Doctors need to warn EBV patients to avoid sexual contact until they fully recover, Risk factor for CFS

[gbells]

One pet peeve I have about medical doctors is that they didn't warn me to stop nonmonogamous intimate contact until after I had fully recovered from Epstein Barr virus. CFS ME looks like it is actually a superinfection of HHV-6 post EBV infection during the acute or convalescent phases, up to 6 months post infection. For me kissing a sick girlfriend while I was still recovering from EBV was what triggered the CFS. Had the doctor warned me I could have recovered from the EBV and never developed CFS.

They still don't warn people. Everyone should eventually get a vaccine to prevent HHV-6 infection as kids, that would probably prevent a good deal of CFS patients from ever developing the disease.

 

[Rufous McKinney]

while I was still recovering from EBV was what triggered the CFS. Had the doctor warned me I could have recovered from the EBV and never developed CFS.

I can sure understand being really upset about that. Like this is trivial.

Similar with the blood transfusions. I had enough sense to NOT ever donate my blood to anyone but nobody much else gives a darn.

 

[linusbert]

Had the doctor warned me I could have recovered from the EBV and never developed CFS.

maybe, but most humans do have this kiss within the 6 month and dont get cfs.

imho, your body was already compromised and if that didnt trigger it, something else (maybe corona) would have.

 

[gbells]

maybe, but most humans do have this kiss within the 6 month and dont get cfs.

imho, your body was already compromised and if that didnt trigger it, something else (maybe corona) would have.

You aren't getting that the EBV allowed HHV6 to penetrate more cells than it normally could. The disease is a superinfection that requires EBV to start. EBV alone isn't enough to do it.

Simply having doctors warn patients to avoid intimate contact for six months after EBV infection would drastically cut down the CFS rates by avoiding the superinfection yet they aren't doing it. This makes the CDC, infectious disease doctors and primary care providers complicit to some extent in perpetuating the disease.

One would think that the government's interest in lowering the cases to prevent disability payments would motivate them to start warning patients.

 

[linusbert]

You aren't getting that the EBV allowed HHV6 to penetrate more cells than it normally could. The disease is a superinfection that requires EBV to start. EBV alone isn't enough to do it.

i am getting this very well.
but 90% of society are infected with EBV and a lot have EBV and HHV6 contact at the same time, and yet only a fraction become cfs... or not?

of course the doctors should do everything to reduce risks. its like with everything, reducing unnecessary risks should be taken into consideration, or at least the people informed so they can decide for themselves.
i compare this too smokers risk of getting bad diseases later on. smokers should know the risk, and in this ebvhhv6 connection case too.

the government has the interests of those who pay them. and those are the same people who make big cash with sick people.
there is no powerful rich lobby for healthy or sick people. only for the very rich and powerful.

 

[gbells]

but 90% of society are infected with EBV and a lot have EBV and HHV6 contact at the same time, and yet only a fraction become cfs... or not?

I think it's the timing. EBV convalescence must impair the immune system and create a reservoir for the HHV6. Normally, post EBV infection EBV is limited to the lymph tissues then the body recovers. However, to get to adaptive immunity with EBV antibodies it can take several months. HHV6 causes problems in people with low immune function. What appears to be happening is that EBV convalescence creates a larger reservoir for the HHV6. The likely mechanism is that the EBV makes infected cells more inflammatory due to upregulating Nf-kB, making them leaky and this opens up to cells that would normally be resistant to HHV6 colonization due to a lack of CD134.

So without superinfection EBV is limited to some cells and HHV6 to other cells but with coinfection all of them are vulnerable. The periostitis effects I am seeing in myself is likely HHV6 infected B cells and these would normally not be vulnerable..

the government has the interests of those who pay them. and those are the same people who make big cash with sick people.
there is no powerful rich lobby for healthy or sick people. only for the very rich and powerful.

The government hates having to pay disability claims. It should be highly motivated to find ways to reduce them. I wrote to a NIH official I know and proposed a dual infection animal study in monkeys to prove the hypothesis that EBV plus HHV6 cause CFS. Hopefully, they will do it.

