have been testing specifically for EBV , especially in patients with fatigue, heart disease and recurrent infection. In so many of these cases the creature exists and is thriving.
I always recommend testing a 5 antibody panel to accurately see if the organism is actively multiplying, and will recommend skin testing to evaluate immune response.
The best of mechanisms to help kill it include IV vitamins and immune stimulating protocols.
It has become ever important to aggressively look for organisms and address them before serious medical conditions appear.
Thanks,
Dr. Chris Calapai
Relapsing acute disseminated encephalomyelitis associated with chronic Epstein-Barr virus infection: MRI findings.
Summary A 25-year-old women had a fever, left cervical lymphadenopathy, neurological symptoms and signs, CSF pleocytosis and persistent high serum antibodies to the Epstein-Barr virus (EBV); she had a recurrence 1 year later. She was thought to have relapsing acute disseminated encephalomyelitis associated with chronic EBV infection. MRI revealed abnormalities, mainly in the right basal ganglia and left midbrain. At the time of the recurrence, further abnormalities appeared in the opposite basal ganglia and right cerebral white matter.
Epstein-Barr virus and the nervous system.
The neurological complications of Epstein-Barr virus infection include viral meningitis, encephalitis and neuromuscular complications. The introduction of cerebrospinal fluid polymerase chain reaction for Epstein-Barr virus DNA has improved diagnosis of these conditions and of primary central nervous system lymphoma in acquired immune deficiency syndrome, and has enabled cerebrospinal fluid monitoring of .
Prognosis remains good for most Epstein-Barr virus-related neurological complications; for primary central nervous system lymphoma in acquired immune deficiency syndrome the prognosis is still poor.
Encephalomyeloradiculopathy associated with Epstein-Barr virus: primary infection or reactivation?
INTRODUCTION: Encephalomyeloradiculopathy (EMR) is a new syndrome, characterized by extensive involvement of the nervous system at different levels, including brain, medulla and spinal roots. We describe a patient presenting with prodromal febrile illness, followed by a wide infection of the nervous system with transverse myelitis and less severe meningitis, encephalitis and polyradiculopathy. The patient was treated with high-dose corticosteroids, antibiotics and acyclovir; in spite of his condition improved very slowly, with severe neurological sequelae.
MATERIAL AND METHODS: Antiviral antibodies were searched for in serum and cerebrospinal fluid (CSF) by commercially available ELISA kits. Viral investigations were performed by cell culture isolation and search for viral antigens, and genomic nucleic acids were investigated by polymerase chain reaction (PCR).
RESULTS: Virological and serological studies evidenced a primary infection by cytomegalovirus (CMV), possibly responsible for the prodromal illness, persisting in the course of the disease. PCR performed in the peripheral blood mononuclear cells (PBMCs), DNA collected early and in the CSF drawn 30 days after the onset of the disease showed Epstein-Barr virus (EBV) DNA. The serum panel of EBV antibodies was typical of an intercurrent virus reactivation, more than of a primary infection.
CONCLUSION: EBV is known to be highly infectious for the nervous system, in this case of EMR the presence of DNA sequences in the PBMCs and CSF suggests that EBV plays a role in the development of this newly described syndrome.
Gastric Carcinoma: Monoclonal Epithelial Malignant Cells Expressing Epstein-Barr Virus Latent Infection.
In 1000 primary gastric carcinomas, 70 (7.0%) contained Epstein-Barr virus (EBV) genomic sequences detected by PCR and Southern blots. The positive tumors comprised 8 of 9 (89%) undifferentiated lymphoepithelioma-like carcinomas, 27 of 476 (5.7%) poorly differentiated adenocarcinomas, and 35 of 515 (6.8%) moderately to well-differentiated adenocarcinomas.
In situ EBV-encoded small RNA 1 hybridization and hematoxylin/eosin staining in adjacent sections showed that the EBV was present in every carcinoma cell but was not significantly present in lymphoid stroma and in normal mucosa.
