Immune profiles of a COVID-19 adolescent with mild symptoms and anti-viral antibody deficiency

Yang-Dian Lai¹, Ying-Ying Chen¹, Ji-Ping Sun¹, Yun Ling², Jie Xu³, Youqiong Ye¹, Lei Shen¹, Hong-Zhou Lu², Bing Su¹, Ying Wang^{1

4}

Affiliations

¹ Shanghai Institute of Immunology, Department of Immunology and Microbiology, and the Ministry of Education Key Laboratory of Cell Death and Differentiation, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
² Department of Infectious Disease, Shanghai Public Health Clinical Center, Shanghai, 201052, China.
³ Department of Infectious Disease, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011,China.
⁴ Key Laboratory of Emergency Prevention, Diagnosis and treatment of Respiratory Disease, Shanghai, 200025, China.

PMID: 40477411
PMCID: PMC7889007
DOI: 10.1016/j.fmre.2021.02.004

Immune profiles of a COVID-19 adolescent with mild symptoms and anti-viral antibody deficiency

Yang-Dian Lai et al. Fundam Res. 2021 Mar.

. 2021 Mar;1(2):117-123.

doi: 10.1016/j.fmre.2021.02.004. Epub 2021 Feb 17.

Authors

Yang-Dian Lai¹, Ying-Ying Chen¹, Ji-Ping Sun¹, Yun Ling², Jie Xu³, Youqiong Ye¹, Lei Shen¹, Hong-Zhou Lu², Bing Su¹, Ying Wang^{1

4}

Affiliations

¹ Shanghai Institute of Immunology, Department of Immunology and Microbiology, and the Ministry of Education Key Laboratory of Cell Death and Differentiation, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
² Department of Infectious Disease, Shanghai Public Health Clinical Center, Shanghai, 201052, China.
³ Department of Infectious Disease, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011,China.
⁴ Key Laboratory of Emergency Prevention, Diagnosis and treatment of Respiratory Disease, Shanghai, 200025, China.

PMID: 40477411
PMCID: PMC7889007
DOI: 10.1016/j.fmre.2021.02.004

No abstract available

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Conflict of interest statement

The funders had no role in study design, data collection, analysis, decision to publish or preparation of the manuscript. All the authors declare no conflict of interests.

Figures

Fig 1 — **Fig. 1**
Clinical manifestations and humoral immune responses of the COVID-19 adolescent patient during the disease process. (A) Timeline of the COVID-19 adolescent patient during the disease process, including body temperature; RT-PCR results of SARS-CoV-2 virus from oropharyngeal swabbing, urine, and feces; and the treatments. (B) Computed tomography (CT) on admission day (Feb 6), day 8 and day 11 (hospitalization in the Shanghai Public Health Clinic Center), and day 21 (the first follow-up visit). Red arrows indicate the inflammation lesion in the lung. (C) Dynamics of blood C-reactive protein (CRP) levels from admission to the follow-up visit. (D-E) Dynamics of SARS-CoV-2 spike (S) protein-specific IgG (D) and IgM (E) in the plasma of the adolescent patient. Limit of detection (LOD): anti-S IgG $\leq$ 15 RU/mL, anti-S IgM $\leq$ 3.4 RU/mL. Three adult convalescent COVID-19 patients (blue triangles) and three healthy controls (black diamonds) were used as controls. (F) UAMP plots of B cell gene signatures, including *CD19, CD27, MS4A1, CD38, IGHD, IGHM, IGHA1, IGHG1, IGHG2, IGHG3, IGHG4*, and *IGHE*. (G) Distribution percentages of each isotype of immunoglobulin. (H) Antigen-specific IFN-γ releasing cells in PBMCs were determined by an ELISpot assay upon stimulation with tuberculin pure protein derivative (PPD), SARS-CoV-2 spike protein fragment (S-RBD), nucleocapsid protein (N), and envelope protein (E). PHA: positive control; culture medium (blank): negative control.

Fig 2 — **Fig. 2**
NK/T cell profiles in the periphery of the COVID-19 adolescent. (A) A UMAP plot showed three clusters, including NK cells, CD4⁺ and CD8⁺ T cells, according to the expression of marker genes. Cells were color-coded according to gene signatures. (B) The features of UMAP plots defined NK/T cell types with specific genes, including *CD3E, CD4, CD8A, NCAM1*, and *FCGR3A*. (C-D) UMAP plots (C) and violin plots (D) showed the expression of cytokines across NK/T cell subtypes, including *IFNG, TNF, GZMB, CSF2, IL2*, and *IL17RA*. (E-G) Cytokine expression upon 12-myristate 13-acetate (PMA) and ionomycin stimulation in CD3⁺CD8^- cells (E) CD3⁺CD8⁺ T cells (F), and CD3-CD56⁺ NK cells (G), including IFN-γ, IL-2, TNF-α, GM-CSF, GzmB, and IL-17. (H) Feature plot of *KLRC2* expression.

Fig 3 — **Fig. 3**
Characterization of myeloid cell subsets in the periphery of the COVID-19 child (A) A UMAP plot showed five clusters among 1120 myeloid cells based on the expression of marker genes. Cells were color-coded according to defined myeloid subtypes. (B) The feature plots of UMAP showed subtype-specific gene expression for myeloid cells, including *CD14, FCGR3A, HLA-DRA, ITGAX, CD1C*, and *IL3RA*. (C-D) UMAP (C) and violin plots (D) showed cytokine expression in different myeloid subtypes, including IFNAR1, IFNAR2, IL1B, IFNG, TNF, CSF2, and IL6. (E-F) Cytokine production in monocyte subsets after LPS stimulation, including IL-1β, GM-CSF, IL-6, IFN-γ, and TNF-α.(G-H) Co-expression of three cytokines (IL-1β, IL-6, TNF-α) in CD14^low (G) and CD14^hi (H) monocytes.

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Immune profiles of a COVID-19 adolescent with mild symptoms and anti-viral antibody deficiency

Affiliations

Immune profiles of a COVID-19 adolescent with mild symptoms and anti-viral antibody deficiency

Authors

Affiliations

Conflict of interest statement

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