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1.
Clin Infect Dis ; 74(Suppl_3): S219-S221, 2022 05 15.
Article in English | MEDLINE | ID: covidwho-1868252

ABSTRACT

This supplement demonstrates the profound reach of social media across several domains: improved clinical care and advocacy, data analysis, broad reach to diverse patient populations, educational access, best practices in medical education, peer review, digital strategy for individuals and institutions, and combating misinformation.


Subject(s)
Communicable Diseases , Social Media , Communicable Diseases/epidemiology , Communication , Humans
4.
J Infect Dis ; 224(11): 1810-1820, 2021 12 01.
Article in English | MEDLINE | ID: covidwho-1545969

ABSTRACT

The coronavirus disease 2019 (COVID-19) pandemic has disproportionately impacted lesbian, gay, bisexual, transgender, and queer (LGBTQ+) communities. Many disparities mirror those of the human immunodeficiency virus (HIV)/AIDS epidemic. These health inequities have repeated throughout history due to the structural oppression of LGBTQ+ people. We aim to demonstrate that the familiar patterns of LGBTQ+ health disparities reflect a perpetuating, deeply rooted cycle of injustice imposed on LGBTQ+ people. Here, we contextualize COVID-19 inequities through the history of the HIV/AIDS crisis, describe manifestations of LGBTQ+ structural oppression exacerbated by the pandemic, and provide recommendations for medical professionals and institutions seeking to reduce health inequities.


Subject(s)
COVID-19 , Health Inequities , Sexual and Gender Minorities , Transgender Persons , COVID-19/epidemiology , Female , HIV Infections/history , History, 20th Century , History, 21st Century , Humans , Male , Pandemics
5.
Open Forum Infect Dis ; 8(9): ofab417, 2021 Sep.
Article in English | MEDLINE | ID: covidwho-1440640

ABSTRACT

During the coronavirus disease 2019 (COVID-19) pandemic, we have witnessed profound health inequities suffered by Black, Indigenous, and People of Color (BIPOC). These manifested as differential access to testing early in the pandemic, rates of severe disease and death 2-3 times higher than white Americans, and, now, significantly lower vaccine uptake compared with their share of the population affected by COVID-19. This article explores the impact of these COVID-19 inequities (and the underlying cause, structural racism) on vaccine acceptance in BIPOC populations, ways to establish trustworthiness of healthcare institutions, increase vaccine access for BIPOC communities, and inspire confidence in COVID-19 vaccines.

6.
Open Forum Infect Dis ; 8(2): ofab027, 2021 Feb.
Article in English | MEDLINE | ID: covidwho-1254809

ABSTRACT

Rapid information dissemination is critical in a world changing rapidly due to global threats. Ubiquitous internet access has created new methods of information dissemination that are rapid, far-reaching, and universally accessible. However, inaccuracies may accompany rapid information dissemination, and rigorous evaluation of primary data through various forms of peer review is crucial. In an era in which high-quality information can save lives, it is critical that infectious diseases specialists are well versed in digital strategy to effectively disseminate information to colleagues and the community and diminish voices spreading misinformation. In this study, we review how social media can be used for rapid dissemination of quality information, benefits and pitfalls of social media use, and general recommendations for developing a digital strategy as an infectious diseases specialist. We will describe how the Infectious Diseases Society of America has leveraged digital strategy and social media and how individuals can amplify these resources to disseminate information, provide clinical knowledge, community guidance, and build their own person brand. We conclude in providing guidance to infectious diseases specialists in aiming to build and preserve public trust, consider their audience and specific goals, and use social media to highlight the value of the field of infectious diseases.

7.
Open Forum Infectious Diseases ; 7(Supplement_1):S320-S321, 2020.
Article in English | Oxford Academic | ID: covidwho-1010546
8.
J Infect Dis ; 222(6): 890-893, 2020 08 17.
Article in English | MEDLINE | ID: covidwho-990713

ABSTRACT

The coronavirus disease 2019 (COVID-19) pandemic has unveiled unsettling disparities in the outcome of the disease among African Americans. These disparities are not new but are rooted in structural inequities that must be addressed to adequately care for communities of color. We describe the historical context of these structural inequities, their impact on the progression of COVID-19 in the African American (black) community, and suggest a multifaceted approach to addressing these healthcare disparities. (Of note, terminology from survey data cited for this article varied from blacks, African Americans, or both; for consistency, we use African Americans throughout.).


Subject(s)
Betacoronavirus , Black or African American , Coronavirus Infections/epidemiology , Healthcare Disparities/ethnology , Pneumonia, Viral/epidemiology , COVID-19 , Coronavirus , Coronavirus Infections/ethnology , Health Services Accessibility , Health Status Disparities , Humans , Pandemics , Pneumonia, Viral/ethnology , Risk Factors , SARS-CoV-2 , Social Determinants of Health/ethnology , Socioeconomic Factors , United States/epidemiology
9.
J Infect Dis ; 222(12): 1951-1954, 2020 Nov 13.
Article in English | MEDLINE | ID: covidwho-952024

ABSTRACT

The coronavirus disease 2019 (COVID-19) pandemic in the United States has revealed major disparities in the access to testing and messaging about the pandemic based on the geographic location of individuals, particularly in communities of color, rural areas, and areas of low income. This geographic disparity, in addition to deeply rooted structural inequities, have posed additional challenges to adequately diagnose and provide care for individuals of all ages living in these settings. We describe the impact that COVID-19 has had on geographically disparate populations in the United States and share our recommendations on what might be done to ameliorate the current situation.