Two-color immunofluorescence and hematoxylin/eosin staining in parallel sections revealed that every keratin-positive epithelial malignant cell expressed EBV-determined nuclear antigen 1 (EBNA1) but did not significantly express CD45+ infiltrating leukocytes.
A single fused terminal fragment was detected in each of the EBNA1-expressing tumors, thereby suggesting that the EBV-carrying gastric carcinomas represent clonal proliferation of cells infected with EBV. The carcinoma cells had exclusively EBNA1 but not EBNA2, -3A, -3B, and -3C; leader protein; and latent membrane protein 1 because of methylation.
The patients with EBV-carrying gastric carcinoma had elevated serum EBV-specific antibodies. The EBV-specific cellular immunity was not significantly reduced; however, the cytotoxic T-cell target antigens were not expressed. These findings strongly suggest a causal relation between a significant proportion of gastric carcinoma and EBV, and the virus-carrying carcinoma cells may evade immune surveillance
Detection of Epstein-Barr Virus in Invasive Breast Cancers.
BACKGROUND: Epstein-Barr virus (EBV) may be a cofactor in the development of different malignancies, including several types of carcinomas. In this study, we investigated the presence of EBV in human breast cancers.
METHODS: We used tissues from 100 consecutive primary invasive breast carcinomas, as well as 30 healthy tissues adjacent to a subset of the tumors. DNA was amplified by use of the polymerase chain reaction (PCR), with the primers covering three different regions of the EBV genome. Southern blot analysis was performed by use of a labeled EBV BamHI W restriction fragment as the probe. Infected cells were identified by means of immunohistochemical staining, using monoclonal antibodies directed against the EBV nuclear protein EBNA-1.
RESULTS: We were able to detect the EBV genome by PCR in 51% of the tumors, whereas, in 90% of the cases studied, the virus was not detected in healthy tissue adjacent to the tumor (P<.001). The presence of the EBV genome in breast tumors was confirmed by Southern blot analysis. The observed EBNA-1 expression was restricted to a fraction (5%-30%) of tumor epithelial cells. Moreover, no immunohistochemical staining was observed in tumors that were negative for EBV by PCR. EBV was detected more frequently in breast tumors that were hormone-receptor negative (P = .01) and those of high histologic grade (P = .03). EBV detection in primary tumors varied by nodal status (P = .01), largely because of the difference between subjects with more than three lymph nodes versus less than or equal to three lymph nodes involved (72% versus 44%).
CONCLUSIONS: Our results demonstrated the presence of the EBV genome in a large subset of breast cancers. The virus was restricted to tumor cells and was more frequently associated with the most aggressive tumors. EBV may be a cofactor in the development of some breast cancers.
Epstein–Barr Virus — Increasing Evidence of a Link to Carcinoma.
In this issue of the Journal, Pathmanathan et al.1 add a new dimension to the etiologic link between Epstein–Barr virus (EBV) infection and anaplastic nasopharyngeal carcinoma. Genetic and environmental factors have also been implicated in nasopharyngeal carcinoma.2 In southern Chinese and some North African and Native American populations, it is a common cancer that causes substantial morbidity and mortality, even among young people. Although the carcinoma usually responds to radio , recurrences are frequent and difficult to treat.
Microorganisms in the aetiology of atherosclerosis.
Recent publications have suggested that infective pathogens might play an important role in the pathogenesis of atherosclerosis. This review focuses on these microorganisms in the process of atherosclerosis. The results of in vitro studies, animal studies, tissue studies, and serological studies will be summarised, followed by an overall conclusion concerning the strength of the association of the microorganism with the pathogenesis of atherosclerosis.
The role of the bacteria Chlamydia pneumoniae and Helicobacter pylori, and the viruses human immunodeficiency virus, coxsackie B virus, cytomegalovirus, Epstein-Barr virus, herpes simplex virus, and measles virus will be discussed.