Long COVID and severe COVID-19 infections associated with Epstein-Barr virus reactivation

[2Cor.12:19]

"“We ran Epstein-Barr virus serological tests on COVID-19 patients at least 90 days after testing positive for SARS-CoV-2 infection, comparing EBV reactivation rates of those with long COVID symptoms to those who never experienced long COVID symptoms,” says lead study author Jeffrey E. Gold of World Organization in a media release. “We found over 73% of COVID-19 patients who were experiencing long Covid symptoms were also positive for EBV reactivation.” Long COVID and severe COVID-19 infections associated with Epstein-Barr virus reactivation
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1. Investigation of Long COVID Prevalence and Its Relationship to Epstein-Barr Virus Reactivation by Jeffrey E. Gold 1,*, Ramazan A. Okyay 2, Warren E. Licht 3 and David J. Hurley
2. Positive Epstein–Barr virus detection in coronavirus disease 2019 (COVID-19) patients Ting Chen,#1 Jiayi Song,#1 Hongli Liu,1 Hongmei Zheng,1 and Changzheng Chencorresponding author

 

[Woof!]

Wow. One door opening...

 

[Pyrrhus]

Investigation of Long COVID Prevalence and Its Relationship to Epstein-Barr Virus Reactivation by Jeffrey E. Gold 1,*, Ramazan A. Okyay 2, Warren E. Licht 3 and David J. Hurley

Abstract:

Coronavirus disease 2019 (COVID-19) patients sometimes experience long-term symptoms following resolution of acute disease, including fatigue, brain fog, and rashes. Collectively these have become known as long COVID.

Our aim was to first determine long COVID prevalence in 185 randomly surveyed COVID-19 patients and, subsequently, to determine if there was an association between occurrence of long COVID symptoms and reactivation of Epstein–Barr virus (EBV) in 68 COVID-19 patients recruited from those surveyed.

We found the prevalence of long COVID symptoms to be 30.3% (56/185), which included 4 initially asymptomatic COVID-19 patients who later developed long COVID symptoms. Next, we found that 66.7% (20/30) of long COVID subjects versus 10% (2/20) of control subjects in our primary study group were positive for EBV reactivation based on positive titers for EBV early antigen-diffuse (EA-D) IgG or EBV viral capsid antigen (VCA) IgM. The difference was significant (p < 0.001, Fisher’s exact test). A similar ratio was observed in a secondary group of 18 subjects 21–90 days after testing positive for COVID-19, indicating reactivation may occur soon after or concurrently with COVID-19 infection.

These findings suggest that many long COVID symptoms may not be a direct result of the SARS-CoV-2 virus but may be the result of COVID-19 inflammation-induced EBV reactivation.

Positive Epstein–Barr virus detection in coronavirus disease 2019 (COVID-19) patients Ting Chen,#1 Jiayi Song,#1 Hongli Liu,1 Hongmei Zheng,1 and Changzheng Chencorresponding author

Abstract:

The objective of this study was to detect the Epstein–Barr virus (EBV) coinfection in coronavirus disease 2019 (COVID-19). In this retrospective single-center study, we included 67 COVID-19 patients with onset time within 2 weeks in Renmin Hospital of Wuhan University from January 9 to February 29, 2020.

Patients were divided into EBV/SARS-CoV-2 coinfection group and SARS-CoV-2 infection alone group according to the serological results of EBV, and the characteristics differences between the two groups were compared. The median age was 37 years, with 35 (52.2%) females.

Among these COVID-19 patients, thirty-seven (55.2%) patients were seropositive for EBV viral capsid antigen (VCA) IgM antibody. EBV/SARS-CoV-2 coinfection patients had a 3.09-fold risk of having a fever symptom than SARS-CoV-2 infection alone patients (95% CI 1.11–8.56; P = 0.03). C-reactive protein (CRP) (P = 0.02) and the aspartate aminotransferase (AST) (P = 0.04) in EBV/SARS-CoV-2 coinfection patients were higher than that in SARS-CoV-2 infection alone patients. EBV/SARS-CoV-2 coinfection patients had a higher portion of corticosteroid use than the SARS-CoV-2 infection alone patients (P = 0.03).

We find a high incidence of EBV coinfection in COVID-19 patients. EBV/SARS-CoV-2 coinfection was associated with fever and increased inflammation. EBV reactivation may associated with the severity of COVID-19.

 

[SWAlexander]

My eyes are cloudy today and I can´t read anything or write much, so I listen to this Epstein–Barr virus presentation:
"Reactivated Viruses Causing Chronic Fatigue Syndrome and Long-Haul COVID-19" https://play.acast.com/s/smartest-d...uses-causing-chronic-fatigue-syndrome-and-lon

 

[2Cor.12:19]

@SWAlexander - thanks for sharing!

