Dr Avindra Nath, NIH USA, views on ME/CFS and Long Covid

5/16/21, Body Politic: 'Dr. Nath Presents on the "Neurological Complications with COVID"

Nath: "This is a protein called fibrinogen and this protein is present only in the blood - it's never been in the brain, it's a big protein - it doesn't get through the blood vessel, the only way it can get through the blood vessel, the blood vessel has to be damaged. And so when we saw this in the olfactory bulb, okay that told us immediately these blood vessels, something is wrong with the blood vessels."

"...macrophages, so they're all these immune cells are getting in there too..the primary target of the virus are the endothelial cells in the blood vessel..."

"PEM..I'm very curious to figure out how on earth and why this really happens.."

"The thing is that what i'm excited about is that Congress appropriated $1.5 billion dollars just to study this Long COVID phenomenon - I mean that's the most money you would ever get or ever hope to - to study this phenomenon that has far-reaching consequences for all these other syndromes.."

“…I am told about 270 some grants were submitted from all around the country..the fact that so many groups of people are interested in studying this around the country, that's unprecedented..”

“What I’m excited about is once these studies get going, and the federal government is not the only one pumping money into it, we have other agencies looking at it as well - if we don't understand the pathophysiology now, we will never do it – so, I’m excited will be some answers now there's going to be a second phase to this thing and they're going to now invite proposals for clinical trials and my guess is you'll see the same kind of enthusiasm for clinical trials. So, we should not only understand the disease, we should find reasonable treatments for the disease too. And that is the most exciting thing I think that's happening at the moment.”

“…if you want to boost your T-cells there’s a number of things you can do, if you have exhaustion markers you can reverse them, they're called checkpoint inhibitors..”

"..you have a whole world full of scientists and physicians who have devoted their energies towards studying this thing...I'm very hopeful that we'll come up with something.."

 

10/4/22, AME: 'Neurologic Sequelae of Acute Viral Infections - Avindra Nath, MD'

Nath: "I think all the pathology is really in the blood vessels and viral-mediated stuff – and the parenchyma, it's all innate immune activation and there's leakiness in the blood vessels, you'll get fibrinogen and all kinds of blood products into the parenchyma and then the macrophages come in and they once they get in, they don’t leave. So you have persistent activated microphages in the brain."

 

8/8/22, GVN: Forefront of Virology COVID-19 Webinar Featuring Dr. Avindra Nath

Nath: "The reality is that ultimately the socioeconomic consequences long-term disability is almost all from neurological complications so I think understanding these things early on is absolutely critical.”

“My bias is we need to study pathophysiology in the context of clinical trials because we have millions of people affected and we can't be waiting too much longer or years before we do clinical trials - we need to start with clinical trials now and not wait”

 

Maybe the type of person who prioritises career ambition instead of truth. I mean it takes a lot of that type of thinking to get into such a prestigious position has his.

Maybe he didn’t want to stir up any drama within his field or within the NIH, to benefit his career , so he let Wallitt run free

 

yes I’ve found the latest stuff interesting for similar insight re Nath

Was that Walitts paper back then? I don’t know how things precisely work re the names of authors for all things but got the impression if you have deliver a paper by a certain date and one person has ended up in charge of doing that then it’s hard to have a strong opinion if they want include certain bits or angles because if that theoretical of academic literature of people can always just write their own paper if they disagree (although I think we know it doesn’t work like that in practice easily either)

 

10/20/20: “Neurological Complications of COVID-19 and NINDS Clinical Research by Dr. Avindra Nath”

Nath: "Post-viral syndromes..we think are largely immune-mediated..these COVID patients..it brings an opportunity for us to try & figure out underlying cause"

 

I don’t think so. I can recall the transcript of a conference he went too where there were nearly only psychsomatisers and he spent his whole speech and Q&A pushing back against them.

