The public defence will be held as a video conference over Zoom.
The defence will follow regular procedure as far as possible, hence it will be open to the public and the audience can ask ex auditorio questions when invited to do so.
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Due to copyright reasons, an electronic copy of the thesis must be ordered from the faculty. In order for the faculty to have time to process the order, it must be received by the faculty no later than 2 days prior to the public defence. Orders received later than 2 days before the defence will not be processed. Inquiries regarding the thesis after the public defence must be addressed to the candidate.
Digital Trial Lecture – time and place
Adjudication committee
- First opponent: Professor and Director of the Standford Center for Narcolepsy Emmanuel Mignot, Stanford Center for Sleep Sciences and Medicine, US
- Second opponent: Senior Consultant/Head of Nasjonal kompetansetjeneste for CFS/ME Ingrid B. Helland, Oslo University Hospital
- Third member and chair of the evaluation committee: Professor Marit Inngjerdingen, University of Oslo
Chair of the Defence
Associate Professor Andreas Lossius, University of Oslo
Principal Supervisor
Researcher Marte Kathrine Viken, Oslo University Hospital
Summary
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a serious and complex disease characterized by medically unexplained chronic fatigue, post-exertional malaise and a variety of additional symptoms. The etiology is unknown, and many different disease mechanisms have been proposed. Several immunologic changes have been reported among patients in different studies. A central hypothesis is that autoimmunity is involved in the pathogenesis of ME/CFS.
Autoimmune diseases (AID) are complex diseases with large variation in symptoms and severity. Genetic associations with the immunologically important human leukocyte antigen (HLA) genes are hallmarks of AID, typically manifested by a higher prevalence of specific HLA risk alleles among patients.
The main aim of this thesis was to evaluate the hypothesis that autoimmunity is involved in ME/CFS pathogenesis. First, we wanted to conduct a large and high resolution genetic HLA association study in ME/CFS. Next, we wanted to assess safety and potential effect of the immunosuppressive agent cyclophosphamide in a smaller group of ME/CFS patients. Finally, we wanted to see whether potential HLA risk alleles were associated with questionnaire-based clinical information or therapeutic effect.
We identified two novel HLA associations for adult, Norwegian ME/CFS patients, represented by a significantly higher prevalence of the alleles HLA-C*07:04 and HLA-DQB1*03:03 among 426 patients than among 4511 healthy controls. 22 out of 40 patients reported substantial clinical improvement after receiving cyclophosphamide, but the results must be cautiously interpreted since there was no control group. The HLA risk alleles were further significantly associated with comorbid autoimmunity among patients, and with clinical improvement after cyclophosphamide treatment.
Our results are in favor of immunological involvement in ME/CFS pathogenesis, possibly in a subgroup of patients, but the results need to be reproduced in additional studies before they can be regarded as established.
Additional information
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