Do COVID-19 'long haulers' have biochemical and physiological changes seen in Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome (ME/CFS)?
- Funded by Brain Research New Zealand
- Total publications:1000 publications
Grant number: N/A
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Key facts
Disease
COVID-19start year
-99Known Financial Commitments (USD)
$0Funder
Brain Research New ZealandPrincipal Investigator
Emeritus Professor Warren TateResearch Location
New ZealandLead Research Institution
N/AResearch Priority Alignment
N/A
Research Category
Clinical characterisation and management
Research Subcategory
Disease pathogenesis
Special Interest Tags
N/A
Study Type
Unspecified
Clinical Trial Details
N/A
Broad Policy Alignment
Pending
Age Group
Adults (18 and older)
Vulnerable Population
Unspecified
Occupations of Interest
Unspecified
Abstract
A concerning development from the COVID-19 pandemic is the number of individuals that show prolonged debilitating symptoms long after the expected recovery time to normal health. Called 'long COVID', an estimated 30% of 'recovered' COVID-19 patients report ongoing symptoms, with many unable to return to work or perform physically or mentally taxing activities. With over 63 million cases of COVID-19 currently recorded and the numbers still rising rapidly, this is a concerning statistic and an urgent matter for public health. Many of the symptoms reported by long COVID patients, particularly the persistent fatigue and 'brain fog', are characteristic of another long-term debilitating disease, Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), that often arises after infectious disease outbreaks. Using cutting edge analytical techniques including mass spectrometry to profile the immune cell proteins, and specialised sequencing technology to derive sites of DNA methylation, we plan to compare the molecular profiles of long COVID-19 patients with those of ME/CFS and healthy controls. We have very recently identified specific molecular changes characteristic of ME/CFS patients that allow us to better understand the systemic disruptions occurring in patients. This has highlighted abnormal regulation of energy production and oxidative stress, and abnormal neurological activity of the brain and the nervous system. By comparing the molecular similarities or differences of long COVID to ME/CFS we can better understand the underlying pathophysiology of these long COVID patients, and suggest potential therapeutic interventions that might be applied based on our understanding of ME/CFS. This will be achieved by recruiting a small cohort of 5 long COVID-19 patients in the practice of our collaborating physician Dr Rosamund Vallings, and, in combination with cohorts of 5 ME/CFS patients and 5 matched healthy controls, we will perform a thorough molecular analysis based on in-depth strict principles of precision or personalised medicine.
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