 

Nath complained vigorously about his own workload around the time the intramural was gearing up and I think said pretty directly that he didn't have time to do it. He seemed very grateful that Wallitt was willing to take it off his hands.
This complaint about not having time to do it was repeated when it was time to write it up. Nath and Wallitt wrote it up at weekends, with Nath complaining again about workload.
Goodness knows how he thought Wallitt would handle it. Jeanette Burmeister write her excoriating piece about Wallitt at that time so criticisms of Wallitt were rife.

It doesn't make sense does it?

 

12/18, Neurology Journal: “Reemerging Infectious Diseases and Neuroimmunologic Complications”

By Avindra Nath & Dennis L. Kolson

“We are ill-equipped to handle this crisis. We need targeted treatments based on our understanding of the current pathophysiology of the disease. While we have made substantial progress…we lack disease-modifying therapies and the medical personnel to provide long-term care.”

https://www.neurology.org/doi/10.1212/NXI.0000000000200356

 

9/1/22, Neurology Podcast: “September 2022 Neurology Recall: Cognitive Impairment From Less Common Causes”

(host) “What do you envision as the important contributors to this syndrome (Long COVID)? And this may be a good opportunity to draw some parallels, as this article does, between COVID brain fog and things like chemo brain or sequelae after other neuroinfectious diseases. What are your thoughts on that?”

Avindra Nath: “Yeah, so I think there's a fair bit of excitement in the field because we're starting to understand some of the pathophysiological mechanisms. We still don't understand a lot, but at least we're starting to solve some of these things out. And there are some important observations that have been made now from autopsy studies as well as some of the new emerging animal models.

And I think this paper that you refer to, tries to draw parallels between patients who received chemotherapy, and really what they're talking about is that you have activation of glial cells within the brain. And I think a lot of various kinds of things can do that that don't really invade the brain but yet can cause a systemic inflammation. And the brain also shows evidence of microglial activation at the same time. And I think the importance of that is that most people do not find virus within the brain. Or if they do, there's just very small amounts of virus within the brain.”

“So, that alone cannot explain the symptoms or the pathology that we see in the brain. So you have to somehow explain it by some additional pathophysiological mechanism. What this paper found was that there was a lot of microglial cell activation within the brain, some macrophage infiltrates, and suggesting that this persistent glial cell activation is bad.

In the acute phase, if you have glial cell activation, it's good because it tries to repair whatever pathology there is. But if it persists for a long period of time, then it ends up causing bystander damage. So that's at least one of the mechanisms, but that may not be the only one.

So we've looked at some autopsy cases ourselves, and what we found was that another component that is important is vascular damage. In a sizable number of individuals, you can find a fair bit of microvascular pathology. These blood vessels become leaky, and there are proteins that are coming out of the small blood vessels leaking into the brain. You have perivascular macrophages there. What you do not find is T cells, very few T cells. If this was a viral encephalitis of some sort, you would find a lot of T cells. You actually don't find them at all. What we do find is that the endothelial cells themselves are not only damaged, they're also activated. You will find platelets will aggregate there. You can find small thrombosis that can occur. Sometimes you can get micro hemorrhages also. We think that in part that may be mediated because of antibody deposition on the endothelial cells itself.

There may be an immune component that is beyond just microglial cell activation, but that is mediating vascular damage and then causing a series of events leading to neural injury.”

(Host): “I think the key take-home points here, what you've said about this, what we're looking at, what we think are the main contributors to post-COVID syndromes, are really indirect effects of viral infections…I'd like to know your views on whether the parallels that we're discussing today between long COVID and these other syndromes, does this open up the possibility that maybe some of these trials might include clinical trials using medications to try to improve symptoms in our patients or mediate these end effects?”

Nath: “You have such a large population that's been affected by it. How long, the patients are going to ask you and physicians too, how long do you want to wait to study the pathophysiology before you're going to do some kind of treatment trials? And the answer is you can't.

You know, even if you don't understand all the pathophysiology, you've got to do something for them. I and others will also agree that you can study a lot of pathophysiology in the context of a clinical trial. And we know enough already that we can start designing clinical trials.”