DIAGNOSTIC CRITERIA OF VIRAL PERSISTENCE FOR PATIENTS WITH

SWAlexander

Senior Member
Messages
2,108
LONG COVID
CHRONIC POST-VAC SYN.
ME/CFS
FIBROMYALGIA
ARTHRITIS
AUTOIMMUNE DIS.
POTS,
DYSAUTONOMIA
OTHER DISEASES POST-VIRAL
There are 3 Diagnostic Criteria
A. CLINICAL
B. THERAPEUTIC
C. LABORATORY
In patients who present persistent symptoms associated with or suggestive of a viral infection, it is recommended to sequentially apply the following diagnostic criteria for viral persistence: A. CLINICAL CRITERION. The patient will meet the clinical diagnostic criteria if he or she has one or more of the following symptoms or syndromes: 1) If the patient scores 10 or more points on the free HHM test questionnaire for microclots, available at: https://www.researchgate.net/publication/362634538 2) Low-grade fever, fever and/or night sweats (or very early in the morning). 3) Persistent anosmia, hyposmia and/or dysgeusia (alteration of taste). If the clinical criteria are met, it is justified to apply the therapeutic criteria. B. THERAPEUTIC CRITERION. The application of this criterion consists of carrying out therapeutic tests using drugs against the viral load. Details of these therapeutic tests can be found in the documents at the following links: https://www.researchgate.net/publication/366412536 https://www.researchgate.net/publication/351051024 https://www.researchgate.net/publication/372413948 https://www.researchgate.net/publication/373799663 To meet this criterion, patients must respond favorably to viral load treatment, with a significant decrease or disappearance of persistent symptoms. C. LABORATORY CRITERION. To meet this criterion, the existence of the causative viruses must be identified through laboratory tests. This criterion could be applied before the therapeutic criterion, however, the percentage of false negative results is still very high. See details at: https://www.researchgate.net/publication/343931153 and https://www.researchgate.net/publication/354528386 For the diagnosis of persistent viral infections, the use of samples for molecular tests (PCR) that contain cells or tissues (very few available) is indicated. See 1st step in: https://www.researchgate.net/publication/353325113 IN PRACTICE, IF THE THERAPEUTIC CRITERION IS MET, IT IS SUFFICIENT TO MAKE THE DIAGNOSIS OF VIRAL PERSISTENCE.
https://www.researchgate.net/public...POTS_AND_OTHER_DISEASES_CONSIDERED_POST-VIRAL
 

Rufous McKinney

Senior Member
Messages
13,524
I posted stuff here in PR from Dr. Aguirre-Chang several times including links you posted here.

I think his work and treatment approach is very interesting.
 

Rufous McKinney

Senior Member
Messages
13,524
ME/CFS
FIBROMYALGIA
ARTHRITIS
AUTOIMMUNE DIS.
POTS,
DYSAUTONOMIA
OTHER DISEASES POST-VIRAL
out of all these types of things, I feel like I enjoy some odd version that is unlike most other peoples' versions.

But I suppose alot of folks around here would say the same thing.

I've avoided COVID so far, but how much longer? with a granddaughter going to preschool conveying germs here every day?
 

SWAlexander

Senior Member
Messages
2,108
active COVID
no. Cytokines don't stop even when the virus is gone. They keep attacking. As long as one has inflammation one has Cytokines.
Danielle Beckman writes.
"I directly see the virus in the brain using microscopy, and you can see it as well in the video I made below. Viral protein (red, viral nucleocapsid) is found mainly inside neurons (blue, neun) in the olfactory cortex. Glial cells such as astrocytes (white, gfap) and microglia (green, iba1( are attacking these infected neurons, trying to slow down the viral spreading across the brain. Although beneficial, this mechanism also generates more neuroinflammatory propagation, with additional collateral damage to the circuits besides the death of infected neurons. You can deny as much as you want that this is happening, but science is here clearly proving what is going on. Our first study was published last year:" https://cell.com/cell-reports/fulltext/S2211-1247(22)01434-6?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2211124722014346%3Fshowall%3Dtrue
 
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SWAlexander

Senior Member
Messages
2,108
SARS-CoV-2 infection is associated with intestinal permeability, systemic inflammation, and microbial dysbiosis in hospitalized COVID-19 patients.

"The rectal swabs of COVID-19 patients had reduced abundances of several commensal bacteria including Faecalibacterium prausnitsii, and an increased abundance of the opportunistic pathogens"

Faecalibacterium prausnitzii is one of the most important bacteria in the human gut flora and makes up to 5-10% of the total number of bacteria

see post: https://forums.phoenixrising.me/thr...osis-in-hospitalized-covid-19-patients.91201/
 
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