From HHV-6 reactivation to autoimmune reactivity against tight junctions
and neuronal antigens, to inflammation, depression, and chronic fatigue
syndrome due to Long COVID.
Abstract
Background: Inflammation and autoimmune responses contribute to
the pathophysiology of Long COVID, and its affective and chronic fatigue
syndrome (CFS) symptoms, labeled “the physio-affective phenome.”
Objectives: To investigate whether Long COVID and its
physio-affective phenome are linked to autoimmunity to the tight
junction proteins, zonulin and occludin (ZOOC), and immune reactivity to
lipopolysaccharides (LPS), and whether the latter are associated with
signs of human herpes virus-6 reactivation (HHV-6), autoimmunity
directed against oligodendrocyte and neuronal proteins, including myelin
basic protein (MBP). Methods: IgA /IgM/IgG responses
to Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), HHV-6,
ZOOC, and neuronal proteins, C-reactive protein (CRP) and advanced
oxidation protein products (AOPP), were measured in 90 Long COVID
patients and 90 healthy controls. The physio-affective phenome was
conceptualized as a factor extracted from physical and affective symptom
domains. Results: Neural network identified IgA directed to LPS
(IgA-LPS), IgG-ZOOC, IgG-LPS, and IgA-ZOOC as the most important
variables associated with Long COVID diagnosis with an area under the
ROC curve of 0.755. Partial Least Squares analysis showed that 40.9% of
the variance in the physio-affective phenome was explained by CRP,
IgA-MPB and IgG-MBP. A large part of the variances in both autoimmune
responses to MBP (36.3-39.7%) was explained by autoimmunity (IgA and
IgG) directed to ZOOC. The latter was strongly associated with indicants
of HHV-6 reactivation, which in turn was associated with increased
IgM-SARS-CoV-2. Conclusions: Autoimmunity against components of
the tight junctions and increased bacterial translocation may be
involved in the pathophysiology of Long COVID’s physio-affective
phenome.