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Background: An asymptomatic respiratory viral infection during cardiac surgery could lead to pulmonary complications and increased mortality. For elective surgery, testing for respiratory viral infection before surgery or vaccination could reduce the number of these pulmonary complications. The aim of this study was to investigate the association between influenzalike illness (ILI) seasons and prolonged mechanical ventilation and inhospital mortality in a Dutch cohort of adult elective cardiac surgery patients. Methods: Cardiac surgery patients who were admitted to the intensive care unit between January 1, 2014, and February 1, 2020, were included. The primary endpoint was the duration of invasive mechanical ventilation in the ILI season compared with baseline season. Secondary endpoints were the median PaO2 to fraction of inspired oxygen ratio on days 1, 3, and 7 and postoperative inhospital mortality. Results: A total of 42,277 patients underwent cardiac surgery, 12,994 (30.7%) in the ILI season, 15,843 (37.5%) in the intermediate season, and 13,440 (31.8%) in the baseline season. No hazard rates indicative of a longer duration of invasive mechanical ventilation during the ILI season were found. No differences were found for the median PaO2 to fraction of inspired oxygen ratio between seasons. However, inhospital mortality was higher in the ILI season compared with baseline season (odds ratio 1.67; 95% CI, 1.14-2.46). Conclusions: Patients undergoing cardiac surgery during the ILI season were at increased risk of inhospital mortality compared with patients in the baseline season. No evidence was found that this difference is caused by direct postoperative pulmonary complications.

Background Co-infections with SARS-CoV-2 and influenza virus may become more prevalent now that many countries are easing restrictions to reduce the spread of SARS-CoV-2. Co-infected patients are more likely to receive invasive mechanical ventilation (IMV) and have higher odds of in-hospital mortality. In the RECOVERY trial, dexamethasone was found to reduce the risk of 28-day mortality in hospitalised COVID-19 patients. On June 16, 2020, corticosteroids were included in clinical guidelines for the treatment of COVID-19 patients requiring supplemental oxygen. However, corticosteroid treatment in severe influenza virus infection may increase mortality. The effect of steroids in influenza and COVID-19 co-infected patients is unknown. Methods Adult patients with RT-PCR confirmed SARS-CoV-2 and influenza virus co-infection were evaluated. Patients without supplemental oxygen during admission were excluded. Patients who were hospitalised prior to June 16, 2020 were included in the ‘early’ group and patients who were hospitalised on or after June 16, 2020 were included in the ‘late’ group. Results 171 co-infected patients were included, 123 patients in the early group (table 1) and 48 in the late group (table 2). In the early group, 25 patients received steroids. In the late group, 40 patients received steroids. In the early group, the proportion of patients who were admitted to critical care was slightly lower in the group that received steroids. IMV was similar in both groups. In-hospital mortality was slightly higher in the group treated with steroids. In the late group, critical care admission and receipt of IMV were higher in the group not treated with corticosteroids than the group with corticosteroid treatment. In-hospital mortality was slightly lower in the group not treated with steroids. Conclusion There are differences between co-infected patients who were treated and not treated with corticosteroids and differences between the early and late groups. A limitation is that no dates were collected for the start of steroid treatment, making it impossible to draw conclusions on the causality of the need for IMV and treatment with steroids in this analysis. Future research should focus on the effect of steroids in COVID-19 and influenza co-infected patients. Disclosures Peter Openshaw, PhD, Bavarian Nordic: Advisor/Consultant|Cepheid: Advisor/Consultant|GlaxoSmithKline: Advisor/Consultant|Janssen: Advisor/Consultant|Pfizer: Advisor/Consultant Calum Semple, PhD, Integrum Scientific: Scientific Advisory Board|Integrum Scientific: Stocks/Bonds.

An increasing body of literature describes the role of host factors in COVID-19 pathogenesis. There is a need to combine diverse, multi-omic data in order to evaluate and substantiate the most robust evidence and inform development of future therapies. We conducted a systematic review of experiments identifying host factors involved in human betacoronavirus infection (SARS-CoV-2, SARS-CoV, MERS-CoV, seasonal coronaviruses). Gene lists from these diverse sources were integrated using Meta-Analysis by Information Content (MAIC). This previously described algorithm uses data-driven gene list weightings to produce a comprehensive ranked list of implicated host genes. 5,418 genes implicated in human betacoronavirus infection were identified from 32 datasets. The top ranked gene was *PPIA*, encoding cyclophilin A. Pharmacological inhibition with cyclosporine in vitro exerts antiviral activity against several coronaviruses including SARS-CoV. Other highly-ranked genes included proposed prognostic factors (*CXCL10*, *CD4*, *CD3E*) and investigational therapeutic targets (*IL1A*) for COVID-19, but also previously overlooked genes with potential as therapeutic targets. Gene rankings also inform the interpretation of COVID-19 GWAS results, implicating *FYCO1* over other nearby genes in a disease-associated locus on chromosome 3. Pathways enriched in gene rankings included T-cell receptor signalling, protein processing, and viral infections. We identified limited overlap of our gene list with host genes implicated in ARDS (innate immune and inflammation genes) and Influenza A virus infection (RNA-binding and ribosome-associated genes). We will continue to update this dynamic ranked list of host genes as the field develops, as a resource to inform and prioritise future studies. Updated results are available at https://baillielab.net/maic/covid19.