Is Apheresis an effective treatment for Long Covid and ME?

[SNT Gatchaman]

These are crucial steps as most monocytes die within a few days, and having very long-lived (up to at least 16 months) coronavirus protein-carrying monocytes is a critical aspect of Patterson’s hypothesis.

It seems quite a stretch to suggest monocytes can be "immortalised" to this degree.

A simpler explanation is that these are ordinary, non-classical monocytes that have scavenged up persistent micro-clots that contain the spike protein.

This of course is arguing that micro-clots can be persistent while monocytes can not be. I think it's a bit easier to accept that possibility for a biological construct vs a living cell.

This is the implication of the apheresis observations and the findings described in the Pretorius paper: "Persistent clotting protein pathology in Long COVID/Post-Acute Sequelae of COVID-19 (PASC) is accompanied by increased levels of antiplasmin"

 

[andyguitar]

It seems quite a stretch to suggest monocytes can be "immortalised" to this degree.

Yes it does!

This of course is arguing that micro-clots can be persistent while monocytes can not be.

But would they need to be persistant? They might well be resistant to the normal process that would break them down so they hang around for a while, but for years? Decades even in some cases of me/cfs? Seems more probable that if they exist in me/cfs their creation is an on-going process.

 

[SNT Gatchaman]

But would they need to be persistant? They might well be resistant to the normal process that would break them down so they hang around for a while, but for years? Decades even in some cases of me/cfs? Seems more probable that if they exist in me/cfs their creation is an on-going process.

Yes, absolutely! I think the interplay between micro-clots containing inflammagens, activated platelets, dysfunctional endothelium and probably RBCs allow the creation of more micro-clots to maintain the population. (We have evidence to suggest that at least some are being mopped up be monocytes).

I think there must be a threshold where self-perpetuation via this interplay is beyond the fibrinolytic process to control. Remove enough of the micro-clots (eg apheresis) and get below threshold. Eventually the residual will clear.

An attractive explanation for the remitting / relapsing histories that are so commonly described.

(Not all ME need be this exact process, but I'd be surprised if it wasn't very similar.)

 

[andyguitar]

I think there must be a threshold where self-perpetuation via this interplay is beyond the fibrinolytic process to control.

Yeah, sounds about right to me.

 

[Martin aka paused||M.E.]

The question is: how do other viruses do that? Take EV as an example. There is no spike protein. So I think it’s possible that other viral proteins do the same.

 

[andyguitar]

The question is: how do other viruses do that? Take EV as an example. There is no spike protein. So I think it’s possible that other viral proteins do the same.

In my mind @Martin aka paused||M.E. the question is bigger than that as not everyone who has me/cfs can say that their illness began with a viral infection. And if it was caused by a virus how come they did'nt get it before? Viral infection is common during a persons life so how could they get through all the viral infections of childhood and not get me/cfs and then they do? Must be something else going on.

 

[Martin aka paused||M.E.]

In my mind @Martin aka paused||M.E. the question is bigger than that as not everyone who has me/cfs can say that their illness began with a viral infection. And if it was caused by a virus how come they did'nt get it before? Viral infection is common during a persons life so how could they get through all the viral infections of childhood and not get me/cfs and then they do? Must be something else going on.

I had a very long conversation with William Weir on that. We both think that every ME is caused by one ore more infections. Please keep in mind that viral infections are mostly asymptomatic so you don't know if you had one when it all started.
Re your question I like the PolyBio explanation that multiple infections, toxic metals, drugs, etc. (“hits”) might lead to ME. Furthermore there might be a genetic predisposition.

ME/CFS has a big problem: diagnosis. I think the prevalence of ppl that don’t have ME but a psychosomatic illness with a ME/CFS diagnosis might also play a role.

And then there are subgroups. I seem to fit in one subgroup as many things in my case (lab results, success with drugs) are different from most ME/CFS-patients (except Abilify where I seem to fit in the main group… or what I think is that Abilify does sth that has an effect on the most subgroups underlying pathomechanism… same with Ativan).

 

[Shanti1]

VEGF is high in Long Covid and is the marker for polyneuropathy. It is low in ME (!) (despite neuropathy in about 1/3….another cause?)

Interesting because Dr. Shoemaker also notes low VEGF in CIRS patients. CIRS has symptoms that can be identical to ME/CFS, including PEM. The difference seems to be that in CIRS there is an identifiable cause.

Hmmmm - “none of the 13,000 LC patients had microclots” Didn’t Dr Resia Pretorius have a specific way she identified microclots - that hardly anyone knows how to do at this point, not the least Bruce Patterson? I wonder how his method differed from hers.

"None of the 13 000 LC patients had microclots nor the 1000 severe acute patients after using CCR5 antagonist as it reduces platelet activation and reduced vascular inflammation." I think he is saying that the intervention cleared the microclots, not that the LC patients didn't have them to begin with.... but it is a good question on how he is identifying the microclots. Also, 13,000 that all responded to the therapy completely seems a bit unbelievable, how did he manage to give that many people an expensive off-label HIV medication? Maybe there is an extra '0' in the number? @Countrygirl

 

[andyguitar]

. Also, 13,000 that all responded to the therapy completely seems a bit unbelievable, how did he manage to give that many people an expensive off-label HIV medication?

It does sound a bit over the top. I hope he will be able to publish some solid evidence to verify this.

