LAUSR

Individuals susceptible to infection with coronavirus 2019 (COVID-19) represent heterogeneous populations presenting a large risk spectrum. Risk stratification is critical to define clinically relevant subpopulations to more accurately target screening, prevention, and therapeutic interventions and allocate resources. Patients over age of 65 and those with comorbidities including obesity, cardiovascular disease, chronic pulmonary disease, and diabetes mellitus are at higher risk for severe COVID-19 disease [1]. Various common viral agents including influenza and adenovirus are associated with an increased risk of a severe disease course and respiratory complications in immunocompromised patients; however, this has not been the case with coronaviruses [2]. It is unclear at this time whether rheumatic disease patients on chronic immunosuppressive therapy are at higher risk of developing a more severe disease course when infected with COVID-19 as data regarding this topic are limited and conflicting. One small study conducted in Italy, involving thirteen patients—four patients with confirmed COVID-19 identification through nasopharyngeal swab, four with symptoms highly suggestive of COVID-19, and five asymptomatic patients with a known exposure to COVID-19—treated with a biologic DMARD, a targeted synthetic DMARD, or a combination of the two, showed no increase risk of developing severe symptoms [3]. None of the thirteen patients developed severe respiratory complications, and only one patient (age 65) required short-term hospitalization [3]. All patients in this study had a diagnosis of rheumatoid arthri t is (RA) or spondyloarthritis (SpA) [3]. In a recent larger cohort in New York City of 86 patients with immune-mediated diseases and either confirmed or highly suspected COVID-19 symptomatic infection studied prospectively, the incidence of hospitalization among patients with immune-mediated inflammatory disease was consistent with that among patients with COVID-19 in the general population, suggesting that the baseline use of biologics is not associated with worse COVID-19 outcomes [4]. Another report, however, suggests that systemic lupus erythematosus (SLE) patients may be prone to severe COVID19 disease independent of their immunosuppression from lupus treatment. Hypomethylation and overexpression of angiotensin-converting enzyme-2 (ACE-2) in lupus patients may facilitate viral entry into the cells [5]. Recent data indicates that a small fraction of patients infected with COVID-19 develop rheumatic disease symptoms including arthralgia, interstitial pneumonia, myocarditis, leucopenia, thrombocytopenia, and coagulopathy with antiphospholipid antibodies [6, 7]. Significant efforts to assess the efficacy of anti-rheumatic drugs in COVID-19 patients are currently underway. All coronaviruses express a surface glycoprotein termed a “spike”which binds to the host receptor for entry [8]. This receptor has been identified as the ACE-2 which is expressed in mature lung epithelial cells, enterocytes, kidney proximal tubular cells, and endothelial cells [8]. This distribution of ACE-2 would explain the risk for multiorgan involvement of this viral infection. When the lysosomal proteases cleave the spike protein, it releases signal peptide that facilitates viral entry into the cells [8]. Low synthesis of antiviral cytokines, including interferon alpha and beta, and increased pro-inflammatory cytokines, including IL-1 and IL-6, * Kiana Vakil-Gilani [email protected]