COVID-19 and Inflammatory Bowel Diseases: Risk Assessment, Shared Molecular Pathways, and Therapeutic Challenges

• Published in: Gastroenterology research and practice 2020, Vol.2020 (2020), p.1-7
• Main Authors: Cijevschi-Prelipcean, Cristina, Mihai, Cătălina, Diculescu, Mircea, Popa, Iolanda Valentina, Burlacu, Alexandru
• Format: Article
• Language: English
• Subjects: Adalimumab; Care and treatment; Comorbidity; Computational linguistics; Coronaviruses; COVID-19; Datasets; Disease susceptibility; Genetic translation; Health aspects; Infections; Inflammatory bowel disease; Inflammatory bowel diseases; Intensive care; Interferon; Language processing; Middle East respiratory syndrome; Mortality; Natural language interfaces; Pandemics; Patients; Population; Queries; Questioning; Review; Risk assessment; Severe acute respiratory syndrome coronavirus 2; Studies; Tofacitinib
• ISSN: 1687-6121; 1687-630X
• DOI: 10.1155/2020/1918035

Background. The novel coronavirus SARS-CoV-2 causing COVID-19 disease is yielding a global outbreak with severe threats to public health. In this paper, we aimed at reviewing the current knowledge about COVID-19 infectious risk status in inflammatory bowel disease (IBD) patients requiring immunosuppressive medication. We also focused on several molecular insights that could explain why IBD patients appear not to have higher risks of infection and worse outcomes in COVID-19 than the general population in an attempt to provide scientific support for safer decisions in IBD patient care. Methods. PubMed electronic database was interrogated for relevant articles involving data about common molecular pathways and shared treatment strategies between SARS-CoV-2, SARS-CoV-1, MERS-CoV, and inflammatory bowel diseases. Besides, Neural Covidex, an artificial intelligence tool, was used to answer queries about pathogenic coronaviruses and possible IBD interactions using the COVID-19 Open Research Dataset (CORD-19). Discussions. Few molecular and therapeutic interactions between IBD and pathogenic coronaviruses were explored. First, we showed how the activity of soluble angiotensin-converting enzyme 2, CD209L other receptors, and phosphorylated α subunit of eukaryotic translation initiation factor 2 might exert protective impact in IBD in case of coronavirus infection. Second, IBD medication was discussed in the context of possible beneficial effects on COVID-19 pathogeny, including “cytokine storm” prevention and treatment, immunomodulation, interferon signaling blocking, and viral endocytosis inhibition. Conclusions. Using the current understanding of SARS-CoV-2 as well as other pathogenic coronaviruses immunopathology, we showed why IBD patients should not be considered at an increased risk of infection or more severe outcomes. Whether our findings are entirely applicable to the pathogenesis, disease susceptibility, and treatment management of SARS-CoV-2 infection in IBD must be further explored.