Clinical, Immunological, and Virological SARS-CoV-2 Phenotypes in Obese and Nonobese Military Health System Beneficiaries

Abstract

Background: The mechanisms underlying the association between obesity and coronavirus disease 2019 (COVID-19) severity remain unclear. After verifying that obesity was a correlate of severe COVID-19 in US Military Health System (MHS) beneficiaries, we compared immunological and virological phenotypes of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in both obese and nonobese participants.

Methods: COVID-19-infected MHS beneficiaries were enrolled, and anthropometric, clinical, and demographic data were collected. We compared the SARS-CoV-2 peak IgG humoral response and reverse-transcription polymerase chain reaction viral load in obese and nonobese patients, stratified by hospitalization, utilizing logistic regression models.

Results: Data from 511 COVID-19 patients were analyzed, among whom 24% were obese and 14% severely obese. Obesity was independently associated with hospitalization (adjusted odds ratio [aOR], 1.91; 95% confidence interval [CI], 1.15-3.18) and need for oxygen therapy (aOR, 3.39; 95% CI, 1.61-7.11). In outpatients, severely obese had a log10 (1.89) higher nucleocapsid (N1) genome equivalents (GE)/reaction and log10 (2.62) higher N2 GE/reaction than nonobese (P = 0.03 and P < .001, respectively). We noted a correlation between body mass index and peak anti-spike protein IgG in inpatients and outpatients (coefficient = 5.48, P < .001).

Conclusions: Obesity is a strong correlate of COVID-19 severity in MHS beneficiaries. These findings offer new pathophysiological insights into the relationship between obesity and COVID-19 severity.

Keywords: COVID-19 severity; antibody response; obesity; viral load.

Figure 1.

Body mass index (BMI) distribution by severity, stratified into inpatient and outpatient (A), and medical oxygen requirements, stratified into oxygen supplement yes and oxygen supplement no, respectively (B). Statistically significant differences by nonparametric t tests are noted. Each dot represents a subject. Boxplots denote median, first quartile (25th percentile), and third quartile (75th percentile); statistical significance was determined by Wilcoxon rank sum test.

Figure 2.

Viral load as measured by qPCR N1 GE/reaction (A) and N2 GE/reaction (B), log₁₀ transformed and plotted by symptom day and stratified by obesity status. Each dot represents a subject. Local polynomial regression curves were fit to nonobese and obese groups; 95% confidence intervals are shaded for nonobese and obese groups; statistical significance was determined by Wilcoxon rank sum test. Abbreviations: Ct, cycle threshold; GE, genome equivalent; N, nucleocapsid; qPCR, quantitative polymerase chain reaction.

Figure 3.

Anti-spike IgG MFI plotted by sampling day and stratified by obesity status. Each dot represents a subject. Local polynomial regression curves were fit to nonobese and obese groups; 95% confidence intervals are shaded for nonobese and obese groups; statistical significance was determined by Wilcoxon rank sum test. Abbreviations: IgG, immunoglobulin G; MFI, median fluorescence intensity.