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Background and Aims

The coronavirus disease 2019 (COVID-19) pandemic has affected populations, societies, and lives for more than 2 years. Long-term sequelae of COVID-19, collectively termed the post-acute COVID-19 syndrome, are rapidly emerging across the globe. Here, we investigated whether severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) antigen persistence underlies the post-acute COVID-19 syndrome.

Methods

We performed an endoscopy study with 46 inflammatory bowel disease (IBD) patients 219 days (range 94-257) after a confirmed COVID-19 infection. SARS-CoV-2 antigen persistence was assessed in the small and large intestine by qPCR of four viral transcripts, immunofluorescence of viral nucleocapsid, and virus cultivation from biopsy tissue. Post-acute COVID-19 was assessed by a standardized questionnaire, and a systemic SARS-CoV-2 immune response was evaluated by flow cytometry and ELISA at endoscopy. IBD activity was evaluated by clinical, biochemical, and endoscopic means.

Results

We report expression of SARS-CoV-2 RNA in the gut mucosa ∼7 months after mild acute COVID-19 in 32 of 46 patients with IBD. Viral nucleocapsid protein persisted in 24 of 46 patients in gut epithelium and CD8+ T cells. Expression of SARS-CoV-2 antigens was not detectable in stool and viral antigen persistence was unrelated to severity of acute COVID-19, immunosuppressive therapy, and gut inflammation. We were unable to culture SARS-CoV-2 from gut tissue of patients with viral antigen persistence. Post-acute sequelae of COVID-19 were reported from the majority of patients with viral antigen persistence, but not from patients without viral antigen persistence.

Conclusion

Our results indicate that SARS-CoV-2 antigen persistence in infected tissues serves as a basis for post-acute COVID-19. The concept that viral antigen persistence instigates immune perturbation and post-acute COVID-19 requires validation in controlled clinical trials.

You can read an interview with two of the study authors here.