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. 2021 Nov 6;13(11):2235.
doi: 10.3390/v13112235.

Epidemiological and Immunological Features of Obesity and SARS-CoV-2

Affiliations

Epidemiological and Immunological Features of Obesity and SARS-CoV-2

Eric J Nilles et al. Viruses. .

Abstract

Obesity is a key correlate of severe SARS-CoV-2 outcomes while the role of obesity on risk of SARS-CoV-2 infection, symptom phenotype, and immune response remain poorly defined. We examined data from a prospective SARS-CoV-2 cohort study to address these questions. Serostatus, body mass index, demographics, comorbidities, and prior COVID-19 compatible symptoms were assessed at baseline and serostatus and symptoms monthly thereafter. SARS-CoV-2 immunoassays included an IgG ELISA targeting the spike RBD, multiarray Luminex targeting 20 viral antigens, pseudovirus neutralization, and T cell ELISPOT assays. Our results from a large prospective SARS-CoV-2 cohort study indicate symptom phenotype is strongly influenced by obesity among younger but not older age groups; we did not identify evidence to suggest obese individuals are at higher risk of SARS-CoV-2 infection; and remarkably homogenous immune activity across BMI categories suggests immune protection across these groups may be similar.

Keywords: COVID-19; SARS-CoV-2; body mass index; clinical features; epidemiology; immunity; obesity.

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Conflict of interest statement

G.A. is a founder of Seromyx Systems Inc., a company developing platform technology that describes the antibody immune response. G.A.’s interests were reviewed and are managed by Massachusetts General Hospital in accordance with their conflict-of-interest policies. M.J.G. (Matthew J. Gluck), S.B., Y.H., J.R., E.P., B.M., A.S.M. and E.R.M. are employees of Space Exploration Technologies Corp. All other authors have declared that no conflict of interest exist.

Figures

Figure 1
Figure 1
Forest plots of adjusted odds ratio for seropositivity by BMI as a categorical variable with normal BMI (18.5–<25) as reference. (A) Includes participants with BMI measures and demonstrates a non-significant trend to declining seroprevalence with BMI ≥40 kg/m2 when compared to normal/healthy weight (BMI 18.5–24 kg/m2) (n = 4270). (B) Includes only participants from a single high seroprevalence (22.5%) location in South Texas, where the high force of infection may more clearly delineate infection risks (n = 629).
Figure 2
Figure 2
Forest plot of odds ratios of reported COVID-19 compatible symptoms among obese (n = 85) versus non-obese (n = 179) SARS-CoV-2 seropositive individuals.
Figure 3
Figure 3
Forest plot of odds ratios of COVID-19 compatible symptoms among obese versus non-obese SARS-CoV-2 seropositive individuals stratified by (A) <40 years (n = 195) and (B) ≥40 years (n = 67).
Figure 4
Figure 4
Symptom reporting by age group and obesity status among SARS-CoV-2 seropositive individuals. (A) Heatmap shows consistently higher symptom reporting amongst obese individuals in the 19–29 and 29–39 year age groups but not ≥40-year age group. Number of individuals in each category are listed below obesity markers. (B) Table lists relevant values. * indicates p < 0.05 for difference between obese and non-obese in that age category with Chi-squared test for proportions and ANOVA for test of mean.
Figure 5
Figure 5
Limited influence of BMI on SARS-CoV-2 antibody profiles (n = 77). (A) The dot plots show similar mean fluorescent intensity levels of IgG1, IgM, IgG3, and IgA levels across individuals classified as normal weight (n = 29), overweight (n = 23), and obese (n = 25). (B) The uniform manifold approximation and projection (UMAP) shows the relationship between antibody profiles and BMI (dot size, color intensity), highlighting the limited influence of BMI on shaping SARS-CoV-2 antibody responses. (C) Correlation plot of shows limited correlation between BMI and 20 immunological features.
Figure 6
Figure 6
Role of obesity in inflammatory response to infection. Adipocyte-secreted factors (e.g., adiponectin, leptin, Type I IFNs, and IL-6) contribute to normal homeostatic immune responses against infectious pathogens among healthy/normal weight. Obesity-dependent changes in adipocyte function can contribute to (1) immunosenescence (suppressed immune response against pathogens); (2) delayed immune inflammation (reduced pathogen clearance and compensatory exacerbated adipocyte inflammation); and (3) “cytokine storm” (IL-). Modified from Alarcon, 2021 [29].

Update of

  • Epidemiological and immunological features of obesity and SARS-CoV-2.
    Nilles EJ, Siddiqui SM, Fischinger S, Bartsch YC, de Saint Aubin M, Zhou G, Gluck MJ, Berger S, Rhee J, Petersen E, Mormann B, Loesche M, Chen Z, Yu J, Gebre M, Atyeo C, Gorman MJ, Lee Zhu A, Burke J, Slein M, Hasdianda MA, Jambaulikar G, Boyer E, Sabeti P, Barouch DH, Julg BD, Kucharski AJ, Musk ER, Lauffenburger DA, Alter G, Menon AS. Nilles EJ, et al. medRxiv [Preprint]. 2020 Dec 11:2020.11.11.20229724. doi: 10.1101/2020.11.11.20229724. medRxiv. 2020. Update in: Viruses. 2021 Nov 06;13(11):2235. doi: 10.3390/v13112235. PMID: 33200139 Free PMC article. Updated. Preprint.

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