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 August 2nd, 2021

Long Covid and its association with Epstein Barr Virus, EBV, reactivation

The article notes that a 6.7x increase in EBV reactivation in long COVID patients based on antibody titer measurements. We do not know if EBV is driving the long COVID so much as a reflection of the inadequate immune T helper cell activity that should be present in immune solvent individuals attempting to clear a viral pathogen. It has been shown in different studies over the past year that individuals with poor T cell activity, TH1, Natural killer cells, NK and poorly polarized macrophages, MAC2, are at increased risk for a worse COVID morbidity and/or mortality outcome.

The science: My friend, Dr. Sam Yanuck, writes: We could imagine the patient’s Th1 system becoming suppressed in several ways, leading to expansion of EBV burdens, even in a patient who had managed to eradicate SARS-CoV-2 from their system. 1) GI or respiratory involvement of COVID-19 would be expected to increase epithelial inflammatory activation, driving Th2-promoting cytokines, at the expense of Th1, 2) stress chemistry from the biological and psychological stresses of COVID-19 infection would be expected to induce apoptosis, programmed cell death, of Th1 cells and NK cells, and 3) inflammatory effects from COVID-19 would be expected to upregulate MDSC’s, myeloid derived suppressor cells, driving down Th1 response. In this third option, we would expect to see high TGFβ. There are likely plenty of other ways to get to low Th1, given the moving parts involved in SARS-CoV-2 infection.

If a patient is suffering from COVID but survives, it is highly possible and likely that the immune system was so tasked fighting the SARS2 virus that the ability to tackle the indolent EBV virus is compromised allowing for a resurgence and a chronic fatigue fighting state to ensue. This is hypothetical only but plausible based on the fact that SARS2 does suppress immune viral killing capacity and herpes virus sit dormant in many of us waiting for a time of stress to reactivate from dormancy. EBV is known to infect and become indolent in over 90% of Americans. The measurement of a biomarker is NOT conclusion of cause and effect. However, there are patients that appear to have long COVID and feel well when they are on an antiviral medicine that theoretically contains EBV's growth. More time and data will answer these questions, yet, I am aligned with the physiological premise that our stress chemistry, nutritional chemistry and microbiome are somehow driving a dysregulated immune activation and response leading to a chronic brain fog and fatigue state that we are calling long covid.

Very important to search for clues as to why so many people are suffering from prolonged post COVID symptoms. This is just the beginning,

Dr. M

Gold Pathogens