 

[smithsj]

In my mind @Martin aka paused||M.E. the question is bigger than that as not everyone who has me/cfs can say that their illness began with a viral infection. And if it was caused by a virus how come they did'nt get it before? Viral infection is common during a persons life so how could they get through all the viral infections of childhood and not get me/cfs and then they do? Must be something else going on.

When I got mono, my grandma rolled her eyes and said, "In my time, we didn't have this 'mono'...we just got a cold" (she was born in Romania in 1930). And I had a Mexican-American friend who said something similar when I first started complaining about crippling fatigue – "this is a white person disease." This – and things like calling CFS "yuppy flu" – was insensitive and cruel, it hurt me a lot and I will never trust these people again enough to talk about my health issues, but there is a small grain of truth to it: the richer a society, the later people tend to get Epstein-Barr infections (in the US, poorer people get it younger than wealthier people; I can't find it now, but I've seen a study that said in some country that got wealthy in the latter half of the 20th century, younger people were getting it later than their older relatives).

And the later you get EBV, the more likely (I think) you are to be symptomatic, and therefore to get post-viral complications. This is not to say that nobody who gets it young has post-viral issues – I think @Martin aka paused||M.E. is onto something when he points out that many viral infections are asymptomatic, and that can explain many people who have POTS or CFS but no apparent viral onset – but I think we've seen pretty clearly with Covid that you are more likely to get long Covid if you are symptomatic than asymptomatic, and that very young people are at less risk of getting post-viral fatigue than teenagers or young adults.

Of course, Covid may change this, since unlike with EBV, nobody had preexisting immunity. I think in very poor countries where the average age is young, there is still likely to be less long Covid because it seems like children are less susceptible to it than adults, but still, there will be a lot of people being exposed to the virus for the first time, which I don't think is the case with EBV, which people in poorer countries almost all get when they're young.

 

[Martin aka paused||M.E.]

but I think we've seen pretty clearly with Covid that you are more likely to get long Covid if you are symptomatic than asymptomatic

It’s no different with ME. And that’s not a contradiction (you said “but”) to what I said and what Weir and I think.

 

[smithsj]

It’s no different with ME. And that’s not a contradiction (you said “but”) to what I said and what Weir and I think.

I let the parenthetical go on for too long and it got confusing – the "but" was to modify "This is not to say that nobody who gets it young has post-viral issues," not what you said.

 

[Martin aka paused||M.E.]

@Shanti1 Patterson is a salesman. 13.000 would be one of the biggest drug studies ever. To monitor this with acceptable scientific methods would cost millions.

 

[Martin aka paused||M.E.]

I let the parenthetical go on for too long and it got confusing – the "but" was to modify "This is not to say that nobody who gets it young has post-viral issues," not what you said.

Oops sorry. Thanks for clarification

 

[SNT Gatchaman]

And I had a Mexican-American friend who said something similar when I first started complaining about crippling fatigue – "this is a white person disease."

You could imagine geographic and racial variations in predisposing factors. An obvious example that could work to predispose to a micro-clotting pathology would be Factor V Leiden mutation (mentioned previously). This is present in up to 5% of those with European ancestry. Would be interesting to see if there was any correlation with LC rates in various countries.

Eg LC not common in Singapore.

 

[Martin aka paused||M.E.]

You could imagine geographic and racial variations in predisposing factors. An obvious example that could work to predispose to a micro-clotting pathology would be Factor V Leiden mutation (mentioned previously). This is present in up to 5% of those with European ancestry. Would be interesting to see if there was any correlation with LC rates in various countries.

Eg LC not common in Singapore.

That is very interesting. Though I personally know Chinese and Latin American patients but I have never seen a patient with black skin. Most patients are white in my experience. Maybe there is a genetic factor.
What would also be interesting is the prevalence of EV and herpes infections in Africa.

 

[SNT Gatchaman]

What would also be interesting is the prevalence of EV and herpes infections in Africa.

Well for part of that question - famously EBV is responsible for endemic Burkitt lymphoma (aka African variant). See Wikipedia. Plenty of EBV exposure in that continent, so that does favour variation in host response.

 

[junkcrap50]

More details on microclot detection via light microscopy. Claim that only a blood smear is needed. I sort of doubt that as it would be hard to see the microclots among the RBCs, platelets, & other cells. Pertorius used Platelet Free Plasma (PFP), which is plasma that's been centrifuged twice. A smear of PFP would be clearer, I'd think.

One Long Covid patient, who is a doctor, discovered microclots in here blood using a light microscope. She is a dermatologist, so you'd think she'd definitely have a microscope in her office.

She describes her procedure on how she detected them here. At only 40x (I assume x10 w/ eye piece, so 400x total), a child's microscope or cheapest microscope on amazon for $150 should be able to see that. Maybe even those digital ones for $50.

Images of her results, and description of procedure:

 

[Countrygirl]

Hmmmm - “none of the 13,000 LC patients had microclots” Didn’t Dr Resia Pretorius have a specific way she identified microclots - that hardly anyone knows how to do at this point, not the least Bruce Patterson? I wonder how his method differed from hers.

I understood that by treating early that he prevented the micro clots from forming. Without treatment at the very early stage, they would need HELP apheresis.

 

[Martin aka paused||M.E.]

I understood that by treating early that he prevented the micro clots from forming. Without treatment at the very early stage, they would need HELP apheresis.

Pretorius said the same IIRC. But AFAIK she mentioned the use of drugs against clotting in early stage of Covid infections.