Georgia Hunter said...
There are about 100 different bacteria in the body that share the exact same nucleic acid sequence with SARS-Cov2. There are multiple human genes that share the same nucleic acid sequence with SARS-Cov2. Is it a result of molecular mimicry? With the vaccine trigger VAERD reactions in the future?

It's important to differentiate between the whole virus (natural infection), and just the spike protein (vaccines). But here is something I would like to know about the current vaccines: do they use the whole spike protein with all of its immunogenic epitopes? I was thinking they did.. but maybe not. Maybe findings in the study below (April 2020) were considered in the developmental stages:

"SAR-CoV-2 spike proteins, and all other SARS-CoV-2 proteins, immunogenic epitopes in each SARS-CoV-2 protein were compared to human proteins in search of high local homologous matching. Only one immunogenic epitope in a SARS-CoV-2 had no homology to human proteins. If all of the parts of the epitopes that are homologous to human proteins are excluded from consideration due to risk of pathogenic priming, the remaining immunogenic parts of the epitopes may be still immunogenic and remain as potentially viable candidates for vaccine development."

https://pubmed.ncbi.nlm.nih.gov/32292901/

Regarding triggers, I checked out the study cited by the paper in the op. The title is "Molecular mimicry and autoimmune thyroid disease". This is from the abstract:

"Bioinformatics data published by our group support and explain the triggering role of Borrelia, Yersinia, Clostridium botulinum, Rickettsia prowazekii and Helicobacter pylori. Our new data suggest the potential pathogenic importance of Toxoplasma gondii, some Bifidobacteria and Lactobacilli, Candida albicans, Treponema pallidum and hepatitis C virus in autoimmune thyroid disease, indicating specific molecular targets for future research."

https://pubmed.ncbi.nlm.nih.gov/27307072/

Honestly, this is starting to bum me out a little.. feeling less certain that I'll ever be able to curb my own remaining symptoms.

Anyway I'm now looking into that TLR4 stuff, reading this:

"TLR2 and TLR4 in autoimmune diseases: a comprehensive review "

https://pubmed.ncbi.nlm.nih.gov/24352680/

In case you guys aren't already aware, this is a site that helps you through paywalls:

https://sci-hub.se

Post Edited (potsnpans) : 2/8/2021 5:34:44 PM (GMT-7)

dcd2103 said...
What are your remaining symptoms?

I should probably start a new thread. It's mostly PEM that comes with a tightness in my lower throat/upper chest area. I don't think it's thyroiditis.. no noticeable swelling and TSH is always normal. There are some other symptoms that come and go unexpectedly.

dcd2103 said...
I think HLA-DR4 means HLA-DRB1*04:01, but not sure.

Looks like the "B" in "DRB" stands for "Beta".. was reading that the "A" or "Alpha" is invariable, so it seems likely that you are right.. HLA-DR4 is probably short for HLA-DRB1*04:01

https://en.m.wikipedia.org/wiki/hla-dra

dcd i - know your question was aimed at pots - but since I have PEM also - in case it helps I will describe my PEM type symptoms.

typically mine is more like classical PEM as discussed in the CFS sphere.
a delayed malaise after exertion

the malaise in my case would be intensified fatigue, headache, feeling sensitive to light, sound, pain, pressure etc. and the intensity would depend mostly on the amount of exertion - but with some variability.

The onset would typically be delayed around 24hours after the exertion - but could start to kick in the same day with feelings of sore head etc. sometimes, in severe cases, the peak would be 48hrs after - and from there it would typically recede by about half each day until i would be somewhat back at baseline a few days to a week later.

the exertion in my case may be physical - especially anything aerobic - like trying to run - even for 100yards
or maybe due to some kind of mental exertion - eg anything that exercises the brain - this could include socializing - trying to work on a PC - or in my case driving a car for any distance over 30mins would typically trigger it. so weird as I used to be able to drive 4hours - mountain bike in the hills for 4 hours and then drive back 4 hours in a day without any ill effects.

thankfully, as I generally improve, this effect is lessening also - in that I can do more before the PEM is triggered - but it's still there and means I have to be measured in what i do.

Pots - I wanted to say you are not alone in your challenge with making sense of the science-based literature in and around the chronic Lyme subject.

