Discussion about Lehrner's abortive infection hypothesis

gbells

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I'm writing this post to see if anyone has any insight into abortive infections. Researcher Dr. Lehrner put forth the hypothesis that he felt SEIDs was actually the result of persistent infections (EBV, HHv6, CMV) that are difficult to diagnose because they can't replicate. I think this is an excellent theory. If someone has one infection during the period of time before antibodies are made then another different infection exposure then the combination would allow infections to spread more rapidly through the body. Once the body could make antibodies the spread of these infections should be checked however infected cells would still stay infected, be inflammed and painful which would be the source of the CFS symptoms. It is very common that EBV and other viruses stay dormant in the body after an initial infection. I think this is an excellent hypothesis for the cause of SEIDs.
 

Wishful

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Counterevidence: ME can switch state between healthy and full symptoms over the space of hours if not less. Hidden viruses don't seem to fit that time frame.
 

Wishful

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@Hip do you think the abortive infection theory can fit the time frame for temporary remissions? I don't really have a good feel for the time frames for immune system responses. How likely is it that the body's response to abortive infections can abruptly switch state, and a few hours later, switch back again?
 

Hip

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How likely is it that the body's response to abortive infections can abruptly switch state, and a few hours later, switch back again?
Temporary remissions seem very rare; personally I've never experienced one, my ME/CFS is very stable.

The ones I heard about seem more like a clearing of brain fog; I am not sure if any other ME/CFS symptoms cleared up during these remissions.
 
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Wishful

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I had probably more than half a dozen temporary remissions. They seemed like full remissions: I felt completely healthy again, and, after being ill, felt bouncy with energy. Other people here have reported temporary remissions, particularly after taking one of the cortisol drugs. I had temporary remission from my first and second trial of prednisone, lasting the duration of the course (took 5 days for the first course to trigger remission; 2 for the second). I also triggered remissions from the first couple of iodine supplements and T2 supplements. In the early part of my ME, I had several remissions with no identified trigger.

So yes, temporary full remissions do seem to occur, and it's an abrupt switch of states. I've posted a poll asking about it.
 

Hip

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I was referring to spontaneous remissions, rather than remissions achieved from drugs. I had a near remission for 2 weeks from Wellbutrin, my mind became really clear, then it just stopped working.
 

Wishful

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Well, it's hard to tell whether my remissions from unidentified triggers were actually spontaneous, or if they were triggered by something I ate. Hard to tell whether the artificial colouring or preservative in something isn't an effective trigger for biological changes. Thus no one can guarantee that any 'spontaneous' remission is actually different from one from a known trigger.
 

Hip

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Thus no one can guarantee that any 'spontaneous' remission is actually different from one from a known trigger.
Sure, a spontaneous remission must have some cause, even if that cause is unknown. All I am saying is that these spontaneous remissions are quite rare, from what I have read on these forums. People report them happening only once or twice in a decade, or not all.

Dr Goldstein's top 23 ME/CFS drugs however were well known for creating flash in the pan temporary remissions. In that respect, I think his treatments were somewhat gimmicky: they looked like they worked, but they never panned out long term.

My own temporary remission was from Wellbutrin, which is one of those 23 drugs.
 
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Wishful

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I had several spontaneous remission in the first few months of my ME. Each time I thought that whatever I had had finally been dealt with...and then the symptoms would return the next day. Possibly the type IV sensitivity kept retriggering my ME. The time between remissions kept increasing, until they stopped. Then I had several more remissions from the treatments I listed in the poll. I haven't managed to have another since the T2, quite a few years ago. *sigh* Remissions feel so wonderful. :angel:

It would be nice if there were some relatively reliable triggers, so most PWME could at least experience one remission. It's very good for giving hope for a cure.
 

sb4

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I had 2 very short lived (1-2 days) remissions very early on, they proceeded dietary changes (cutting out cheese, and then fodmaps). I went out drinking very soon after both times and woke up the next morning with symptoms returned.
 

Wishful

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My guess about the early-stage remissions is that ME involves some two-state switch (positive feedback loop), and at some point in our lives, changes occur which pull the switch more towards the ME state. In the early stages, random fluctuations might be strong enough to flip the switch occasionally. The bias towards the ME state grows stronger, and spontaneous flips become less likely. Later, some things can still flip the switch, but something seems to adapt to prevent it from working again.
 

