[Preprint] Evidence of a Sjögren’s disease-like phenotype following COVID-19, 2022, Shen et al

Evidence of a Sjögren’s disease-like phenotype following COVID-19

Spoiler: Researchers including NIH craniofacial research unit, NCI Pathology, Colleges of Medicine and Veterinary Medicine at Uni of Florida

Yiran Shen, Alexandria Voigt, Laura Goranova, Mehdi Abed, David E. Kleiner, Jose O. Maldonado, Margaret Beach, Eileen Pelayo, John A. Chiorini, William F. Craft, David A. Ostrov, Vijay Ramiya, Sukesh Sukumaran, Apichai Tuanyok, Blake M. Warner, Cuong Q. Nguyen

Objectives Sjögren’s Disease (SjD) is a chronic and systemic autoimmune disease characterized by lymphocytic infiltration and the development of dry eyes and dry mouth resulting from the secretory dysfunction of the exocrine glands. SARS-CoV-2 may trigger the development or progression of autoimmune diseases, as evidenced by increased autoantibodies in patients and the presentation of cardinal symptoms of SjD. The objective of the study was to determine whether SARS-CoV-2 induces the signature clinical symptoms of SjD.

Methods The ACE2-transgenic mice were infected with SARS-CoV-2. SJD profiling was conducted. COVID-19 patients’ sera were examined for autoantibodies. Clinical evaluations of convalescent COVID-19 subjects, including minor salivary gland (MSG) biopsies, were collected. Lastly, monoclonal antibodies generated from single B cells of patients were interrogated for ACE2/spike inhibition and nuclear antigens.

Results Mice infected with the virus showed a decreased saliva flow rate, elevated antinuclear antibodies (ANAs) with anti-SSB/La, and lymphocyte infiltration in the lacrimal and salivary glands. Sera of COVID-19 patients showed an increase in ANA, anti-SSA/Ro52, and anti-SSB/La. The male patients showed elevated levels of anti-SSA/Ro52 compared to female patients, and female patients had more diverse ANA patterns. Minor salivary gland biopsies of convalescent COVID-19 subjects showed focal lymphocytic infiltrates in four of six subjects, and 2 of 6 subjects had focus scores >2. Lastly, we found monoclonal antibodies produced in recovered patients can both block ACE2/spike interaction and recognize nuclear antigens.

Conclusion Overall, our study shows a direct association between SARS-CoV-2 and SjD. Hallmark features of SjD salivary glands were histologically indistinguishable from convalescent COVID-19 subjects. The results potentially implicate that SARS-CoV-2 could be an environmental trigger for SjD.

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Mice and small numbers of patients. Presumably a much less common outcome than the ME/CFS-like phenotype.

 

I have some signs of Sjogren, like more-or-less permanently (moderately) enlarged and sore glands, and reduced saliva flow (to the point where I need to keep water handy, and use moisturising oral gels at night, and I have had doctors and dentists remark unprompted on the oral dryness).

Did have an ultrasound of the relevant glands for other reasons, and they showed no overt pathology.

Have sometimes wondered if this is something I should get checked more thoroughly (mainly gland biopsies and blood tests). The major symptoms overlap considerably with ME: fatigue (79%); dry eyes (75%); dry mouth (73%); joint pain (65%); trouble sleeping (64%); eye discomfort (60%); muscle pain (56%); and brain fog (54%).

Interestingly, it is apparently the second most common cause of dysautonomia, and is commonly comorbid with other auto-immune disorders.

Main reason I have not pursued it further is that there is no specific test for it, and there is no treatment or cure, only symptom management and risk reduction, and I am doing most of that anyway for ME.