Ron Davis's trypanosome 'signature' finding (IIMER conference 2018)

The question which strikes me about this is whether this is another manifestation of the TH2 shift which according to Dr Cheney some viral infections can induce. EBV produces a viral IL-10 analogue for example, which is considered a TH2 cytokine.

The reason viruses evolve to do this is that the TH2 response tends to suppress the TH1 response due to feedback mechanisms. This makes sense for viruses because the TH1 response is aimed squarely at them, intracellular infections i.e. viruses inside cells, so by activating the TH2 pathway they take the heat off themselves and throw the immune system a red herring.

TH2 responses handle extracellular threats like trypanosomes.

So the question I am asking myself is, wouldn't a TH2 shift in progress activate the same immune genes as a trypanosome infection activating the TH2 pathway for real?

In other words if Ron does not find a trypanosome then he could look at finding out if there is a TH2 shift in progress due to another cause.

I guess first though he has to eliminate the obvious "looks like a duck" possibility.
 
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Sasha said:
He wonders if we all have a trypansome infection or whether having a trypanosome infection is one route to ME.
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I'm just guessing the latter would be more likely, because of the male-female ratio in ME? (Well, I confess I haven't read up on whether trypansome vectors choose their meals based on the gender offered on the menu:))
 
Sasha said:
Oh! I thought everyone would have them if I did. I guess not!


Another thing he mentions is that trypanosomes cause sleeping sickness and that the treatment for that is suramin, which of course Robert Naviaux used in his autism trial and is interested in for ME.

Ron said he doesn't know what to make of that connection.
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cc : @Hip

The connection might be that EBV, Coxsackie Virus, HHV-6, Cytomegalovirus and many many more viruses disrupt Liver function :

Regarding Trypanosomes :


Trypanosoma cruzi, the etiological agent of Chagas' disease, causes an intense inflammatory response in several tissues, including the liver. Since this organ is central to metabolism, its infection may be reflected in the outcome of the disease. 15-deoxy-Δ12,14 prostaglandin J2(15dPGJ2), a natural agonist of peroxisome-proliferator activated receptor (PPAR) γ, has been shown to exert anti-inflammatory effects in the heart upon T. cruzi infection. However, its role in the restoration of liver function and reduction of liver inflammation has not been studied yet. BALB/c mice were infected with T. cruzi. The effects of in vivo treatment with 15dPGJ2 on liver inflammation and fibrosis, as well as on the GOT/GPT ratio were studied and the role of NF-κB pathway on 15dPGJ2-mediated effects was analysed. 15dPGJ2 reduced liver inflammatory infiltrates, proinflammatory enzymes and cytokines expression, restored the De Ritis ratio values to normal, reduced the deposits of interstitial and perisinusoidal collagen, reduced the expression of the pro-fibrotic cytokines and inhibited the translocation of the p65 NF-κB subunit to the nucleus. Thus, we showed that 15dPGJ2 is able to significantly reduce the inflammatory response and fibrosis and reduced enzyme markers of liver damage in mice infected with T. cruzi.
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https://www.ncbi.nlm.nih.gov/pubmed/27693222


Here is another list of viruses that may affect Liver function :

The first virus capable of causing hepatitis was the yellow fever virus, a mosquito-borne flavivirus. Other viruses than can cause hepatitis include:

KIs-V is a virus isolated in 2011 from four patients with raised serum alanine transferases without other known cause. A causal role is suspected.[23]
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I hypothesize that Suramin is relevant to ME/CFS because it ameliorates Liver Injury :


In recent years, research interest has turned to a new use for this old drug. For example, recent studies have shown that suramin protects against liver injury after D-galactosamine and lipopolysaccharide (LPS) exposure in mice (Eichhorst et al., 2004; Liu and Zhuang, 2011). Suramin also reduces ischemia/reperfusion-induced brain and kidney injury in rodents (Kharlamov et al., 2002; Zhuang et al., 2009). The mechanisms by which suramin protects these organs from injury are associated with inhibition of apoptosis, suppression of nuclear factor-κB (NF-κB) activation, and decrease toxic/proinflammatory cytokine formation
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EDIT : @Jonathan Edwards Would you like to comment on these two hypotheses?
 
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Parasitic Illness From a Bug That Bites People at Night Is Spreading Worldwide, Doctors Warn

https://www.sciencealert.com/chagas-disease-parasite-spreading-and-causing-heart-problems-us-europe

Doesn't seem like there are any similarities to ME, but it does persist without symptoms (or so we think) in many cases. From wiki:
After 8–12 weeks, individuals enter the chronic phase of disease and in 60–70% it never produces further symptoms.[5][2] The other 30 to 40% of people develop further symptoms 10 to 30 years after the initial infection,[2] including enlargement of the ventricles of the heart in 20 to 30%, leading to heart failure.[1] An enlarged esophagus or an enlarged colon may also occur in 10% of people.[1]
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This current news article claims that there are 300,000 people in the US with Chagas and it is "spreading."

However, I strongly suspect that the news article is irresponsibly leading people to believe Chagas transmission is rampant in the U.S. when it is not.

This paper from 2011 says:
A total of 7 autochthonous [indigenous] vector-borne human infections have been reported in Texas, California, Tennessee, and Louisiana; many others are thought to go unrecognized. Nevertheless, most T. cruzi-infected individuals in the United States are immigrants from areas of endemicity in Latin America. Seven transfusion-associated and 6 organ donor-derived T. cruzi infections have been documented in the United States and Canada.
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So, in all likelihood, when the current article claims that Chagas is "spreading" in the US, it is referring to a growing number of people who have been infected elsewhere, but who are now being recognized/diagnosed in the US.
 
just so... how funny when i read @alex3619 post on phoenix, where he was told something like "yes, if you had been to vietnam"
think, it was him who told here, he was born in africa ?
maybe i mix up

but funny, because i was in vietnam and asked for a test.
was told "yes, if you had been to africa previously"

i declared (by mail) i had been to africa previously.
then, when in the tropical hospital, they asked where...
when i said "egypt" they felt outright insulted
 
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regarding parasite travels/transmissions:

1) for some 3000 years or more .. animals have traveled on ships - as foods, as pets/mice, rats, cats etc. insects and artrophods as well.
apart from the humans on board.
importing exotic "pets" has been popular since all times (snakes, budgies, exotic birds, monkeys)

2) migrating birds
they may travel all the 1000s of km with their mites on board. if not the bird, then the mite can be easily infected.

3) i remember some "study" or it was just an idea on some of these study publishing sites, where two guys wondered if vaccines could have been contaminated with trypanosomes.
why would they think that? its definitely possible, and vaccine contaminations with serious pathogens happen.
(sorry no link)

4) i saw some studies on publishing sites, that found trypanosoma in cattle in nordic countries and in france. they were looking for that. numbers were low.
but how much meat do we eat in a lifetime?
how often gets cattle bitten by mosquitoes, that may take up parasites when sucking blood and transfer them further ?
nobody checks for such parasites by default in our areas. only veterinaries may. in rare cases. tests are expensive and require much effort. what for - it so super rare, isnt it?
(sorry no link)

5) a lot of vectors can transfer trypanosomes. when only a few are named in the context of the parasite/pathogen, then because no other vectors have been tested. others are not ruled out. thats my take, may be wrong.
 
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Climate change has been affecting vector borne disease for the past 10 years- it's one of the early indicators as entropy rates are higher for insects etc
Malaria in particular is now in places that were previously relatively free of the disease......
 
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