I don't think it's you - I think we all have it - and I think even lifelong academics would struggle

one of the main issues is the sheer breadth and depth of the subject matter
it clearly everything from infectious diseases, immune system complexities, diet lifestyle and functional health, genomics, mind-body medicine, effects, neurology, auto-immunity .....the list goes on and on

each of these fields is an extremely deep subject in itself, that people study for a lifetime and still don't know everything there is to know. in our academic model, people specialize pretty early on and focus narrower and narrower in order to go deeper - so few people ( including trained professionals) have even a very good overview of all of these areas.

the second major issue as I see it is that, in each of these fields - as it stands today - we only have partial knowledge of what is going on - the rest of the scientific work remains yet to be done or worse falls in an area where there are conflicting scientific opinions on what is true - so in many cases, we may only have 50% of the jigsaw pieces to work with and the rests are yet to be discovered.

this being the case - my view is we just have to accept that there is a great deal we will never know with certainty - and the best we can do is to make the best decisions we can based on a more probabilistic approach of what could help us most and hopefully the least likely to hurt us - and then keep moving forward to try things that may help.

don't lose hope - as long as we are alive and able to keep trying there is certainly hope.

just wanted to reach out and say i hear you and feel the same humbling by the sheer scale of the puzzle.

So, are they saying that the virus itself alters the microbiome? I’m sure they are not testing people’s microbiomes to determine what is there before they get sick. How do they determine whether the microbiome differences were already present before sickness or whether the virus is altering the microbiome?

By microbiome, I am assuming they are looking at the gut, correct? How are they testing the patients’ microbiomes?

Thanks, Garzie. I know Georgia Hunter believes that borrelia alters the gut microbiome in ways to protect itself. I suppose we should suspect that any microbe has the potential to do this - bacteria, viruses, fungi, yeast, parasites. Scary thought.

Garzie said...
Pots - I wanted to say you are not alone in your challenge with making sense of the science-based literature in and around the chronic Lyme subject.
...
just wanted to reach out and say I hear you and feel the same humbling by the sheer scale of the puzzle.

Thanks for that Garzie! I really shouldn't complain.. I'm much better off than most members here but the ups and downs still get to me sometimes.

Haven’t had time to dig thru this information but someone recommended I check out this guys stuff.

Lots of papers on microbiome and autoimmunity and infection and autoimmunty, seems interesting

https://www.trevormarshall.com/

Edit: the first paper from 2018 seems particularly relevant to this discussion. It implies microbes affect the microbiome by lower immune response, affecting gene expression and screwing w vitamin and peptide activity (vit d/vdr for example) to maintain survival

Post Edited (dcd2103) : 2/22/2021 6:17:12 PM (GMT-7)

dcd2103 said...
Anyone look at that link, there’s a ton of good information in there.

My buddy was just telling me post-covid that his stomach is screwed up 2m later and he’s concerned. Altered microbiome...

My husband told me this a few days ago! He's having to run to the bathroom. He had COVID last year (spring)

potsnpans said...

Garzie said...
interestingly the Toll-like receptors can enter a kind of self-sustaining inflammation loop once triggered - so a mechanism like this could be at work

I wonder if urtica dentate would be useful (see below).. can't seem to find much info about it. I also wonder if coumarins can be found in the more common urtica dioica (stinging nettle):

"Celastrol, a pentacyclic-triterpene extract from Tripterygium wilfordii Hook might inhibit FLS migration and invasion by suppressing TLR4/NF-kB-mediated MMP9expression[120]. And coumarins, the major components of Urtica dentate Hand, can maintain the DCs in an immature tolerogenic state partially by down-regulating TLR4-signaling pathways in DCs and promote Treg differentiation [121]. Different molecules can target different components in TLR2 or TLR4 signaling pathways to regulate inflammatory responses, thereby ameliorating autoimmune diseases"

i did some digging pots - but couldn't find much at all on that particular species
but yes coumarins are present in common stinging nettle - mostly in the root
as it happens I have tried taking both the root ( as a tincture ) and the leaf as a tea and cannot say i have noticed either having a noticeable effect on my illness / symptoms.
quantities of coumarins are however pretty small -
see this paper

