Older patients are more susceptible to infective complications postoperatively, particularly chest complications. Surgeons should alter their practice to reduce morbidity, such as adopting protocols requiring early physiotherapy.
An analysis of SARS-CoV-2 cell entry genes identifies the intestine and colorectal cancer as susceptible tissues Editor SARS-CoV-2 is the causative agent for the COVID-19 pandemic. COVID-19 has necessitated rapid changes in surgical practice and organisation through both the initial peak and ongoing recovery period 1. SARS-CoV-2 infects cells by interacting with the host cell surface protein ACE2 and utilises TMPRSS2 in viral spike protein priming to facilitate cell entry (Fig. 1a) 2. Whilst COVID-19 is predominantly a respiratory disease approximately 15% of patients have concurrent gastrointestinal symptoms 3. SARS-CoV-2 RNA and live virus have been identified in stool from COVID-19 patients and SARS-CoV-2 readily infects intestinal organoids 4-6. Despite these circumstantial data, gastrointestinal transmission has not yet been formally confirmed. Cancers commonly express different genes from the tissue of origin and it is largely unexplored whether tumours can be infected with SARS-CoV-2. We sought to explore the expression of ACE2 and TMPRSS2 in large publicly available normal tissue and pan-cancer expression data sets to understand whether levels of these genes identify susceptible tissues. Analysis of the normal tissue Genotype Tissue Expression project (GTEx) dataset showed high ACE2 expression in the testis, small intestine, kidney, heart, thyroid and adipose tissue (Fig. S1a, supporting information). TMPRSS2 levels were highest in the prostate, stomach, small intestine, pancreas, lung, salivary gland, kidney, thyroid and liver (Fig. S1b, supporting information). Whilst initial analysis suggested only kidney and thyroid co-expressed high levels of ACE2 and TMPRSS2 closer inspection of small
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