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HLA alleles, disease severity, and age associate with T-cell responses following infection with SARS-CoV-2.

ABSTRACT: Memory T-cell responses following SARS-CoV-2 infection have been extensively investigated but many studies have been small with a limited range of disease severity. Here we analyze SARS-CoV-2 reactive T-cell responses in 768 convalescent SARS-CoV-2-infected (cases) and 500 uninfected (controls) Icelanders. The T-cell responses are stable three to eight months after SARS-CoV-2 infection, irrespective of disease severity and even those with the mildest symptoms induce broad and persistent T-cell responses. Robust CD4⁺ T-cell responses are detected against all measured proteins (M, N, S and S1) while the N protein induces strongest CD8⁺ T-cell responses. CD4⁺ T-cell responses correlate with disease severity, humoral responses and age, whereas CD8⁺ T-cell responses correlate with age and functional antibodies. Further, CD8⁺ T-cell responses associate with several class I HLA alleles. Our results, provide new insight into HLA restriction of CD8⁺ T-cell immunity and other factors contributing to heterogeneity of T-cell responses following SARS-CoV-2 infection.

SUBMITTER: Olafsdottir TA

PROVIDER: S-EPMC9446630 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature

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HLA alleles, disease severity, and age associate with T-cell responses following infection with SARS-CoV-2.

Olafsdottir Thorunn A TA Bjarnadottir Kristbjorg K Norddahl Gudmundur L GL Halldorsson Gisli H GH Melsted Pall P Gunnarsdottir Kristbjorg K Ivarsdottir Erna E Olafsdottir Thorhildur T Arnthorsson Asgeir O AO Theodors Fannar F Eythorsson Elias E Helgason Dadi D Eggertsson Hannes P HP Masson Gisli G Bjarnadottir Sólveig S Saevarsdottir Saedis S Runolfsdottir Hrafnhildur L HL Olafsson Isleifur I Saemundsdottir Jona J Sigurdsson Martin I MI Ingvarsson Ragnar F RF Palsson Runolfur R Thorgeirsson Gudmundur G Halldorsson Bjarni V BV Holm Hilma H Kristjansson Mar M Sulem Patrick P Thorsteinsdottir Unnur U Jonsdottir Ingileif I Gudbjartsson Daniel F DF Stefansson Kari K

Communications biology 20220906 1

Memory T-cell responses following SARS-CoV-2 infection have been extensively investigated but many studies have been small with a limited range of disease severity. Here we analyze SARS-CoV-2 reactive T-cell responses in 768 convalescent SARS-CoV-2-infected (cases) and 500 uninfected (controls) Icelanders. The T-cell responses are stable three to eight months after SARS-CoV-2 infection, irrespective of disease severity and even those with the mildest symptoms induce broad and persistent T-cell r ...[more]

PMID: 36068292

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Project description:ObjectiveBeginning in October 2021 in the US and elsewhere, cases of severe pediatric hepatitis of unknown etiology were identified in young children. While the adenovirus and adenovirus-associated virus have emerged as leading etiologic suspects, we attempted to investigate a potential role for SARS-CoV-2 in the development of subsequent liver abnormalities.DesignWe conducted a study utilizing retrospective cohorts of de-identified, aggregated data from the electronic health records of over 100 million patients contributed by US health care organizations.ResultsCompared to propensity-score-matched children with other respiratory infections, children aged 1-10 years with COVID-19 had a higher risk of elevated transaminases (Hazard ratio (HR) (95% Confidence interval (CI)) 2.16 (1.74-2.69)) or total bilirubin (HR (CI) 3.02 (1.91-4.78)), or new diagnoses of liver diseases (HR (CI) 1.67 (1.21-2.30)) from one to six months after infection. Patients with pre-existing liver abnormalities, liver abnormalities surrounding acute infection, younger age (1-4 years), or illness requiring hospitalization all had similarly elevated risk. Children who developed liver abnormalities following COVID-19 had more pre-existing conditions than those who developed abnormalities following other infections.ConclusionThese results indicate that SARS-CoV-2 may prime the patient for subsequent development of liver infections or non-infectious liver diseases. While rare (∼1 in 1,000), SARS-CoV-2 is a risk for subsequent abnormalities in liver function or the diagnosis of diseases of the liver.What is already known on this topicClusters of severe hepatitis in children in 2022 coincident with the increase in COVID-19 infections in children raised the question of the contribution of SARS-CoV-2 to the hepatitis outbreak, though it was soon determined that SARS-CoV-2 was not the primary etiologic agent.What this study addsSARS-CoV-2 may prime the patient for subsequent development of liver infections or non-infectious liver diseases.How this study might affect research practice or policyDespite the mild initial disease in children, there may be longer term consequences of COVID-19, such as liver abnormalities, that warrants further investigation.

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HLA alleles, disease severity, and age associate with T-cell responses following infection with SARS-CoV-2.

Publications

HLA alleles, disease severity, and age associate with T-cell responses following infection with SARS-CoV-2.

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