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

Why do I get the impression that Nath has just read about all this stuff in the Daily Express or heard it from someone on a bus? He doesn't even seem to get the jargon right - "mental fog", "Long-Haul Covid". It's almost as if, if you work oat NIH it doesn't matter if you don't know half of what you are talking about because people at the NIH are right by definition.

He seems to bundle together fatal brain infarction with blood escaping, with inflammation, and with Long Covid where there isn't even inflammation.

I don't see any justification for using immunomodulatory therapies at this stage when nobody has any idea what is going on.

 

4/3/23, SABPA: 'Long-COVID: Clinical manifestations, pathophysiology and therapeutics targets by Avindra Nath M.D.'

“..there was one neurologist I talked to, and after she developed COVID, she was talking to me on the phone and she says that I have to lie down to talk to you I can't even sit up in my bed to talk she would get dizzy every time..”

“..there are other kinds of syndromes that we've known for awhile and they've remained a mystery nobody really understands what's going on with these patients for one is Chronic Fatigue Syndrome, the other is post-Lyme disease, then you have Gulf War Illness..”

‘it's been a real dilemma as to how to really manage these patients and study them so one hope is that as we study Long COVID, all the other illnesses will also benefit from the knowledge gained here..’

“is it possible that there's a persistent viral infection or is it possible that there's immune dysregulation or the two may be interacting with one another, what really is the pathophysiology of Long COVID is the mystery..’

“…what we found was that the biggest pathology really was here in these perivascular region of these blood vessels and we found a lot of fibrinogen over here and this fibrinogen should actually be inside the blood vessel - not outside - and there was leakage of fibrogen suggesting that the there's compromise of the blood-brain barrier and leading to leakage of all these proteins..”

“..what I'm going to show you is that the most of it is likely mediated by antibodies or by macrophages…’

“…you can see there's just excessive amounts of microglia cell activation within the brain so the inflammation really is a key part of what is happening in these individuals…”

“…people have also reported increase in neural filament so it suggests that there's ongoing neural injury taking place and there's protein aggregation taking place in the brains of patients with Long COVID.."

“…if you look at these blood vessels here, you will find that a number of these blood vessels have activated platelets…we found a lot of platelets aggregated around the blood vessels… when we looked at the brain stem, here we found that there were neurons that were atrophic and there’s microglia around them and that suggests that there's neuronophagia taking place…suggests to us that two phenomenon taking place - one was within the blood vessels and the second phenomenon that was taking place was all within the brain stem leading to neuronal damage..”

“..what we think is happening is that most of the pathology occurs at the blood vessel… we think the antibodies attached to the blood vessel, there's rupture of the adhesion molecules - cells and protein then come in, then macrophages that come in and kind of clean up the mess -you get some micro hemorrhages here - the microglial cells then get activated, and then they will attack the neurons and cause neuronal injury..”

“so how do we treat patients..? So we think that a lot of this is immune-mediated…I assured you that there is activation of innate immune responses and hence there are several potential candidates that can be used to dampen the innate immune responses - if there is immune exhaustion in these patients, one can use checkpoint inhibitors – there is a subgroup of patients in which there is there are auto-antibodies that people have reported and so for that subgroup, one can use anti-b cell therapies. And then certainly one can use corticosteroids, but that's not a long-term solution - I will tell you that at least it's an immune phenomenon and you can use it for short periods of time.."

"So, I'd like to conclude by saying that direct invasion of the brain by SARS-CoV-2 is rare and does not explain the neurological complications. Neuroimmune dysfunction is driven by activation of innate immunity immune exhaustion and antibody-mediated phenomenon and clinical trials with immunotherapies could be considered in patients with Long COVID and maybe relevant to other post-infection syndromes."

 

??

??

This 'biology' is new to me.

 

7/15/21, Patient-Led Research Collaborative: "Q&A with Dr. Nath at the NIH Neurologic and Psychiatric Effects of SARS-CoV-2 Infection conference"

Nath: "Ninety percent of medicine is actually listening to the patient"

 

Ninety two percent I would say.

 

https://www.pharmgkb.org/pathway/PA154444041
Effects of antiplatelet drugs on platelet aggregation pathway.

 

Was this already shared?

3/19/25, Frontiers: Post-Exertional Malaise in Long COVID: Subjective Reporting Versus Objective Assessment Provisionally accepted

By Avindra Nath, Brian Walitt et al.

(If any have thoughts on feel free to share)

 

I am unclear what they mean by objective assessment of PEM. There isn't any that I know of.
I get the impression that this is a case of measuring-osis. Measure, measure, measure, regardless of whether the measurements mean anything.

 

National Deafness and Other Communication Disorders Advisory Council - September 2021 (Day 2)

(1 hour 26 min mark) Nath: "There were decreased interferon responses and exhausted T-cells...this milieu is terrible, because what it means is your adaptive innate immune responses are gone, your innate immune responses are highly activated, and the innate immune responses are very difficult to shut down. And so once these are activated, they remain activated for long periods of time. So it's quite possible that a lot of what we see in Long COVID is driven by persistent activation of innate immune response. I also showed you in the pathology that largely it was macrophages that were present in the brain."

 

American Academy of Neurology, 4/7/25 - '2025 Annual Meeting | C101 - Sequelae of COVID-19'

'Participants should become familiar with recent advances in understanding mechanisms for neurological sequlae of COVID-19 ("long COVID") including factors contributing to post-COVID-19 cognitive impairment, as well as immunological mechanisms that may drive symptomatology. Lessons from the RECOVER (Researching COVID to Enhance Recovery) studies will be presented.'

'Speaker: Pathophysiology and Therapeutics of Long-COVID - Avindra Nath, MD, MBBS, FAAN'

 

I cannot see any good basis for vague statements like this. The innate and adaptive responses are integrated into a seamless whole. One up and one down is the same old story that never made sense. We need specific mechanisms and pathways. I think 'T cell exhaustion' is going to turn out to be the big disinformation term of the 2020s.

 

Neurocritical Care Society: 'NIH Protocol for Encephalitis and Emerging Neuroimmune Infections'

"..there has been an emergence of new pathogens and reemergence or others many of which may cause encephalomyelitis..." - Avindra Nath, MD