Hip

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I had several spontaneous remission in the first few months of my ME.
I've seen it mentioned that some patients experience a relapsing-remitting onset, where there are initially large ups and downs in symptom severity, before their ME/CFS eventually settles into a steady state.



I just found this paper, which says that 7% of patients report a relapsing-remitting course to their ME/CFS, where as 59% report their illness persists with little change.
 

Sidny

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Well when you think about it, the very nature of Human herpes viruses like HSV,EBV, HHV6 is a “relapsing remitting” existence. Usually “latent” but with periodic reactivation throughout the life of the host. Not to mention much work pointing in the direction that even during latency they are interfering with host cell metabolic functions.

Back to the topic of this thread, it seems like the late Dr Martin Lerner isnt alone in his theory of abortive herpes virus contributing to ME/CFS.

http://simmaronresearch.com/tag/dutpase/


It’s not that the virus is reactivating; in fact, they believe the virus may be most dangerous in ME/CFS when it fails to reactivate properly and produces kind of a very low-level, smoldering infection. Even as the immune system in people with ME/CFS is mostly smothering EBV, the virus is producing a protein that’s causing harm.
It turns out that in herpesviruses a failure to replicate produces something called “abortive lytic replication”. As it does that, it produces proteins that get ejected into the blood stream or get inserted in vesicles called exosomes, which then travel through the blood. These exosomes are now believed to play important roles in cell to cell communication. (Maureen Hanson is now studying exosomes in ME/CFS).
The protein released during abortive lytic replication is an enzyme called deoxyuridine triphosphate nucleotidohydrolase or EBV-dUTPase. The unusual herpesvirus dUTPase saga at Ohio State University began way back in 1985 with a Williams/Glaser study. It gathered force in the mid-2000’s with a series of papers suggesting the protein might be a good target for chemotherapy, produced “sickness behavior” in mice, and triggered pro-inflammatory cytokine production.
In 2010 Ronald Glaser won an NIH grant to study the protein titled Stress Effects on Virus Protein induced inflammation and sickness behavior and the hunt was on to determine dUTPase’s effects in ME/CFS. (This long standing grant continues today under Ariza and Williams’ name.)
A 2013 paper suggested dUTPase might provide a way to reconcile the studies which had not found herpesvirus reactivation in ME/CFS with others suggesting that the virus could be having profound effects. It found that even under conditions of low viral load, herpesvirus dUTPases were able to trigger a pro-inflammatory response strong enough to promote atherosclerosis and perhaps even precipitate a heart attack.
In 2012, Williams, Ariza , Glaser and Martin Lerner and Lenny Jason produced the first direct evidence that dUTPases may be producing problems in ME/CFS. The small study found a prolonged antibody response to the protein in a large subset of ME/CFS patients.
A 2014 study indicated that during EBV’s last gasp while undergoing lytic replication, the virus was pouring enough dUTPase into exosomes to produce major immune effects that supported or promoted the establishment/maintenance of further EBV infections
.
 

Pyrrhus

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@Hip do you think the abortive infection theory can fit the time frame for temporary remissions? I don't really have a good feel for the time frames for immune system responses. How likely is it that the body's response to abortive infections can abruptly switch state, and a few hours later, switch back again?
The symptoms of a viral infection are often primarily due to the immune response to the virus, rather than due to the virus’s direct effects. Therefore, you can get sudden relief from viral symptoms by suppressing the immune system with anti-inflammatories. This is most dramatically seen with cortisone injections, which can shut down the inflammation and symptoms without altering the virus. Hope this helps.
 

Wishful

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Therefore, you can get sudden relief from viral symptoms by suppressing the immune system with anti-inflammatories.
Yes, but I'm not sure that that mechanism can abruptly switch to off, then abruptly switch back several hours alter. The mechanism also has to be triggerable by the other triggers mentioned, such as T2 and Wellbutrin. I think there should be more effort made to define the observed characteristics of temporary remissions, and work those results into any models for ME. That could redirect resources away from models that are more likely modelling downstream effects.