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Click on the blue text above and pay attention to our new research using cells, genetically modified mouse models, and cultured human lung tissue.
The evidence suggests that the ability to trigger programmed cell death (or apoptosis) may be The highly pathogenic coronavirus spreads in the host body very successfully
.
The study went on to prove that targeting this process may reduce the severity of coronavirus disease
.
Although scientists have realized that highly pathogenic coronaviruses can cause a large number of cell deaths after infiltrating the body, the importance of apoptosis to the spread of coronavirus infections in the body and the underlying mechanism that cause the virus to be highly pathogenic remain unclear.
.
To fill the gap in this research, Hin Chu and colleagues first observed the MERS-CoV virus in cultured human lung tissue and the lungs of infected transgenic mice, and found that these viruses induce severe cell apoptosis
.
To explore how the virus triggers programmed cell death in the cells of its host organ, the researchers analyzed the mRNA transcripts in human bronchial epithelial cells at 12 and 24 hours after infection with MERS-CoV; it was found that the receptor protein Genes regulated by kinase R-like endoplasmic reticulum kinase (PERK) are highly expressed; PERK is related to cell death
.
When Chu et al.
inhibited PERK signaling in infected human lung tissue, they found that the cell-to-cell transmission of MERS-CoV and cell death induced by the virus were significantly reduced
.
The researchers also tested the inhibition of PERK signaling in transgenic mice infected with the virus
.
This treatment down-regulated genes involved in apoptosis and reduced lung damage
.
Although the authors found that PERK inhibitors cannot inhibit cell apoptosis caused by SARS-CoV or SARS-CoV-2, they have truly observed that an inhibitor of apoptosis inherent in the body can effectively inhibit SARS-infection.
This process in CoV or SARS-CoV-2 mice reduces the lung damage caused by SARS-CoV-2
.
These findings indicate that the three highly pathogenic human coronaviruses, namely SARS-CoV, MERS-CoV and SARS-CoV-2, may trigger cell apoptosis through different mechanisms.
Therefore, inhibiting cell apoptosis may reduce this Pathogenicity of 3 kinds of viruses
.
Welcome to pay attention to Science's official public account.
Click "Read the original text" below to access the open access papers.
This issue of Science Advances lights up yours.
The evidence suggests that the ability to trigger programmed cell death (or apoptosis) may be The highly pathogenic coronavirus spreads in the host body very successfully
.
The study went on to prove that targeting this process may reduce the severity of coronavirus disease
.
Although scientists have realized that highly pathogenic coronaviruses can cause a large number of cell deaths after infiltrating the body, the importance of apoptosis to the spread of coronavirus infections in the body and the underlying mechanism that cause the virus to be highly pathogenic remain unclear.
.
To fill the gap in this research, Hin Chu and colleagues first observed the MERS-CoV virus in cultured human lung tissue and the lungs of infected transgenic mice, and found that these viruses induce severe cell apoptosis
.
To explore how the virus triggers programmed cell death in the cells of its host organ, the researchers analyzed the mRNA transcripts in human bronchial epithelial cells at 12 and 24 hours after infection with MERS-CoV; it was found that the receptor protein Genes regulated by kinase R-like endoplasmic reticulum kinase (PERK) are highly expressed; PERK is related to cell death
.
When Chu et al.
inhibited PERK signaling in infected human lung tissue, they found that the cell-to-cell transmission of MERS-CoV and cell death induced by the virus were significantly reduced
.
The researchers also tested the inhibition of PERK signaling in transgenic mice infected with the virus
.
This treatment down-regulated genes involved in apoptosis and reduced lung damage
.
Although the authors found that PERK inhibitors cannot inhibit cell apoptosis caused by SARS-CoV or SARS-CoV-2, they have truly observed that an inhibitor of apoptosis inherent in the body can effectively inhibit SARS-infection.
This process in CoV or SARS-CoV-2 mice reduces the lung damage caused by SARS-CoV-2
.
These findings indicate that the three highly pathogenic human coronaviruses, namely SARS-CoV, MERS-CoV and SARS-CoV-2, may trigger cell apoptosis through different mechanisms.
Therefore, inhibiting cell apoptosis may reduce this Pathogenicity of 3 kinds of viruses
.
Welcome to pay attention to Science's official public account.
Click "Read the original text" below to access the open access papers.
This issue of Science Advances lights up yours.