Gene editing to inactivate the HHV6 is the way to cure this. DARPA has developed designer receptors. If they could tag the EBV cells and gene edit them to turn it off it should cure the mitochondral fragmentation and other CFS effect to return people to normal.

Dr. Charles Morgan on Psycho-Neurobiology and War​

Youtube. Modern War Institute.

see 32 min for designer receptors.

 

[linusbert]

So without superinfection EBV is limited to some cells and HHV6 to other cells but with coinfection all of them are vulnerable. The periostitis effects I am seeing in myself is likely HHV6 infected B cells and these would normally not be vulnerable..

yikes this is creepy.
i always assumed that the body when fighting one disease is in alert state and other disease would have it harder.

 

[JES]

I think it's the timing. EBV convalescence must impair the immune system and create a reservoir for the HHV6. Normally, post EBV infection EBV is limited to the lymph tissues then the body recovers. However, to get to adaptive immunity with EBV antibodies it can take several months. HHV6 causes problems in people with low immune function. What appears to be happening is that EBV convalescence creates a larger reservoir for the HHV6. The likely mechanism is that the EBV makes infected cells more inflammatory due to upregulating Nf-kB, making them leaky and this opens up to cells that would normally be resistant to HHV6 colonization due to a lack of CD134.

So without superinfection EBV is limited to some cells and HHV6 to other cells but with coinfection all of them are vulnerable. The periostitis effects I am seeing in myself is likely HHV6 infected B cells and these would normally not be vulnerable..

Interesting hypothesis, but what is the concrete evidence that this combination of viruses and their interaction is the thing causing ME/CFS in you and others? Doctors aren't going to make new recommendations based on hypotheses. Heck, doctors are lazy to make new recommendations even when the evidence sits straight in front of them.

If there is one thing that would be EBV related and possibly advance in the next decade is the link of EBV to MS. If that research goes further (and it already seems clear EBV is a necessary component in triggering MS), then what seems to be an obvious next step is to create a vaccine against EBV. That might also reduce the occurence of ME/CFS if it allowed your immune system to better deal with EBV than if unvaccinated.

Whether such a vaccine would help the patients who already got MS or ME/CFS is another question.

 

[gbells]

Interesting hypothesis, but what is the concrete evidence that this combination of viruses and their interaction is the thing causing ME/CFS in you and others?

These findings suggest this is going on:
1. History of a subset of CFS patients having EBV and HHV6.
2. These patients having EBV antibodies turn negative but HHV6 positive, hinting at an interaction in the same cells which normally wouldn't happen because they target different receptors.
3. Periosteal reaction in long bones during apoptosis indicating that it's B cells, a target of EBV, but the EBV antibody test is negative and EBV history positive.

This is new ground. I don't think any cellular biologists have ever looked at cells infected with both viruses.

Some viruses that can block the replication of other viruses. For example, pre-infection with a different respiratory tract virus such as a cold virus inhibited SARS-CoV-2 replication, suggesting that interactions between viruses may influence their replication.

Epstein-Barr virus (EBV) and Human herpesvirus-6 (HHV-6) are both members of the herpesvirus family and share some similarities. For example, both viruses establish latency in lymphocytes and possess a strong immunomodulatory capacity that can trigger both immunosuppressive and chronic inflammatory pathways.

Because they are both from the herpesvirus family, HHV6 could block EBV. Virologists just never thought to study it because they targeted different types of cells.

f there is one thing that would be EBV related and possibly advance in the next decade is the link of EBV to MS. If that research goes further (and it already seems clear EBV is a necessary component in triggering MS), then what seems to be an obvious next step is to create a vaccine against EBV. That might also reduce the occurence of ME/CFS if it allowed your immune system to better deal with EBV than if unvaccinated.

I don't think a EBV vaccine is being developed. However a HHV-6b vaccine has been developed by a Japanese researcher. That would also prevent it. However, it won't cure already infected SEID patients.

I researched out to the researcher to discuss the connection and any potential interest in research. I'm also keeping OMF in the loop for funding.