Jincun Zhao

First Affiliated Hospital of Guangzhou Medical University

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Jingxian Zhao

First Affiliated Hospital of Guangzhou Medical University

Jing Sun

First Affiliated Hospital of Guangzhou Medical University

Airu Zhu

First Affiliated Hospital of Guangzhou Medical University

Stanley Perlman

University of Iowa

Yanqun Wang

Guangzhou Medical University

Nanshan Zhong

First Affiliated Hospital of Guangzhou Medical University

Zhaoyong Zhang

State Key Laboratory of Respiratory Disease

Zhen Zhuang

First Affiliated Hospital of Guangzhou Medical University

Yanqun Wang

Xichang University

Yimin Li

First Affiliated Hospital of Guangzhou Medical University

Cooperative Institutions

Guangzhou Medical University

487

State Key Laboratory of Respiratory Disease

414

Chinese Academy of Sciences

393

Sun Yat-sen University

372

First Affiliated Hospital of Guangzhou Medical University

342

University of Chinese Academy of Sciences

218

Chinese Academy of Medical Sciences & Peking Union Medical College

205

Shanghai Jiao Tong University

157

Peking University

154

Sichuan University

153

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Kinetics of viral load and antibody response in relation to COVID-19 severity

Journal of Clinical Investigation (2020)

Yanqun Wang Lu Zhang Ling Sang Ye Feng Shicong Ruan

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent for coronavirus 2019 (COVID-19) pneumonia. Little is known about the kinetics, tissue distribution, cross-reactivity, and neutralization antibody response in patients with COVID-19. Two groups of patients with RT-PCR-confirmed COVID-19 were enrolled in this study: 12 severely ill patients in intensive care units who needed mechanical ventilation and 11 mildly ill patients in isolation wards. Serial clinical samples were collected for laboratory detection. Results showed that most of the severely ill patients had viral shedding in a variety of tissues for 20-40 days after onset of disease (8/12, 66.7%), while the majority of mildly ill patients had viral shedding restricted to the respiratory tract and had no detectable virus RNA 10 days after onset (9/11, 81.8%). Mildly ill patients showed significantly lower IgM response compared with that of the severe group. IgG responses were detected in most patients in both the severe and mild groups at 9 days after onset, and remained at a high level throughout the study. Antibodies cross-reactive to SARS-CoV and SARS-CoV-2 were detected in patients with COVID-19 but not in patients with MERS. High levels of neutralizing antibodies were induced after about 10 days after onset in both severely and mildly ill patients which were higher in the severe group. SARS-CoV-2 pseudotype neutralization test and focus reduction neutralization test with authentic virus showed consistent results. Sera from patients with COVID-19 inhibited SARS-CoV-2 entry. Sera from convalescent patients with SARS or Middle East respiratory syndrome (MERS) did not. Anti-SARS-CoV-2 S and N IgG levels exhibited a moderate correlation with neutralization titers in patients' plasma. This study improves our understanding of immune response in humans after SARS-CoV-2 infection.

2019-20 coronavirus outbreak

Betacoronavirus

10.1172/jci138759

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Citations (569)

SARS-CoV-2 Damages Cardiomyocytes Mitochondria and Implicates Long COVID-associated Cardiovascular Manifestations

medRxiv (Cold Spring Harbor Laboratory) (2024)

Wenliang Che Shuai Guo Yanqun Wang Xiaohua Wan Bingyu Tan

Abstract Our study investigates the persistent cardiovascular symptoms observed in individuals long after contracting SARS-CoV-2, a condition commonly referred to as “Long COVID”, which has significantly affected millions globally. We meticulously describe the cardiovascular outcomes in five patients, encompassing a range of severe conditions such as sudden cardiac death during exercise, coronary atherosclerotic heart disease, acute inferior myocardial infarction, and acute myocarditis. All five patients were diagnosed with myocarditis, confirmed through endomyocardial biopsy and histochemical staining, which identified inflammatory cell infiltration in their heart tissue. Crucially, electron microscopy revealed widespread mitochondrial vacuolations and the presence of myofilament degradation within the cardiomyocytes of these patients. These findings were mirrored in SARS-CoV-2-infected mice, suggesting a potential underlying cellular mechanism for the cardiac effects associated with Long COVID. Our report sheds light on the cardiovascular implications of Long COVID and underscores the importance of further research to understand its cellular underpinnings.

