Prevalence and Characteristics of Long COVID 7–12 Months After Hospitalization Among Patients From an Urban Safety-Net Hospital: A Pilot Study

Hua, Miao Jenny; Gonakoti, Sriram; Shariff, Ruhi; Corpuz, Carlos Gabriel D.; Acosta, R. Alfonso Hernandez; Chang, Hillary; Asemota, Iriagbonse; Gobbi, Elizabeth; Rezai, Katayoun

doi:10.1016/j.focus.2023.100091

Cited by 7 publications

(6 citation statements)

References 17 publications

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“…infection of C57Bl6/J mice with B.1.351 produces postacute cognitive deficits. Incidence of neuroCOVID in humans ranges from 15-60%, and in our mouse model we also observe variability, with approximately 50% of mice performing poorly on the NOR test [3][4][5][6][7] . NeuroCOVID risk in humans is increased with hospitalization and in females, however NOR test performance in mice did not correlate with disease severity or with biological sex 4,5,7 .…”

Section: Discussionmentioning

confidence: 99%

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Vaccination prevents IL-1β-mediated cognitive deficits after COVID-19

Klein,

Vanderheiden,

Hill

et al. 2023

Preprint

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Up to 25% of SARS-CoV-2 patients exhibit post-acute cognitive sequelae. Although millions of cases of COVID-19-mediated memory dysfunction are accumulating worldwide, the underlying mechanisms and how vaccination lowers risk are unknown. Interleukin-1, a key component of innate immune defense against SARS-CoV-2 infection, is elevated in the hippocampi of COVID-19 patients. Here we show that intranasal infection of C57BL/6J mice with SARS-CoV-2 beta variant, leads to CNS infiltration of Ly6Chi monocytes and microglial activation. Accordingly, SARS-CoV-2, but not H1N1 influenza virus, increases levels of brain IL-1β and induces persistent IL-1R1-mediated loss of hippocampal neurogenesis, which promotes post-acute cognitive deficits. Breakthrough infection after vaccination with a low dose of adenoviral vectored Spike protein prevents hippocampal production of IL-1β during breakthrough SARS-CoV-2 infection, loss of neurogenesis, and subsequent memory deficits. Our study identifies IL-1β as one potential mechanism driving SARS-CoV-2-induced cognitive impairment in a new murine model that is prevented by vaccination.

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Section: Discussionmentioning

confidence: 99%

“…Current estimates suggest 15-60% of survivors develop post-acute neurologic symptoms of COVID-19 (neuroPASC) [3][4][5][6][7] . Symptoms include new daily headaches, peripheral neuropathy, anosmia, anxiety, memory impairments, and lack of concentration [8][9][10][11] .…”

Section: Introductionmentioning

confidence: 99%

Vaccination prevents IL-1β-mediated cognitive deficits after COVID-19

Klein,

Vanderheiden,

Hill

et al. 2023

Preprint

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“…Because of the absence of a widely accepted case definition and diagnostic criteria for long COVID, national prevalence estimates can range anywhere from 5% to 50%. 14,15 Vaccination status and disease severity can influence the prevalence of long COVID. The prevalence rate for vaccinated individuals is estimated to be 10% to 12%, 16 10% to 30% for nonhospitalized cases, and 50% to 70% for hospitalized cases with severe COVID-19 disease.…”

Section: Prevalencementioning

confidence: 99%

“…Because of the absence of a widely accepted case definition and diagnostic criteria for long COVID, national prevalence estimates can range anywhere from 5% to 50% 14,15 . Vaccination status and disease severity can influence the prevalence of long COVID.…”

Section: Medical Aspectsmentioning

confidence: 99%

Long COVID and Occupational Medicine Practice

Howard,

Cloeren,

Vanichkachorn

2023

J Occup Environ Med

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T he national public health emergency declared in response to the worldwide pandemic of "coronavirus disease 2019" or COVID-19 ended on May 11, 2023, in the United States. 1 Whereas most Americans infected with the causative agent of COVID-19-the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-recover their usual state of health, others experience a broad array of new or continuing debilitating symptoms. Grouped together, these various post-COVID-19 symptoms are collectively known by the patient-generated term, "long COVID; by the term, "postacute sequelae of SARS-CoV-2 infection 2 ; or by the World Health Organization's term, "post-COVID-19 condition." 3,4 In this editorial, the term "long COVID" will be used.Although a single case definition has not been widely accepted, the World Health Organization has defined long COVID as "the continuation or development of new symptoms 3 months after the initial SARS-CoV-2 infection, with these symptoms lasting for at least 2 months with no other explanation." 5 The US Department of Health and Human Services emphasizes that "long COVID is not one condition. It represents many potentially overlapping entities, likely with different biological causes and different sets of risk factors and outcomes." 6

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“…UU. un 10-30% del total de los pacientes infectados 21 . Conocer las características diferenciales de estos enfermos, así como la prevalencia en diferentes regiones sanitarias del mundo tendría interés clínico para conocer el perfil del paciente de riesgo.…”

Section: Introductionunclassified