 

[Rufous McKinney]

I can´t read anything or write much, so I listen to this

Me, too!

I listened to part of this yesterday. Amy's story of her childhood sounded almost just like my version.

Except Amy got her ME treated and Amy is now well. She certainly speaks rapidly.

And I have not, over the last 68 years, solved my medical mystery. So I am sharing this made me feel bad, and like I am some type of failure, unable to work a medical system, unable to get any help or meaningful treatments.

so just sharing my petty, unevolved emotional response.

Its just wonderful we have this amazing motivated smart person working on our troubles.

 

[Tammy]

Makes a lot of sense to me.

 

[SWAlexander]

Epstein-Barr Virus May Be Leading Cause of Multiple Sclerosis
Multiple sclerosis (MS), a progressive disease that affects 2.8 million people worldwide and for which there is no definitive cure, is likely caused by infection with the Epstein-Barr virus (EBV), according to a study led by Harvard T.H. Chan School of Public Health researchers.

Their findings will be published online in Science on January 13, 2022.

“The hypothesis that EBV causes MS has been investigated by our group and others for several years, but this is the first study providing compelling evidence of causality,” said Alberto Ascherio, professor of epidemiology and nutrition at Harvard Chan School and senior author of the study.

“This is a big step because it suggests that most MS cases could be prevented by stopping EBV infection, and that targeting EBV could lead to the discovery of a cure for MS.”

MS is a chronic inflammatory disease of the central nervous system that attacks the myelin sheaths protecting neurons in the brain and spinal cord. Its cause is not known, yet one of the top suspects is EBV, a herpes virus that can cause infectious mononucleosis and establishes a latent, lifelong infection of the host.

Establishing a causal relationship between the virus and the disease has been difficult because EBV infects approximately 95% of adults, MS is a relatively rare disease, and the onset of MS symptoms begins about ten years after EBV infection.
https://neurosciencenews.com/epstein-barr-multiple-sclerosis-19908/

 

[Husband of]

So how do they tell reactivation? More antibodies and antigens? Is it just a threshold that they assume means reactivation? Would you expect more antibodies in a person with an overactive immune system? Is this any different to the old studies showing the same for ME? And also showing the same for ME with hhv6 and coxsackie b?

 

[SWAlexander]

So how do they tell reactivation? More antibodies and antigens? Is it just a threshold that they assume means reactivation? Would you expect more antibodies in a person with an overactive immune system? Is this any different to the old studies showing the same for ME? And also showing the same for ME with hhv6 and coxsackie b?

Researchers have several ideas about why this happens. "It’s clear that genetics play a role in autoimmune disease, but researchers still don’t fully understand how. For example, having a family member with lupus or multiple sclerosis (MS) raises your risk of getting these diseases. Some families have multiple members affected by different autoimmune diseases. However, genetics alone isn’t enough to cause autoimmune disease."
“We know that genes are important, but they aren’t everything,” Orbai says. “You can have family members with lupus or MS and never get them yourself. You can even test positive for lupus-specific DNA and still not have the disease.”
"It’s possible that autoimmune disease occurs based on the immune system’s ability to handle stress. Orbai says that this is an area of intense research. “When does the stress on your body exceed your immune system’s ability to handle it? If we knew this, it could be the key to preventing autoimmune disease before it develops.”
https://www.hopkinsmedicine.org/hea...ease-why-is-my-immune-system-attacking-itself

 

[Learner1]

So how do they tell reactivation? More antibodies and antigens? Is it just a threshold that they assume means reactivation? Would you expect more antibodies in a person with an overactive immune system? Is this any different to the old studies showing the same for ME? And also showing the same for ME with hhv6 and coxsackie b?

A positive PCR test. I had EBV and HHV6 PCR tests before and after my COVID vaccines - HHV6 was negative before but positive after. Zoster is also known to be reactivated and I wouldn't be surprised if all herpesviruses reactivated. I also had HHV6 and EBV reactivate after my cancer treatment, triggering my ME/CFS.

 

[SWAlexander]

Rogue antibodies could be driving severe COVID-19
Evidence is growing that self-attacking ‘autoantibodies’ could be the key to understanding some of the worst cases of SARS-CoV-2 infection.
https://www.nature.com/articles/d41586-021-00149-1

 

[Violeta]

SarS-CoV-2 induces oxidative stress.

SARS-CoV-2 infection pathogenesis is related to oxidative stress as a response to aggression

https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC7357498/
Rubens Cecchini


Oxidative stress favors herpesvirus

Oxidative stress favours herpes virus infection in vertebrates: a meta-analysis
Manrico Sebastiano
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC5829443/

From the first study: "Finally, we suggest a therapeutic strategy to reduce oxidative stress using antioxidants, NF-κB inhibitors, Nrf2 activators, and iron complexing agents. We believe that this hypothesis can guide new studies and therapeutic strategies on this topic."

