Dr. Iwasaki explains that SARS-Cov2 is “one of many unexplained post-acute infection syndromes [that]
occur after encounter with many distinct pathogens” (such as EBV, polio, & dengue). @NIH#LongCovid#LongCovidKids
Dr. Iwasaki says that COVID-19 can cause long-lasting symptoms involving almost all organs and cites @patientled research on symptomology of #LongCovid. @NIH#CovidIsNotOver
Hypotheses on pathogenesis of #LongCovid include 1) viral reservoir 2) autoimmunity 3)dysbiosis/reactivation 4) tissue damage @NIH
Reactive microglia are 1) abundant in the white matter in mild Covid mouse-model & 2) increased in autopsies of patients who were SARS-COV-2 positive at time of death.
This suggests that even respiratory-only SARS-CoV-2 infection leads to prolonged changes in the CNS. #COVID19#LongCovid#CovidIsNotOver
“At 7 days and 7 weeks post infection, Covid19 infected mice have: Increased reactive microglia in the white matter,
Reduced neurogenesis in the hippocampus,
Reduced oligodendrocytes in the white matter,
Reduced myelination of axons”. #LongCovid#COVID19
In another, unpublished study, Dr. Iwasaki worked with @PutrinoLab. The study showed that #LongCovid patients “display significant perturbations in
myeloid and B cell compartments” and “have reduced CD4 T central memory and increased exhausted T cells”.
“A chronic level of antigen may be driving the high level of antibodies in longhaulers”. #LongCovid@NIH
The study showed that “Long COVID is associated with significant differences in circulating cytokines and hormones” and “ high chemokines and lectins are
associated with increased disease severity”. #LongCovid
Other findings: #LongCovid “patients have altered humoral responses to herpesviruses” and they “show specific elevations in anti-EBV IgG targeting gp42”. More research is needed. @NIH#CovidIsNotOver
“Specific immunological perturbations define Long COVID”, such as exhausted T-cells. Also, “decreased cortisol alone efficiently classifies Long COVID”.
Prof. Iwasaki explains that ”Patient Reported Outcomes alone are sufficient to identify long COVID patients with 94% accuracy”. #COVID19#LongCovid
Machine learning demonstrated that “Long COVID can be efficiently predicted from immunological data
alone”. #Covid_19#LongCovid@NIH
Dr. Iwasaki :“randomized clinical trials of cortisol replacement therapy are needed”. “Targeting cytokines or potential viral reservoirs as well as monoclonal antibodies” are interesting areas of study. @NIH#LongCovid
Dr. Bateman speaks of a case study: an identical twin female, 17years, track athlete, who developed severe exhaustion affecting every area of her life. She was able to attend college, but never able to work full-time. #MECFS
At age 24, she suffered an infection and was erroneously diagnosed with a psychiatric disorder. She was seen by Dr. Bateman, who tested for and diagnosed dysautonomia. The patient was able to be upright for 1 hour on worst days. Pyridostigmine was a beneficial therapeutic. #MECFS
Next up at the #IACFSME conference is Dr. Nicola Clague-Baker @ClagueNjc36 presenting on “Feasibility of investigating oxygen consumption (VO2), heart rate variability, blood pressure and lactic acid levels of people with myalgic encephalomyelitis during normal daily activities”.
This was a (successful) feasibility study, with enrollment being closed after 24h, showing that physiological measurement during everyday activity is possible for those patients with mild to severe #MECFS .
Dr. Clague-Baker‘a study adapted for different severities of ME/CFS in order to identify abnormalities and prevent harm to patient health. The outcome measures identified abnormal physiological changes in all patients with #MECFS.