Evidence of SARS-CoV2 entry protein ACE2 in the human nose and olfactory bulb

Usually, pandemic COVID-19 disease, caused by SARS-CoV2, presents with mild respiratory symptoms such as fever, cough but frequently also with anosmia and neurological symptom. Virus-cell fusion is mediated by Angiotensin-Converting Enzyme 2 (ACE2) and Transmembrane Serine Protease 2 (TMPRSS2) with their organ expression pattern determining viral tropism. Clinical presentation suggests rapid viral dissemination to central nervous system leading frequently to severe symptoms including viral meningitis. Here, we provide a comprehensive expression landscape of ACE2 and TMPRSS2 proteins across human, post-mortem nasal and olfactory tissue. Sagittal sections through the human nose complemented with immunolabelling of respective cell types represent different anatomically defined regions including olfactory epithelium, respiratory epithelium of the nasal conchae and the paranasal sinuses along with the hardly accessible human olfactory bulb. ACE2 can be detected in the olfactory epithelium, as well as in the respiratory epithelium of the nasal septum, the nasal conchae and the paranasal sinuses. ACE2 is located in the sustentacular cells and in the glandular cells in the olfactory epithelium, as well as in the basal cells, glandular cells and epithelial cells of the respiratory epithelium. Intriguingly, ACE2 is not expressed in mature or immature olfactory receptor neurons and basal cells in the olfactory epithelium. Similarly ACE2 is not localized in the olfactory receptor neurons albeit the olfactory bulb is positive. Vice versa, TMPRSS2 can also be detected in the sustentacular cells and the glandular cells of the olfactory epithelium. Our findings provide the basic anatomical evidence for the expression of ACE2 and TMPRSS2 in the human nose, olfactory epithelium and olfactory bulb. Thus, they are substantial for future studies that aim to elucidate the symptom of SARS-CoV2 induced anosmia of via the olfactory pathway.

Aerosol-spread during chest compressions in a cadaver model

ObjectiveTo evaluate aerosol-spread in cardiopulmonary resuscitation (CPR) using different methods of airway management. Knowledge about aerosol-spread is vital during the SARS-CoV-2-Pandemic. MethodsTo evaluate feasibility we nebulized ultraviolet sensitive detergents into the artificial airway of a resuscitation dummy and performed CPR. The spread of the visualized aerosol was documented by a camera. In a second approach we applied nebulized detergents into human cadavers by an endotracheal tube and detected aerosol-spread during chest compressions the same way. We did recordings with undergoing compression-only-CPR, with a surgical mask and with an inserted laryngeal tube with and without a connected airway filter. ResultsMost aerosol-spread at the direction of the provider was visualized during compression-only-CPR. The use of a surgical mask deflected the spread. Inserting a laryngeal tube connected to an airway filter lead to a remarkable reduction of aerosol-spread. ConclusionThe early insertion of a laryngeal tube connected to an airway filter before starting chest compression may be good for two things - the treatment of hypoxemia as the likeliest cause of cardiac arrest and for staff protection during CPR.