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6100552/

actually, there are quite a number of herbs that inhibit the NF-kB pathway - which is the one that is triggered by the Toll-Like receptor 4 and 2 i think -

the ones I have come across mostly from buhners writings and some of my own research are
ginger, Chinese Skullcap, licorice, houttuynia, astragalus, Kudzu

interestingly - several of these have been added to my protocol over the last 2 years - as they are also the herbs in his extended protocol for Lyme

in fact, most plant polyphenols inhibit NF-kB - things like quercetin, curcumin, EGCG are common ones

this brings to mind a bunch of research i did a couple of years ago into a mechanism discovered in lab animals where after exposure to a gut pathogen they lost an enzyme needed to process lipopolysaccharide from commensal bacteria and as a result suffered a range of inflammatory disorders and associated symptoms - which persisted long after the pathogen was cleared. the disease state was very reminiscent of CFS or chronic lyme with gut symptoms.

• Inflammation of Colon and Small Intestine
• Leaky Gut (small intestine membrane permeability)
• Weight loss (likely indicates malabsorption)
• Diarrhoea (or altered bowel habit)
• faecal blood - and prolapsed anus ( actually a known thing in chronic Lyme patients - as i can vouch for )
• colon shortening
• systemic inflammation (host of inflammatory cytokines are increased by up to 26-fold)

i will dig out what i found at the time

Post Edited (Garzie) : 2/24/2021 3:23:53 PM (GMT-7)

so i finished the Blautia genus article

its basically one of the most common and abundant genus of bacteria in the human gut - approx 99-100% of samples contain it, and an average of around 10% of total counts by qPCR and regarded as a Keystone genus.

it is generally thought of as a beneficial commensal bacteria that increases the expression of T reg cells in the gut lining and also produces short chain fatty acids - both anti-inflammatory changes
however, research is at an early stage and there are both negative and positive correlations with health conditions) -

its thought to be involved in the breakdown of complex carbs and produces many b vitamins in the gut
• Butyrate ( an anti-inflammatory SCFA)
• Pyridoxine (B6)
• ß-galactosidase (estrogen related)
• Tryptamine
• Vitamin B1 (thiamine)
• Vitamin B12 (Cobalamin)
• Vitamin B2 (riboflavin)
• Vitamin B3 (niacin)
• Vitamin B5 (pantothenic acid/Pantothenate)
• Vitamin B6 (pyridoxine)
• Vitamin B7 (biotin)
• Vitamin B9 (Folic Acid/Folate)

interestingly it also produces bacteriostatic substances that help shape the microbiome
• Bacteriocin: Lanthipeptide I ( these are narrow band Bacteriostatic compounds )
• Bacteriocin: Sactipeptide ( these are narrow band Bacteriostatic compounds )

low abundance is associated with various health conditions including type 2 diabetes, obesity, Crohn's disease to name a few -

it's known to have immunomodulatory effects - notably, people who have bone marrow transplants are much less likely to suffer Graft vs Host disease if they have higher abundance - and bowel cancer and liver cirrhosis rates are lower in those with higher abundance.

however - high abundance is also associated with some health conditions - eg IBS ( so perhaps high abundance makes sense in lyme patients ) also ulcerative colitis

the upshot is - research is at an early stage - and whilst there are signs of its immunomodulatory behavior and disease associations we do not yet seem to understand the landscape of the gut in sufficient detail to understand all the mechanism at play ie why exactly its abundance is raised in Lyme patients.

so its been an interesting dip into this arena - and may yet prove to be significant - as more and more researchers are focussing on the human gut microbiome and its interaction with human disease - but at present, i don't really see anything actionable.

this is on-topic and may be interesting to those following this

a paper in the Integrative Medicine clinicians Journal

it talks about immune dysfunction following covid and other illnesses - and a potential route to understanding it and treating it by rejuvenating the immune system - via an integrative approach including induced autophagy to remove the population of dysfunctional immune cells

the timeline of just how recent our discoveries of the basics of our immune systems actually is - is interesting
and it mentions the concept of immune resilience that we have discussed here.

some of the reference papers may be of interest too

Post Edited (Garzie) : 3/20/2021 3:32:53 PM (GMT-6)