2019-20 coronavirus outbreak

Betacoronavirus

10.1101/2024.08.18.24311961

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Citations (0)

Author Correction: Interferon-armed RBD dimer enhances the immunogenicity of RBD for sterilizing immunity against SARS-CoV-2

Cell Research (2021)

Shiyu Sun Yueqi Cai Tian‐Zhang Song Pu Yang Lin Cheng

10.1038/s41422-021-00572-z

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Citations (2)

ACE2 Receptor‐Targeted Inhaled Nanoemulsions Inhibit SARS‐CoV‐2 and Attenuate Inflammatory Responses (Adv. Mater. 14/2024)

Advanced Materials (2024)

Hairui Wang Shuang Luo Mingxin Xie Chen Zhao Yunming Zhang

SARS-CoV-2 In article number 2311537 by Jincun Zhao, Xun Sun, and co-workers, a specific ACE2-binding peptide with a superior antiviral activity was identified and used to modified the inhaled nanoemulsions. The inhaled remdesivir nanoemulsions strongly inhibit SARS-CoV-2 not only by blocking the binding of virus to host cells at the cell surface but also restricting virus replication intracellularly.

2019-20 coronavirus outbreak

10.1002/adma.202470103

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Identification and Characterization of Dominant Helper T-Cell Epitopes in the Nucleocapsid Protein of Severe Acute Respiratory Syndrome Coronavirus

Journal of Virology (2007)

Jincun Zhao Qianrong Huang Wei Wang Yan Zhang Ping Lv

By using a series of overlapping synthetic peptides covering 98% of the amino acid sequence of the nucleocapsid protein (NP) of severe acute respiratory syndrome coronavirus (SARS-CoV), four helper T-cell (Th) epitopes (NP11, residues 11 to 25; NP51, residues 51 to 65; NP61, residues 61 to 75; and NP111, residues 111 to 125) in C57BL mice (H-2(b)), four (NP21, residues 21 to 35; NP91, residues 91 to 105; NP331, residues 331 to 345; and NP351, residues 351 to 365) in C3H mice (H-2(k)), and two (NP81, residues 81 to 95; and NP351, residues 351 to 365) in BALB/c mice (H-2(d)) have been identified. All of these peptides were able to stimulate the proliferation of NP-specific T-cell lines or freshly isolated lymph node cells from mice immunized with recombinant NP. Immunization of mice with synthetic peptides containing appropriate Th epitopes elicited strong cellular immunity in vivo, as evidenced by delayed-type hypersensitivity. Priming with the helper peptides (e.g., NP111 and NP351) significantly accelerated the immune response induced by recombinant NP, as determined by the production of NP-specific antibodies. When fused with a conserved neutralizing epitope (SP1143-1157) from the spike protein of SARS-CoV, NP111 and NP351 assisted in the production of high-titer neutralizing antibodies in vivo. These data provide useful insights regarding immunity against SARS-CoV and have the potential to help guide the design of peptide-based vaccines.

Priming (agriculture)

Coronaviridae

Coronavirus

Cellular immunity

10.1128/jvi.02568-06

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Citations (41)

Broadly Effective ACE2 Decoy Proteins Protect Mice from Lethal SARS-CoV-2 Infection

Microbiology Spectrum (2023)

Mengjia Lu Weitong Yao Yujun Li Danting Ma Zhaoyong Zhang

Engineering soluble ACE2 proteins that function as a receptor decoy to block SARS-CoV-2 infection is a very attractive approach to creating broadly effective and hard-to-escape anti-SARS-CoV-2 agents. This article describes development of two antibody-like soluble ACE2 proteins that broadly block diverse SARS-CoV-2 variants, including Omicron.

Decoy

2019-20 coronavirus outbreak

Sars virus

Coronavirus Infections

Betacoronavirus

10.1128/spectrum.01100-23

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A Rapid and Specific Assay for the Detection of MERS-CoV

Frontiers in Microbiology (2018)

Pei Huang Hualei Wang Zengguo Cao Hongli Jin Hang Chi

Middle East respiratory syndrome coronavirus (MERS-CoV) is a novel human coronavirus that can cause human respiratory disease. The development of a detection method for this virus that can lead to rapid and accurate diagnosis would be significant. In this study, we established a nucleic acid visualization technique that combines the reverse transcription loop-mediated isothermal amplification technique and a vertical flow visualization strip (RT-LAMP-VF) to detect the N gene of MERS-CoV. The RT-LAMP-VF assay was performed in a constant temperature water bath for 30 min, and the result was visible by the naked eye within 2 min. The RT-LAMP-VF assay was capable of detecting 2×101 copies/µl of synthesized RNA transcript and 1×101copies/µl of MERS-CoV RNA. The method exhibits no cross-reactivities with multiple CoVs including SARS-related (SARSr)-CoV, HKU4, HKU1, OC43 and 229E, and thus exhibits high specificity. Compared to the real-time RT-PCR (rRT-PCR) method recommended by the World Health Organization (WHO),the RT-LAMP-VF assay is easy to handle, does not require expensive equipment and can rapidly complete detection within 35 min.

