Epstein-Barr virus: The master of disguise

Most of us carry the Epstein-Barr virus (EBV) but many have never heard of it and fewer still know what it actually is. You may know of it as the Glandular Fever virus. When I was at university in the 70s it was known as the ‘Kissing Virus’ or ‘College Virus’ because most people contracted it through their social activities. Some developed chronic fatigue after an initial infection and were forced to drop out of their courses, while some others never fully recovered the health they had before kissing their classmates.
Epstein-Barre Virus diagram.
The sequence of events leading to the discovery of the Epstein-Barr virus (Human herpesvirus-5), as well as its role in many cancers and autoimmune diseases, is an interesting story. Even today the story is far from complete as its association with various cancers and autoimmune diseases unfolds.
In 1958 Dr Denis Burkitt recognised and described the characteristics of a new tumour that was only occurring in malaria zones of equatorial Africa.  He postulated that possibly an insect born infectious agent was involved in the creation of the tumour. In 1961 Dr Denis Brukitt sent tumour samples to Dr Tony Epstein who together with Dr Yvonne Barr succeeded in culturing a number of the individual lymphoma cells from the tumours and clearly found herpes particles. Hence the virus was named after these two researchers and this was the first time a virus had been directly associated with tumour formation. (Poor Burkitt didn’t get a mention, so he had a cat fight with the other two and they therefore let him name the tumour he found).
In the next few years it became evident that EBV was widespread in all human populations. In most individuals, EBV concentrates in the epithelial mucosal tissue of the throat, is dormant or undergoes low-grade activity in the immune system’s B-cells, and can be found in almost all of the human body’s organ cells.
EBV is a human herpesvirus. Eight types of human herpesviruses have been discovered so far. Most people know of the cold-sore virus (humanherpes-1) or the chickenpox virus (zoster), and the genital herpes virus (humanherpes-2). These viruses are not regarded as any great threat to health, but the other five herpes viruses, including EBV, appear to be potentially lethal when a person’s immune system is compromised.
The human herpesviruses, once in a body, stay there for life. They can infect at any time from birth to old age and always have the ability to reactivate from a state of dormancy to one of rapid infection when the immune system is weakened—then they can cause both acute and chronic symptoms. The conflict between the immune system and these viruses continues throughout life. People who maintain strong immune systems do not experience illnesses due to these viruses.
Human herpesviruses are parasites. They have been infecting our species for many thousands of years, and have evolved some very sophisticated methods to evade and subvert our immune systems. An efficient parasite has no intention of killing the host—their aim is to weaken the defence system so that the host lives a reasonably long life, in poor health. This is achieved by masking the parasite’s true identity, forcing the immune system to squander resources (against other pathogens or the host itself) and subverting and/or manipulating the defence cells. Human herpesviruses interact with each other and have the capacity to use other viruses, such as influenza, to mask their activity from immune system cells.
To understand herpesvirus behaviour, think about the strategies that a spy uses to survive in a foreign country, gather information, and send it out to another country. After herpesviruses infect a person, they aim to replicate, consolidate their infection, and transfer to a new host—similar to the actions of a spy.
To be a successful spy the spy’s true identity needs to be concealed from the authorities. A fake identity, or many identities, indicating the spy is a native citizen would have to be created. If the spy can wipe-out any records of their identity, they can live for life in the host country and continue their nefarious activity. An emergency hiding place, or one where the authorities would never look, would be essential. Blackmailing or bribing the authorities would have its advantages. Having emergency escape plans prepared in case of detection helps survival. A cunning spy might even establish a position as a policeman in the very government organisation established to catch spies.
To be a successful infecting virus and conceal in which cells they are living, herpesviruses change the cell surface identity molecules that are normally present when cells are infected. Some herpesviruses are able to live in the host for life with impunity, because they alter the primary mechanism that instructs immune cells (CD-8 T-cells) to look for particular viruses.  When the immune system detects herpesvirus activity and begins a campaign of focused activity, the herpesviruses change into a dormant life stage which prevents their detection.
Some types of herpesviruses infect nerve cells (including the brain cells) that the immune system will not destroy—in theory because the body cannot replace them.
Herpesviruses subvert the identifying receptors of the immune cells searching for them, so that they cannot recognise these viruses. Herpesviruses alter the adhesion molecules on cells to prevent the immune cells holding on tight to the cell to inject cytokine toxins to kill the cell with the virus colony. Herpesviruses such as EBV  change the replicating codes of B-lymphocyte cells so that they will increase replication and provide more ‘homes’ for their expanding population.
General traits of human herpesviruses:

  • They have latent phases and active phases throughout the entire life of the host person.
  • They evade, subvert, and manipulate immune cells and other pathogens.
  • They are linked with more than 50% of all cancers.
  • They are considered the main cause of many autoimmune diseases.
  • They transfer easily between human hosts through fluids like tears, urine, saliva, lymph and blood.
  • A strong immune system shuts down the herpesviruses.
  • Herpes viruses need only a small gene pool to survive and, unlike other viruses such as influenza, do not have to change their genetic makeup to survive immune identification and attack.

When we are initially infected with EBV, we respond in different ways as our immune system attempts to contain it. Most people experience almost no symptoms, while the rest experience mild symptoms of glandular fever which include flu-like responses, skin rashes, headaches, general aches-pains, and lethargy—all of which stop after several weeks. Some individuals in this latter group experience ongoing fatigue with recurring flu-like symptoms for several months before regaining normal health. Some go on to develop an autoimmune disease without recurring post-viral symptoms. A smaller number develop an autoimmune disease, recurring post-viral symptoms and one of the EBV related cancers.
In underdeveloped countries, the most common cause of weakened immune systems is malnutrition and almost all preadolescent children are infected with EBV. In developed countries, EBV infection occurs in later years probably due to emotional stress, inconsistent sleep, immune-weakening foods and drug abuse.
Because herpes viruses infect and subvert so many different types of immune cells, manipulate other pathogens, and are linked to such a wide variety of terminal diseases, they are considered by many researchers to be the most dangerous of the human viruses when a person’s immune system is weakened.
The good news is that your body has an amazing ability to successfully shut down these viruses.  We have used a successful protocol for decades to help thousands of people strengthen their immune system and shut down all types of herpesvirus activity to regain excellent health. This protocol unloads the immune system and refocuses T-cell activity to the offending virus. Contact us to find out more or download the e-book No More Chronic Fatigue.