Ferrets: A powerful model of SARS-CoV-2

动物学研究, Journal Year: 2023, Volume and Issue: 44(2), P. 323 - 330

Published: Jan. 1, 2023

The rapid spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in recent years not only caused a global pandemic but resulted enormous social, economic, and health burdens worldwide. Despite considerable efforts to combat disease 2019 (COVID-19), various SARS-CoV-2 variants have emerged, their underlying mechanisms pathogenicity remain largely unknown. Furthermore, effective therapeutic drugs are still under development. Thus, an ideal animal model is crucial for studying the pathogenesis COVID-19 preclinical evaluation vaccines antivirals against variant infections. Currently, several models, including mice, hamsters, ferrets, non-human primates (NHPs), been established study COVID-19. Among them, ferrets naturally susceptible infection considered suitable study. Here, we summarize developments application ferret models studies on pathogenesis, agents, vaccines, provide perspective role these preventing spread.

Language: Английский

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RETRACTED: Severe fever with thrombocytopenia syndrome virus induces platelet activation and apoptosis via a reactive oxygen species-dependent pathway

Redox Biology, Journal Year: 2023, Volume and Issue: 65, P. 102837 - 102837

Published: Aug. 1, 2023

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging tick-borne infectious disease caused by the SFTS virus (SFTSV) and a high fatality rate. Thrombocytopenia major clinical manifestation observed in patients, but underlying mechanism remains largely unclear. Here, we explored effects of SFTSV infection on platelet function vivo severely infected IFNar−/− mice mouse human vitro. Results showed that SFTSV-induced clearance acceleration may be main reason for thrombocytopenia. SFTSV-potentiated activation apoptosis were also mice. Further investigation induced reactive oxygen species (ROS) production mitochondrial dysfunction. In vitro experiments revealed administration or glycoprotein (Gn) increased activation, apoptosis, ROS production, dysfunction separated platelets, which could effectively ameliorated application antioxidants (NAC (N-acetyl-l-cysteine), SKQ1 (10-(6′-plastoquinonyl) decyltriphenylphosphonium) resveratrol). partially rescued infection-induced improving excessive down-regulating activation. Furthermore, while Gn directly potentiated it was completely abolished antioxidants. This study can trigger ROS-MAPK-dependent manner, contribute to hemorrhage during infection,

Language: Английский

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Primate-specific BTN3A2 protects against SARS-CoV-2 infection by interacting with and reducing ACE2

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: Jan. 15, 2024

Summary Background Coronavirus disease 2019 (COVID-19) is an immune-related disorder caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The complete pathogenesis of the virus remains to be determined. Unraveling molecular mechanisms governing SARS-CoV-2 interactions with host cells crucial for formulation effective prophylactic measures and advancement COVID-19 therapeutics. Methods We analyzed human lung single-cell RNA sequencing dataset discern association butyrophilin subfamily 3 member A2 ( BTN3A2 ) expression COVID-19. gene edited cell lines transgenic mice were infected live in a biosafety level (BSL-3) laboratory. Immunoprecipitation, flow cytometry, biolayer interferometry competition ELISA assays performed cells. quantitative real-time PCR, histological and/or immunohistochemical analyses tissue samples from or without infection. Findings mRNA was correlated severity. predominantly identified epithelial cells, elevated pathological patients co-occurred ACE2 same subtypes. targeted early stage viral life cycle inhibiting attachment through receptor-binding domain (RBD) Spike protein ACE2. inhibited ACE2-mediated infection reducing vitro vivo . Interpretation These results reveal key role fight against Identifying potential monoclonal antibodies which mimic may facilitate disruption infection, providing therapeutic avenue Funding This study supported National Natural Science Foundation China (32070569, U1902215, 32371017), CAS “Light West China” Program, Yunnan Province (202305AH340006). Research context Evidence before this Our understanding COVID-19, especially events incompletely albeit we witnessed many progresses. knowledge gap hinders finding specific antiviral agents SARS-CoV-2. entry mediated receptor angiotensin-converting enzyme (ACE2) affected defenses. Targeting these universal factors required replication most promising approach prevention treatment Added value revealed that BTN3A2, primate-specific gene, acts as potent inhibitor up-regulation upon competed binding protein, subsequently entry. Implications all available evidence data highlighted novel factor protective effects holds considerable drug mitigating impact its variants concern (VOCs).

Language: Английский

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Primate-specific BTN3A2 protects against SARS-CoV-2 infection by interacting with and reducing ACE2

EBioMedicine, Journal Year: 2024, Volume and Issue: 107, P. 105281 - 105281

Published: Aug. 13, 2024

Language: Английский

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COVID‐19‐associated liver injury: Adding fuel to the flame

Cell Biochemistry and Function, Journal Year: 2023, Volume and Issue: 41(8), P. 1076 - 1092

Published: Nov. 10, 2023

Abstract COVID‐19 is mainly characterized by respiratory disorders and progresses to multiple organ involvement in severe cases. With expansion of SARS‐CoV‐2 research, correlative liver injury has been revealed. It speculated that patients exhibited abnormal function, as previously observed the SARS MERS pandemics. Furthermore, with underlying diseases such chronic disease are more susceptible indicate a poor prognosis accompanied symptoms, systemic inflammation, or metabolic diseases. Therefore, potential impair while individuals preexisting suffer from much worse infected conditions. related may be owing direct cytopathic effect, immune dysfunction, gut−liver axis interaction, inappropriate medication use. However, discussions on these issues infancy. Expanding research have revealed angiotensin converting enzyme 2 (ACE2) expression mediated combination virus target cells, iron metabolism participated life cycle fate amino acid regulated response host which all closely health. Further exploration holds great significance elucidating pathogenesis, facilitating drug development, advancing clinical treatment COVID‐19‐related injury. This article provides review laboratory hepatic characteristics patients, describes etiology impact injury, discusses pathophysiological mechanisms.

Language: Английский

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Cell‐type‐specific mRNA m⁶A landscape and regulatory mechanisms underlying pulmonary injury in COVID‐19

MedComm – Future Medicine, Journal Year: 2024, Volume and Issue: 3(3)

Published: Aug. 26, 2024

Abstract Coronavirus disease 2019 (COVID‐19) pandemic has caused millions of deaths. The risk COVID‐19 spreading still exists after the deconfinement act, Omicron became dominant variant. Although N6‐methyladenosine (m 6 A) regulators been reported to affect pathogenicity COVID‐19, their mechanism in progression lung injury patients remain elusive. Here we show landscape and specific mechanisms m A tissues through single‐nucleus RNA sequencing (snRNA‐Seq) data sets 116,252 cells, external validation was performed using from another snRNA‐Seq data. reader IGF2BP2 specifically upregulated alveolar type I (AT1) resulting impaired regeneration. ALKBH5 expression upregulation macrophages, impairing immune responses. Moreover, WTAP markedly fibroblasts, leading pulmonary fibrosis. In addition, dysregulation induced aberrant cell–cell communication tissue mediated ligand–receptor interactions across diverse cell types by activating TGF‐β signaling pathway. Overall, these results indicated that myeloid fibroblasts may induce patients. development A‐regulator inhibitors could be as one potential antifibrotic drugs for COVID‐19.

Language: Английский

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<i>ZR</i> and <i>ZRDC</i> embrace a new era

动物学研究, Journal Year: 2022, Volume and Issue: 44(1), P. 1 - 2

Published: Dec. 19, 2022

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