Medical hypotheses
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Dental professionals work closely with patients and present an increased risk of person-to-person transmission of SARS-CoV-2. Moreover, the use of ultrasonic scalers, air-water syringes, and slow and high-speed handpieces, which are common in the dental office, generate spatter and aerosol. The use of preprocedural mouthrinses has been proposed to reduce the viral load in saliva and oropharyngeal tissues, thus decreasing viral load in dental aerosol. ⋯ We hypothesized that mouthrinses may reduce SARS-CoV-2 viral load in the oropharynx and its fluids reducing viral load in dental aerosol. The potential use of mouthrinses is discussed, along with proposal of in vitro and clinical studies, in order to evaluate this hypothesis. If this hypothesis holds true, dental professionals and patients may benefit from the routine use of preprocedural mouthrinses.
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This study aimed at identifying human neural proteins that can be attacked by cross-reacting SARS-COV-2 antibodies causing Guillain-Barré syndrome. These markers can be used for the diagnosis of Guillain-Barré syndrome (GBS). To achieve this goal, proteins implicated in the development of GBS were retrieved from literature. ⋯ Based on these results, the study suggests that NCAM may play a significant role in the immunopathogenesis of GBS. NCAM antibodies can be used as a marker for Guillain-Barré syndrome. However, more experimental studies are needed to prove these results.
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Several studies have described unusually high incidence of vascular thrombosis in coronavirus disease-2019 (COVID-19) patients. Pathogenesis of the vascular thrombosis in COVID-19 is least understood for now and presents a challenge to the treating physicians. Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the causative pathogen for COVID-19, has been shown to bind to angiotensin converting enzyme 2 (ACE2) protein in human epithelial cells which facilitates its entry in the organ and mediate tissue specific pathogenesis. ⋯ Existing in situ evidence for SARS-CoV-1 (the causative agent for SARS pandemic of 2002, which shared ACE2 as cell entry receptor) suggested that virus binding can downregulate ACE2, thus can induce endothelial dysfunction. Recently, in situ evidence has been presented that SARS-CoV-2 can infect cells in engineered human vascular endothelium, which can be effectively blocked by using clinical-grade recombinant human ACE2. Based on the circumstantial evidence present in the literature, we propose a SARS-CoV-2 cell entry receptor ACE2 based mechanism for vascular thrombosis in COVID-19 patients.