Dr. Bhupesh Prusty: Herpes virus reactivation as a trigger for #MECFS and #LongCovid
Presenting data on how looking at results can generate different ideas for moving research forward
acute vs chronic contributors in mecfs: fibronectin, peripheral circulation, fibrobalst, mast cell. direct consequence of viral infection/reactivation in: brain and neuronal cells, muscle cells, cardiac myocites
brain muscles, cardia as site of acute disease, then indirect consequences as chronic illness manifested in symptoms such as pots, connective tissue disorder, etc based on the factors involved.
herpesvirus signature in #mecfs and #longcovid immunoglobin detection in pt serum using proteins against herpesvirus dUTPase proteins HSV-1 dUTPase found in over 50% of long covid pts
Autophagy is inhibited under these conditions. Extensive mitochondrial effects are observed.
Autoimmunity is expected to play a role. Can we divide the pts into groups based on what antibodies they are expressing to find patterns? IgG pattern was not found. #mecfs pts have overlapping autoantibodies overlapping with SLE and MS.
IgM against autoantigens can differentiate mecfs patients from healthy controls
Most mecfs pts have increased IgM response against a lot of environmental and common pathogenic antigens
3 very important proteins are depleted in activated immune complex of mecfs patients
serum fibronectin and significantly increased in #MECFS and #LongCovid - it tells us that there is an alteration in the clotting process. The amount of fibronectin correlates with severity.
Both cellular and plasma fibronectin is increased in mecfs
Reaching pathological concentrations of serum fibronectin is easier in females than males.
In a 1995 study of mice, 3 weeks post infection, fibronectin levels went up and IgM-FN1 decreased, this was reversed 4 weeks post infection.
IgM fibronectin can be a natural IgM (doesn't require an antigen). Their job is to clean when cells die. autoimmunity is highly correlated with this type of IgM.
Looking at 2 of the most common natural IgMs (PC and MDA) and you see the same pattern in #LongCovid and #mecfs with these additional natural IgMs
biochemical overlapping of #MECFS and #LongCovid patients is high when comparing FN1
pts that most commonly develop long covid where not hospitalized. This is due to an inhibition of sars-covid-2 expression with the re-activation.
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All of them are risk factors and we need to understand the interrelationships of complex disease and the possibilities for differentiated treatment by patient stratification. Biomarkers remain elusive and clinical subtypes need phenotype & system biology approach
We have just started to define the edges of the puzzle, we need to be able to complete the puzzle by understanding the big picture and what pieces are the components.
How do you determine molecular cause of MECFS and how do you treat and cure it ?
There are many crossroads in the maze of trying to treat MECFS. The decision taken had to do with the experience and perception of the person taking the decision
Before MECFS: a virus, bacteria, physical trauma, childbirth, vaccination, surgery.
TCA cycle - itaconate not discussed prevalently within this cycle. The transformation with CoA-SH was believed to be the end of that part of the process.
Every carbon is avoiding the processes that lead to NAD. The shunt will reduce the amount of ATP depending on the amount of carbon going in the different directions.
Dr Jesper Mehlsen - Towards a uniform treatment regimen
There is knowledge in the Pathobiology of MECFS - using that to direct treatment
Neuro inflammation and human herpes virus - removal of EBV, cmv, hhv6. ; also decrease inflammation with mono/doxy (#remissionbiome ), LDN, aripripazol, SSRI, PEA, cox 2 inhibitors; ATR1 blockers - not one size fits all