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SARS-CoV-2 variants Alpha, Beta, Delta and Omicron show a slower host cell interferon response compared to an early pandemic variant.
Front Immunol. 2022; 13:1016108.FI

Abstract

Since the start of the pandemic at the end of 2019, arising mutations in SARS-CoV-2 have improved its transmission and ability to circumvent the immunity induced by vaccination and previous COVID-19 infection. Studies on the effects of SARS-CoV-2 genomic mutations on replication and innate immunity will give us valuable insight into the evolution of the virus which can aid in further development of vaccines and new treatment modalities. Here we systematically analyzed the kinetics of virus replication, innate immune activation, and host cell antiviral response patterns in Alpha, Beta, Delta, Kappa, Omicron and two early pandemic SARS-CoV-2 variant-infected human lung epithelial Calu-3 cells. We observed overall comparable replication patterns for these variants with modest variations. Particularly, the sublineages of Omicron BA.1, BA.2 and a recombinant sublineage, XJ, all showed attenuated replication in Calu-3 cells compared to Alpha and Delta. Furthermore, there was relatively weak activation of primary innate immune signaling pathways, however, all variants produced enough interferons to induce the activation of STAT2 and production of interferon stimulated genes (ISGs). While interferon mRNA expression and STAT2 activation correlated with cellular viral RNA levels, ISG production did not. Although clear cut effects of specific SARS-CoV-2 genomic mutations could not be concluded, the variants of concern, including Omicron, showed a lower replication efficiency and a slower interferon response compared to an early pandemic variant in the study.

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Authors+Show Affiliations

Laine L
Expert Microbiology Unit, Department of Health Security, Finnish Institute for Health and Welfare, Helsinki, Finland.
Skön M
Expert Microbiology Unit, Department of Health Security, Finnish Institute for Health and Welfare, Helsinki, Finland.
Väisänen E
Expert Microbiology Unit, Department of Health Security, Finnish Institute for Health and Welfare, Helsinki, Finland. Infection and Immunity, Institute of Biomedicine, University of Turku, Turku, Finland.
Julkunen I
Infection and Immunity, Institute of Biomedicine, University of Turku, Turku, Finland.
Österlund P
Expert Microbiology Unit, Department of Health Security, Finnish Institute for Health and Welfare, Helsinki, Finland.

MeSH

Antiviral AgentsCOVID-19HumansInterferonsPandemicsRNA, MessengerRNA, ViralSARS-CoV-2

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

36248817

Citation

Laine, Larissa, et al. "SARS-CoV-2 Variants Alpha, Beta, Delta and Omicron Show a Slower Host Cell Interferon Response Compared to an Early Pandemic Variant." Frontiers in Immunology, vol. 13, 2022, p. 1016108.
Laine L, Skön M, Väisänen E, et al. SARS-CoV-2 variants Alpha, Beta, Delta and Omicron show a slower host cell interferon response compared to an early pandemic variant. Front Immunol. 2022;13:1016108.
Laine, L., Skön, M., Väisänen, E., Julkunen, I., & Österlund, P. (2022). SARS-CoV-2 variants Alpha, Beta, Delta and Omicron show a slower host cell interferon response compared to an early pandemic variant. Frontiers in Immunology, 13, 1016108. https://doi.org/10.3389/fimmu.2022.1016108
Laine L, et al. SARS-CoV-2 Variants Alpha, Beta, Delta and Omicron Show a Slower Host Cell Interferon Response Compared to an Early Pandemic Variant. Front Immunol. 2022;13:1016108. PubMed PMID: 36248817.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - SARS-CoV-2 variants Alpha, Beta, Delta and Omicron show a slower host cell interferon response compared to an early pandemic variant. AU - Laine,Larissa, AU - Skön,Marika, AU - Väisänen,Elina, AU - Julkunen,Ilkka, AU - Österlund,Pamela, Y1 - 2022/09/30/ PY - 2022/08/10/received PY - 2022/09/15/accepted PY - 2022/10/17/entrez PY - 2022/10/18/pubmed PY - 2022/10/19/medline KW - Omicron KW - SARS-CoV-2 KW - innate immunity KW - interferon KW - mutations KW - replication KW - variants SP - 1016108 EP - 1016108 JF - Frontiers in immunology JO - Front Immunol VL - 13 N2 - Since the start of the pandemic at the end of 2019, arising mutations in SARS-CoV-2 have improved its transmission and ability to circumvent the immunity induced by vaccination and previous COVID-19 infection. Studies on the effects of SARS-CoV-2 genomic mutations on replication and innate immunity will give us valuable insight into the evolution of the virus which can aid in further development of vaccines and new treatment modalities. Here we systematically analyzed the kinetics of virus replication, innate immune activation, and host cell antiviral response patterns in Alpha, Beta, Delta, Kappa, Omicron and two early pandemic SARS-CoV-2 variant-infected human lung epithelial Calu-3 cells. We observed overall comparable replication patterns for these variants with modest variations. Particularly, the sublineages of Omicron BA.1, BA.2 and a recombinant sublineage, XJ, all showed attenuated replication in Calu-3 cells compared to Alpha and Delta. Furthermore, there was relatively weak activation of primary innate immune signaling pathways, however, all variants produced enough interferons to induce the activation of STAT2 and production of interferon stimulated genes (ISGs). While interferon mRNA expression and STAT2 activation correlated with cellular viral RNA levels, ISG production did not. Although clear cut effects of specific SARS-CoV-2 genomic mutations could not be concluded, the variants of concern, including Omicron, showed a lower replication efficiency and a slower interferon response compared to an early pandemic variant in the study. SN - 1664-3224 UR - https://www.unboundmedicine.com/medline/citation/36248817/SARS_CoV_2_variants_Alpha_Beta_Delta_and_Omicron_show_a_slower_host_cell_interferon_response_compared_to_an_early_pandemic_variant_ DB - PRIME DP - Unbound Medicine ER -