Abstract
β2-microglobulin (β2-m), a 11.8 kDa protein, pairs non-covalently with the α3 domain of the major histocompatibility class (MHC) I α-chain and is essential for the conformation of the MHC class I protein complex. Shed β2-m is measurable in circulation, and various disorders are accompanied by increases in β2-m levels, including several viral infections. Therefore, we explored whether β2-m levels could also be elevated in Coronavirus disease 2019 (Covid-19) and whether they predict disease severity. Serum β2-m levels were measured in a cohort of 34 patients infected with SARS-CoV-2 on admission to a tertiary care hospital in Riyadh, Saudi Arabia, as well as in an approximately age-sex matched group of 34 uninfected controls. Mean β2-m level was 3.25±1.68 mg/l (reference range 0.8-2.2 mg/l) in patients (mean age 48.2±21.6) and 1.98±0.61 mg/l in controls (mean age 48.2±21.6). 17 patients (mean age 36.9± 18.0) with mean β2-m levels of 2.27±0.64 mg/l had mild disease by WHO severity categorization, 12 patients (mean age 53.3±18.1) with mean β2-m levels of 3.57±1.39 mg/l had moderate disease, and five patients (of whom 2 died; mean age 74.4±13.8) with mean β2-m levels of 5.85±1.85 mg/l had severe disease (P < = 0.001, by ANOVA test for linear trend). In multivariate ordinal regression β2-m levels were the only significant predictor of disease severity. Our findings suggest that higher β2-m levels could be an early indicator of severity of disease and predict outcome of Covid-19. As the main limitations of the study are a single-center study, sample size and ethnicity, these results need confirmation in larger cohorts outside the Arabian Peninsula in order to delineate the value of β2-m measurements. The role of β2-m in the etiology and pathogenesis of severe Covid-19 remains to be elucidated.
Highlights
Immune responses to the infection with SARS-CoV-2, the causative pathogen of Covid-19, were first described in China [1,2,3] and subsequently, in the wake of a global spread, in other countries and ethnicities [4,5,6,7,8,9,10,11,12]
We conducted an observational study at the King Faisal Specialist Hospital & Research Centre (KFSHRC), a large (~1.000.000 outpatient visits/year, 1.600 beds, ~1.000 doctors and ~13.500 employees), non-profit, tertiary referral hospital, located in the city center of Riyadh, Saudi Arabia, where patients are referred from other hospitals from across Saudi Arabia and adjacent regions
The diagnosis of Covid-19 was suspected clinically and confirmed through the detection of SARS-Cov-2 in a nasopharyngeal sample with specific polymerase chain reaction (PCR) (RealStar1SARS-CoV-2 RT-PCR Kit RUO altona-diagnostics, Germany), which was performed in the Section of Medical Microbiology of the Department of Pathology and Laboratory Medicine at KFSHRC
Summary
Immune responses to the infection with SARS-CoV-2, the causative pathogen of Covid-19, were first described in China [1,2,3] and subsequently, in the wake of a global spread, in other countries and ethnicities [4,5,6,7,8,9,10,11,12]. Covid-19 is preponderantly mild and self-limiting with rapidly developing anti-viral immunity. Progression to a well characterized cytokine release syndrome resulting in acute lung injury or acute respiratory distress syndrome in critical cases with a high case fatality ratio occurs in many elderly and in the presence of comorbidities, similar to other (seasonal) viral infections [13,14,15]. In severe or critical disease, a markedly impaired interferon (IFN) type I response was associated with a persistent blood viral load and florid inflammation, which in some patients was related to the presence of autoantibodies against IFN type I [20, 21]. In combination with the clinical presentation and radiographic findings, some of these variables have been used to develop various prognostic models for risk stratification of patients admitted to hospital with Covid-19, but a universally accepted and applicable scoring system has as yet not been established [30]
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