BackgroundRisk factors for severe COVID-19 include older age, male sex, obesity, black or Asian ethnicity and underlying medical conditions. Whether these factors also influence susceptibility to developing COVID-19 is uncertain.MethodsWe undertook a prospective, population-based cohort study (COVIDENCE UK) from 1 May 2020 to 5 February 2021. Baseline information on potential risk factors was captured by an online questionnaire. Monthly follow-up questionnaires captured incident COVID-19. We used logistic regression models to estimate multivariable-adjusted ORs (aORs) for associations between potential risk factors and odds of COVID-19.ResultsWe recorded 446 incident cases of COVID-19 in 15 227 participants (2.9%). Increased odds of developing COVID-19 were independently associated with Asian/Asian British versus white ethnicity (aOR 2.28, 95% CI 1.33 to 3.91), household overcrowding (aOR per additional 0.5 people/bedroom 1.26, 1.11 to 1.43), any versus no visits to/from other households in previous week (aOR 1.31, 1.06 to 1.62), number of visits to indoor public places (aOR per extra visit per week 1.05, 1.02 to 1.09), frontline occupation excluding health/social care versus no frontline occupation (aOR 1.49, 1.12 to 1.98) and raised body mass index (BMI) (aOR 1.50 (1.19 to 1.89) for BMI 25.0–30.0 kg/m2 and 1.39 (1.06 to 1.84) for BMI >30.0 kg/m2 versus BMI <25.0 kg/m2). Atopic disease was independently associated with decreased odds (aOR 0.75, 0.59 to 0.97). No independent associations were seen for age, sex, other medical conditions, diet or micronutrient supplement use.ConclusionsAfter rigorous adjustment for factors influencing exposure to SARS-CoV-2, Asian/Asian British ethnicity and raised BMI were associated with increased odds of developing COVID-19, while atopic disease was associated with decreased odds.Trial registration numberClinicalTrials.gov Registry (NCT04330599).
Since the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections in late 2019, the world has faced a major healthcare challenge. There remains limited understanding of the reasons for clinical variability of coronavirus disease 2019 (COVID-19), and a lack of biomarkers to identify individuals at risk of developing severe lung disease. This article aims to present a hypothesis on a vascular route of transfer of SARS-CoV-2 from the oral cavity to the lungs. Saliva is a reservoir of SARS-CoV-2, thus any breach in the immune defenses of the mouth may facilitate entrance of the virus to the vasculature through the gingival sulcus or periodontal pocket. From the oral vasculature, the virus would pass through veins of the neck and chest, and reach the heart, being pumped into pulmonary arteries, and to the small vessels in the lung periphery. The binding of the virus to the angiotensin-converting enzyme 2 receptor (ACE2), present on the endothelial surface of lung vessels, inactivates ACE2 and increases angiotensin-II levels, leading to pulmonary vasoconstriction and immunothrombosis (inflammatory-mediated clotting). This leads to vascular congestion, proximal vasodilatation, and subsequent lung parenchymal damage mediated by endothelial dysfunction. The biological rationale for the oral-vasculo-pulmonary route of infection is discussed in detail in this article, including pertinent radiological and oral cavity scientific findings. We propose that dental plaque accumulation and periodontal inflammation would further intensify this pathway. Therefore, it is suggested that daily oral hygiene and oral healthcare should be prioritized as such measures could be potentially lifesaving for COVID-19 patients. If this proposed pathological pathway is verified, it would be hugely significant in terms of understanding disease management. Simple low-cost measures, such as use of specific mouthwashes, could decrease the salivary viral load, and help prevent or mitigate the development of lung disease and severe COVID-19.
Introduction COVID‐19 is a transmissible respiratory and multisystem disease caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2). Viral transmission occurs mainly through the spread of salivary droplets or aerosol from an infected subject. Studies suggest that salivary viral load is correlated with disease severity and probability of transmission. Cetylpyridinium chloride mouthwash has been found to be effective in reducing salivary viral load. The aim of this systematic review of randomized controlled trials is to evaluate the efficacy of the mouthwash ingredient cetylpyridinium chloride on salivary viral load in SARS‐CoV‐2 infection. Methods Randomized controlled trials comparing cetylpyridinium chloride mouthwash with placebo and other mouthwash ingredients in SARS‐CoV‐2 positive individuals were identified and evaluated. Results Six studies with a total of 301 patients that met the inclusion criteria were included. The studies reported the efficacy of cetylpyridinium chloride mouthwashes in reduction on SARS‐CoV‐2 salivary viral load compared to placebo and other mouthwash ingredients. Conclusion Mouthwashes containing cetylpyridinium chloride are effective against salivary viral load of SARS‐CoV‐2 in vivo. There is also the possibility that the use of mouthwash containing cetylpyridinium chloride in SARS‐CoV‐2 positive subjects could reduce transmissibility and severity of COVID‐19.
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