Associations of Stay-at-Home Order Enforcement With COVID-19 Population Outcomes: An Interstate Statistical Analysis.

In the United States, state governors initially enacted coronavirus diseases 2019 (COVID-19)-mitigation policies with limited epidemiologic data. One prevailing legislative approach, from March to May 2020, was the implementation of "stay-at-home" (SAH) executive orders. Although social distancing was encouraged, SAH orders varied between states, and the associations between potential legal prosecution and COVID-19 outcomes are currently unknown. Here, we provide empirical evidence on how executive enforcement of movement restrictions may influence population health during an infectious disease outbreak. A generalized linear model with negative binomial regression family compared COVID-19 outcomes in states with law-enforceable stay-at-home (eSAH) orders versus those with unenforceable or no SAH orders (uSAH), controlling for demographic factors, socioeconomic influences, health comorbidities, and social distancing. COVID-19 incidence was less by 1.22 cases per day per capita in eSAH states compared with uSAH states (coefficient = -1.22, 95% confidence interval (CI): -1.83, -0.61; P < 0.001), and each subsequent day without an eSAH order was associated with a 0.03 incidence increase (coefficient = 0.03, 95% CI: 0.03, 0.04; P < 0.001). Daily mortality was 1.96 less for eSAH states per capita (coefficient = -1.96, 95% CI: -3.25, -0.68; P = 0.004). Our findings suggest allowing the enforcement of public health violations, compared with community education alone, is predictive of improved COVID-19 outcomes.

Atopic endotypes as a modulating factor for SARS-CoV-2 infection: mechanisms and implications.

PURPOSE OF REVIEW: Asthma patients are typically at increased risk for severe outcomes from viral respiratory infections. However, asthma and atopy do not appear to be overrepresented comorbidities in COVID-19 patients, and hypotheses attempt to explain this observation. As COVID-19 continues to spread globally, it is imperative to understand how disease outcomes may be influenced in this population to guide patient care. RECENT FINDINGS: Angiotensin converting enzyme 2 (ACE2) is the principal host cell receptor for SARS-CoV-2 entry and Transmembrane Protease Serine 2 (TMRSS2) is the main priming protease. Models have linked atopic endotypes to reductions in ACE2 and increases in TMRSS2 on respiratory epithelia. Epidemiologic and experimental findings imply alterations in ACE2 expression correlate with clinical COVID-19 disease, but limitations restrict the ability to draw direct conclusions. SUMMARY: There is reasonable evidence to assert atopic endotypes modulate COVID-19 susceptibility, but it remains premature to classify this association as protective or deleterious. Asthma is a heterogeneous disease and epidemiologic studies should focus on investigating COVID-19 outcomes by underlying endotype. Direct experimental and clinical evidence is needed to draw definitive conclusions on how the complex interplay of ACE2 and TMRSS2 affect viral entry. VIDEO ABSTRACT: https://www.dropbox.com/sh/9sfwqhz2h78sio3/AAB0JYd4MFzM5JjDFcYwz4CXa?dl=0.

Influence of the Microbiome on Chronic Rhinosinusitis With and Without Polyps: An Evolving Discussion.

Chronic rhinosinusitis (CRS) is widely prevalent within the population and often leads to decreased quality of life, among other related health complications. CRS has classically been stratified by the presence of nasal polyps (CRSwNP) or the absence nasal polyps (CRSsNP). Management of these conditions remains a challenge as investigators continue to uncover potential etiologies and therapeutic targets. Recently, attention has been given to the sinunasal microbiota as both an inciting and protective influence of CRS development. The healthy sinunasal microbiologic environment is largely composed of bacteria, with the most frequent strains including Staphylococcus aureus, Streptococcus epidermidis, and Corynebacterium genera. Disruptions in this milieu, particularly increases in S. aureus concentration, have been hypothesized to perpetuate both Th1 and Th2 inflammatory changes within the nasal mucosa, leading to CRS exacerbation and potential polyp formation. Other contributors to the sinunasal microbiota include fungi, viruses, and bacteriophages which may directly contribute to underlying inflammation or impact bacterial prevalence. Modifiable risk factors, such as smoking, have also been linked to microbiota alterations. Research interest in CRS continues to expand, and thus the goal of this review is to provide clinicians and investigators alike with a current discussion on the microbiologic influence on CRS development, particularly with respect to the expression of various phenotypes. Although this subject is rapidly evolving, a greater understanding of these potential factors may lead to novel research and targeted therapies for this often difficult to treat condition.