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Acute SARS-CoV-2 Infection Impairs Dendritic Cell and T Cell Responses.
Immunity. 2020 10 13; 53(4):864-877.e5.I

Abstract

The SARS-CoV-2 pandemic has resulted in millions of infections, yet the role of host immune responses in early COVID-19 pathogenesis remains unclear. By investigating 17 acute and 24 convalescent patients, we found that acute SARS-CoV-2 infection resulted in broad immune cell reduction including T, natural killer, monocyte, and dendritic cells (DCs). DCs were significantly reduced with functional impairment, and ratios of conventional DCs to plasmacytoid DCs were increased among acute severe patients. Besides lymphocytopenia, although neutralizing antibodies were rapidly and abundantly generated in patients, there were delayed receptor binding domain (RBD)- and nucleocapsid protein (NP)-specific T cell responses during the first 3 weeks after symptoms onset. Moreover, acute RBD- and NP-specific T cell responses included relatively more CD4 T cells than CD8 T cells. Our findings provided evidence that impaired DCs, together with timely inverted strong antibody but weak CD8 T cell responses, could contribute to acute COVID-19 pathogenesis and have implications for vaccine development.

Authors+Show Affiliations

AIDS Institute, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region (SAR), People's Republic of China; Department of Microbiology, State Key Laboratory of Emerging Infectious Diseases, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, People's Republic of China.Department of Microbiology, State Key Laboratory of Emerging Infectious Diseases, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, People's Republic of China.AIDS Institute, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region (SAR), People's Republic of China; Department of Microbiology, State Key Laboratory of Emerging Infectious Diseases, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, People's Republic of China.AIDS Institute, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region (SAR), People's Republic of China; Department of Microbiology, State Key Laboratory of Emerging Infectious Diseases, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, People's Republic of China.AIDS Institute, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region (SAR), People's Republic of China; Department of Microbiology, State Key Laboratory of Emerging Infectious Diseases, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, People's Republic of China.AIDS Institute, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region (SAR), People's Republic of China.AIDS Institute, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region (SAR), People's Republic of China.AIDS Institute, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region (SAR), People's Republic of China; Department of Microbiology, State Key Laboratory of Emerging Infectious Diseases, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, People's Republic of China.AIDS Institute, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region (SAR), People's Republic of China.AIDS Institute, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region (SAR), People's Republic of China.Department of Intensive Care, Queen Mary Hospital, The University of Hong Kong, Hong Kong SAR, People's Republic of China.Department of Adult Intensive Care, Queen Mary Hospital, Hong Kong SAR, People's Republic of China.Department of Microbiology, Pamela Youde Nethersole Eastern Hospital, Hong Kong SAR, People's Republic of China.Department of Medicine, Pamela Youde Nethersole Eastern Hospital, Hong Kong SAR, People's Republic of China.Department of Medicine, Princess Margaret Hospital, Hong Kong SAR, People's Republic of China.Department of Medicine, Princess Margaret Hospital, Hong Kong SAR, People's Republic of China.Department of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, People's Republic of China.Department of Microbiology, State Key Laboratory of Emerging Infectious Diseases, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, People's Republic of China. Electronic address: kyyuen@hku.hk.AIDS Institute, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region (SAR), People's Republic of China; Department of Microbiology, State Key Laboratory of Emerging Infectious Diseases, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, People's Republic of China. Electronic address: zchenai@hku.hk.

Pub Type(s)

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

Language

eng

PubMed ID

32791036

Citation

Zhou, Runhong, et al. "Acute SARS-CoV-2 Infection Impairs Dendritic Cell and T Cell Responses." Immunity, vol. 53, no. 4, 2020, pp. 864-877.e5.
Zhou R, To KK, Wong YC, et al. Acute SARS-CoV-2 Infection Impairs Dendritic Cell and T Cell Responses. Immunity. 2020;53(4):864-877.e5.
Zhou, R., To, K. K., Wong, Y. C., Liu, L., Zhou, B., Li, X., Huang, H., Mo, Y., Luk, T. Y., Lau, T. T., Yeung, P., Chan, W. M., Wu, A. K., Lung, K. C., Tsang, O. T., Leung, W. S., Hung, I. F., Yuen, K. Y., & Chen, Z. (2020). Acute SARS-CoV-2 Infection Impairs Dendritic Cell and T Cell Responses. Immunity, 53(4), 864-e5. https://doi.org/10.1016/j.immuni.2020.07.026
Zhou R, et al. Acute SARS-CoV-2 Infection Impairs Dendritic Cell and T Cell Responses. Immunity. 2020 10 13;53(4):864-877.e5. PubMed PMID: 32791036.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Acute SARS-CoV-2 Infection Impairs Dendritic Cell and T Cell Responses. AU - Zhou,Runhong, AU - To,Kelvin Kai-Wang, AU - Wong,Yik-Chun, AU - Liu,Li, AU - Zhou,Biao, AU - Li,Xin, AU - Huang,Haode, AU - Mo,Yufei, AU - Luk,Tsz-Yat, AU - Lau,Thomas Tsz-Kan, AU - Yeung,Pauline, AU - Chan,Wai-Ming, AU - Wu,Alan Ka-Lun, AU - Lung,Kwok-Cheung, AU - Tsang,Owen Tak-Yin, AU - Leung,Wai-Shing, AU - Hung,Ivan Fan-Ngai, AU - Yuen,Kwok-Yung, AU - Chen,Zhiwei, Y1 - 2020/08/04/ PY - 2020/05/19/received PY - 2020/06/24/revised PY - 2020/07/27/accepted PY - 2020/8/14/pubmed PY - 2020/10/29/medline PY - 2020/8/14/entrez KW - COVID-19 KW - SARS-CoV-2 KW - T cell immune response KW - acute infection KW - convalescent KW - dendritic cell KW - neutralizing antibody KW - nucleocapsid protein KW - receptor-binding domain SP - 864 EP - 877.e5 JF - Immunity JO - Immunity VL - 53 IS - 4 N2 - The SARS-CoV-2 pandemic has resulted in millions of infections, yet the role of host immune responses in early COVID-19 pathogenesis remains unclear. By investigating 17 acute and 24 convalescent patients, we found that acute SARS-CoV-2 infection resulted in broad immune cell reduction including T, natural killer, monocyte, and dendritic cells (DCs). DCs were significantly reduced with functional impairment, and ratios of conventional DCs to plasmacytoid DCs were increased among acute severe patients. Besides lymphocytopenia, although neutralizing antibodies were rapidly and abundantly generated in patients, there were delayed receptor binding domain (RBD)- and nucleocapsid protein (NP)-specific T cell responses during the first 3 weeks after symptoms onset. Moreover, acute RBD- and NP-specific T cell responses included relatively more CD4 T cells than CD8 T cells. Our findings provided evidence that impaired DCs, together with timely inverted strong antibody but weak CD8 T cell responses, could contribute to acute COVID-19 pathogenesis and have implications for vaccine development. SN - 1097-4180 UR - https://www.unboundmedicine.com/medline/citation/32791036/Acute_SARS_CoV_2_Infection_Impairs_Dendritic_Cell_and_T_Cell_Responses_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1074-7613(20)30333-2 DB - PRIME DP - Unbound Medicine ER -