 

[Violeta]

Does the intracellular cytopathic hypoxia cause disfunctional mitochondria, or vice versa?

 

[Ethereal55]

A positive PCR test. I had EBV and HHV6 PCR tests before and after my COVID vaccines - HHV6 was negative before but positive after. Zoster is also known to be reactivated and I wouldn't be surprised if all herpesviruses reactivated. I also had HHV6 and EBV reactivate after my cancer treatment, triggering my ME/CFS.

This is actually a subject that has sadly not really been defined, nor researched much in the West.

The common antibody panel doctors use are the VCA IgM (indicating new or current infection), VCA IgG (indicating past infection) Early Antigen (indicating reactivation mainly, if persistently high in combination with symptoms) and EBNA ( indicating recent infection in the past mainly).

The PCR however is mainly used to detect the amount of copies in your serum, and if positive, might be indicative of CAEBV, however here is where it gets complicated and where we are in desperate need for more research and clarification of this disease/phenomenon by the medical community, which is largely ignored.

CAEBV(chronic active Epstein Barr virus) is a distinct disease in Asia, where it should be more correctly referred to as Severe CAEBV, PCRs in that are positive with copies in the hundreds of thousands often, and that over a period of several months. After researching, there are VERY few studies on this, but the common thread i can see is that it is believed that what we in the West are often experiencing as EBV "reactivation" where people cannot get rid of EBV, is actually either 1) the same entity as severe CAEBV in Asia, only a lot "milder", so call it mild CAEBV if you will or 2) a different entity alltogether.

Personally i am leaning towards 1, because given enough time, the fact that EBV is completely out of control in our organism over years WILL lead to autoimmune disease and cancer inevitably, as a lot of data is now coming out clearly demonstrating the correlation between EBV acting as a trigger for so many different AI diseases and cancers.

Medical science will take decades to catch up to this until large studies have been made to establish this link in a proven scientific way. Until then, we are on our own unfortunately. And i personally have not found a ("serious") doctor yet, even willing to entertain this notion, save prescribing antivirals or other methods to combat this issue, which is a damn shame to say the least.

 

[Learner1]

@Ethereal55
I totally agree, and think you are right about #1.

The best we can do is to bring information to our doctors and make sure we get tested for antibodies and PCR, more than once.

One thing to realize is that EBV antibody testing is done to "stage" the disease IN THE IMMUNOCOMPETENT. If you are immunodeficient, as I was, you may not be producing antibodies. There is only one set of antibodies, to my knowledge for the other herpesviruses, so staging may not make sense and the PCR is more definitive for a doubting doctor. But, the virus may be in the tissue and not the bloodstream at any given point, so repeating the tests would be wise.

Then, once diagnosed, there's the battle of getting treatment.

 

[Ethereal55]

@Ethereal55
I totally agree, and think you are right about #1.

The best we can do is to bring information to our doctors and make sure we get tested for antibodies and PCR, more than once.

One thing to realize is that EBV antibody testing is done to "stage" the disease IN THE IMMUNOCOMPETENT. If you are immunodeficient, as I was, you may not be producing antibodies. There is only one set of antibodies, to my knowledge for the other herpesviruses, so staging may not make sense and the PCR is more definitive for a doubting doctor. But, the virus may be in the tissue and not the bloodstream at any given point, so repeating the tests would be wise.

Then, once diagnosed, there's the battle of getting treatment.

By immunodeficient in your case i assume you mean things like hypogammaglobulinemia where you are unable to produce antibodies in general (PIDs like CVID etc.) right? Because in my case for example i am definitely not immunocompetent (T&B Cell deficiency) but i DO produce Antibodies.
In that case yes, it would not make sense to test those panels. In a lot of cases though where people do produce antibodies, most doctors still have no idea what to do with them because there is simply next to nothing in the literature and they were not educated about it.

Have you managed to get your EBV treated then in the meantime?

 

[Learner1]

By immunodeficient in your case i assume you mean things like hypogammaglobulinemia where you are unable to produce antibodies in general (PIDs like CVID etc.) right? Because in my case for example i am definitely not immunocompetent (T&B Cell deficiency) but i DO produce Antibodies.
In that case yes, it would not make sense to test those panels. In a lot of cases though where people do produce antibodies, most doctors still have no idea what to do with them because there is simply next to nothing in the literature and they were not educated about it.

Have you managed to get your EBV treated then in the meantime?

Valcyte for several months worked well. I had HHV6 and CMV, too.