Coronavirus

Naked eye

10.3389/fmicb.2018.01101

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Citations (155)

Discovery of a subgenotype of human coronavirus NL63 associated with severe lower respiratory tract infection in China, 2018

Figshare (2021)

Yanqun Wang Xin Li Wenkuan Liu Mian Gan Lu Zhang

Human coronavirus NL63 (HCoV-NL63) is primarily associated with common cold in children, elderly and immunocompromised individuals. Outbreaks caused by HCoV-NL63 are rare. Here we report a cluster of HCoV-NL63 cases with severe lower respiratory tract infection that arose in Guangzhou, China, in 2018. Twenty-three hospitalized children were confirmed to be HCoV-NL63 positive, and most of whom were hospitalized with severe pneumonia or acute bronchitis. Whole genomes of HCoV-NL63 were obtained using next-generation sequencing. Phylogenetic and single amino acid polymorphism analyses showed that this outbreak was associated with two subgenotypes (C3 and B) of HCoV-NL63. Half of patients were identified to be related to a new subgenotype C3. One unique amino acid mutation at I507 L in spike protein receptor binding domain (RBD) was detected, which segregated this subgenotype C3 from other known subgenotypes. Pseudotyped virus bearing the I507 L mutation in RBD showed enhanced entry into host cells as compared to the prototype virus. This study proved that HCoV-NL63 was undergoing continuous mutation and has the potential to cause severe lower respiratory disease in humans.

Coronavirus

2019-20 coronavirus outbreak

Respiratory tract

Betacoronavirus

10.6084/m9.figshare.11769900.v2

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Interleukin-1 prevents SARS-CoV-2-induced membrane fusion to restrict viral transmission via induction of actin bundles

eLife (2025)

Xu Zheng Yu Shi Yanqiu Zhou Kuai Yu Yuhui Gao

Innate immune responses triggered by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection play pivotal roles in the pathogenesis of COVID-19, while host factors including proinflammatory cytokines are critical for viral containment. By utilizing quantitative and qualitative models, we discovered that soluble factors secreted by human monocytes potently inhibit SARS-CoV-2-induced cell-cell fusion in viral-infected cells. Through cytokine screening, we identified that interleukin-1β (IL-1β), a key mediator of inflammation, inhibits syncytia formation mediated by various SARS-CoV-2 strains. Mechanistically, IL-1β activates RhoA/ROCK signaling through a non-canonical IL-1 receptor-dependent pathway, which drives the enrichment of actin bundles at the cell-cell junctions, thus prevents syncytia formation. Notably, in vivo infection experiments in mice confirmed that IL-1β significantly restricted SARS-CoV-2 spread in the lung epithelium. Together, by revealing the function and underlying mechanism of IL-1β on SARS-CoV-2-induced cell-cell fusion, our study highlights an unprecedented antiviral function for cytokines during viral infection.

2019-20 coronavirus outbreak

10.7554/elife.98593.3

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Differential Effects of IL-12 on Tregs and Non-Treg T Cells: Roles of IFN-γ, IL-2 and IL-2R

PLoS ONE (2012)

Jingxian Zhao Jincun Zhao Stanley Perlman

Complex interactions between effector T cells and Foxp3+ regulatory T cells (Treg) contribute to clinical outcomes in cancer, and autoimmune and infectious diseases. Previous work showed that IL-12 reversed Treg-mediated suppression of CD4+Foxp3− T cell (Tconv) proliferation. We and others have also shown that Tregs express T-bet and IFN-γ at sites of Th1 inflammation and that IL-12 induces IFN-γ production by Tregs in vitro. To investigate whether loss of immunosuppression occurs when IFN-γ is expressed by Tregs we treated mouse lymphocyte cultures with IL-12. IFN-γ expression did not decrease the ability of Tregs to suppress Tconv proliferation. Rather, IL-12 treatment decreased Treg frequency and Foxp3 levels in Tregs. We further showed that IL-12 increased IL-2R expression on Tconv and CD8 T cells, diminished its expression on Tregs and decreased IL-2 production by Tconv and CD8 T cells. Together, these IL-12 mediated changes favored the outgrowth of non-Tregs. Additionally, we showed that treatment with a second cytokine, IL-27, decreased IL-2 expression without augmenting Tconv and CD8 T cell proliferation. Notably, IL-27 only slightly modified levels of IL-2R on non-Treg T cells. Together, these results show that IL-12 has multiple effects that modify the balance between Tregs and non-Tregs and support an important role for relative levels of IL-2R but not for IFN-γ expression in IL-12-mediated reversal of Treg immunosuppression.

Immunosuppression

Regulatory T cell

10.1371/journal.pone.0046241

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Citations (105)