Subject(s)
COVID-19 Testing/trends , COVID-19/epidemiology , Ethnicity , Geography, Medical , Healthcare Disparities/ethnology , COVID-19/ethnology , Health Services Accessibility , Health Status Disparities , Humans , Poverty , Social Determinants of Health/ethnology , United States/epidemiology
11.
Nat Med ; 26(10): 1636-1643, 2020 10.
Article in English | MEDLINE | ID: covidwho-728994

ABSTRACT

Several studies have revealed that the hyper-inflammatory response induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a major cause of disease severity and death. However, predictive biomarkers of pathogenic inflammation to help guide targetable immune pathways are critically lacking. We implemented a rapid multiplex cytokine assay to measure serum interleukin (IL)-6, IL-8, tumor necrosis factor (TNF)-α and IL-1ß in hospitalized patients with coronavirus disease 2019 (COVID-19) upon admission to the Mount Sinai Health System in New York. Patients (n = 1,484) were followed up to 41 d after admission (median, 8 d), and clinical information, laboratory test results and patient outcomes were collected. We found that high serum IL-6, IL-8 and TNF-α levels at the time of hospitalization were strong and independent predictors of patient survival (P < 0.0001, P = 0.0205 and P = 0.0140, respectively). Notably, when adjusting for disease severity, common laboratory inflammation markers, hypoxia and other vitals, demographics, and a range of comorbidities, IL-6 and TNF-α serum levels remained independent and significant predictors of disease severity and death. These findings were validated in a second cohort of patients (n = 231). We propose that serum IL-6 and TNF-α levels should be considered in the management and treatment of patients with COVID-19 to stratify prospective clinical trials, guide resource allocation and inform therapeutic options.


Subject(s)
Coronavirus Infections/immunology , Interleukin-1beta/immunology , Interleukin-6/immunology , Interleukin-8/immunology , Pneumonia, Viral/immunology , Tumor Necrosis Factor-alpha/immunology , Aged , Betacoronavirus , COVID-19 , Coronavirus Infections/mortality , Coronavirus Infections/physiopathology , Coronavirus Infections/therapy , Cytokines/immunology , Female , Hospitalization , Humans , Male , Middle Aged , Pandemics , Pneumonia, Viral/mortality , Pneumonia, Viral/physiopathology , Pneumonia, Viral/therapy , SARS-CoV-2 , Severity of Illness Index , Survival Rate
12.
Front Immunol ; 11: 1518, 2020.
Article in English | MEDLINE | ID: covidwho-644235

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a member of the genus Betacoronavirus within the family Coronaviridae. It is an enveloped single-stranded positive-sense RNA virus. Since December of 2019, a global expansion of the infection has occurred with widespread dissemination of coronavirus disease 2019 (COVID-19). COVID-19 often manifests as only mild cold-like symptomatology, but severe disease with complications occurs in 15% of cases. Respiratory failure occurs in severe disease that can be accompanied by a systemic inflammatory reaction characterized by inflammatory cytokine release. In severe cases, fatality is caused by the rapid development of severe lung injury characteristic of acute respiratory distress syndrome (ARDS). Although ARDS is a complication of SARS-CoV-2 infection, it is not viral replication or infection that causes tissue injury; rather, it is the result of dysregulated hyperinflammation in response to viral infection. This pathology is characterized by intense, rapid stimulation of the innate immune response that triggers activation of the Nod-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome pathway and release of its products including the proinflammatory cytokines IL-6 and IL-1ß. Here we review the literature that describes the pathogenesis of severe COVID-19 and NLRP3 activation and describe an important role in targeting this pathway for the treatment of severe COVID-19.


Subject(s)
Betacoronavirus/metabolism , Coronavirus Infections/metabolism , Inflammasomes/antagonists & inhibitors , Inflammasomes/metabolism , NLR Family, Pyrin Domain-Containing 3 Protein/antagonists & inhibitors , NLR Family, Pyrin Domain-Containing 3 Protein/metabolism , Pneumonia, Viral/metabolism , Animals , COVID-19 , Coronavirus Infections/complications , Coronavirus Infections/drug therapy , Coronavirus Infections/virology , Cytokine Release Syndrome/drug therapy , Cytokine Release Syndrome/metabolism , Furans , Heterocyclic Compounds, 4 or More Rings/pharmacology , Heterocyclic Compounds, 4 or More Rings/therapeutic use , Humans , Immunity, Innate , Indenes , Interleukin 1 Receptor Antagonist Protein/pharmacology , Interleukin 1 Receptor Antagonist Protein/therapeutic use , Interleukin-1beta/antagonists & inhibitors , Interleukin-1beta/metabolism , Mice , Pandemics , Pneumonia, Viral/complications , Pneumonia, Viral/drug therapy , Pneumonia, Viral/virology , Pyroptosis/drug effects , Respiratory Distress Syndrome/drug therapy , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/metabolism , SARS-CoV-2 , Sesquiterpenes, Guaiane/pharmacology , Sesquiterpenes, Guaiane/therapeutic use , Sulfonamides , Sulfones/pharmacology , Sulfones/therapeutic use
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