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    LitCovid-PubTator

    However, there is another strategy to pursue in this scenario that does not rely on targeting the viral glycoprotein directly. In this strategy, a neutralizing effect could be obtained by targeting the viral receptor protein on the cell surface, thereby blocking the virus from binding to it and gaining entry. Fortunately, scientists have already uncovered the identity of the viral receptor in cell culture. A recent pre-print publication found that the 2019-nCoV uses the angiotensin-converting enzyme 2 (ACE2) as a receptor for cell entry 41, which is the same receptor that the SARS coronavirus uses for entry 42. For both viruses, the coronavirus binds to ACE2 through its S protein on the virion, where after fusion of the viral membrane and cell membrane will occur. Subsequently, the RNA virus will replicate its genome inside the cell, and ultimately make new virions that will be secreted to infect other cells. The coincidence of SARS and 2019-nCoV using ACE2 receptor opens up the possibility of using the extensive research studied on SARS entry and applying it to 2019-nCoV. Based on the SARS literature, several potential blocking strategies could be considered, which were shown to be effective in preventing infection in SARS models.

    LitCovid-PMC-OGER-BB

    However, there is another strategy to pursue in this scenario that does not rely on targeting the viral glycoprotein directly. In this strategy, a neutralizing effect could be obtained by targeting the viral receptor protein on the cell surface, thereby blocking the virus from binding to it and gaining entry. Fortunately, scientists have already uncovered the identity of the viral receptor in cell culture. A recent pre-print publication found that the 2019-nCoV uses the angiotensin-converting enzyme 2 (ACE2) as a receptor for cell entry 41, which is the same receptor that the SARS coronavirus uses for entry 42. For both viruses, the coronavirus binds to ACE2 through its S protein on the virion, where after fusion of the viral membrane and cell membrane will occur. Subsequently, the RNA virus will replicate its genome inside the cell, and ultimately make new virions that will be secreted to infect other cells. The coincidence of SARS and 2019-nCoV using ACE2 receptor opens up the possibility of using the extensive research studied on SARS entry and applying it to 2019-nCoV. Based on the SARS literature, several potential blocking strategies could be considered, which were shown to be effective in preventing infection in SARS models.

    LitCovid-PD-FMA-UBERON

    However, there is another strategy to pursue in this scenario that does not rely on targeting the viral glycoprotein directly. In this strategy, a neutralizing effect could be obtained by targeting the viral receptor protein on the cell surface, thereby blocking the virus from binding to it and gaining entry. Fortunately, scientists have already uncovered the identity of the viral receptor in cell culture. A recent pre-print publication found that the 2019-nCoV uses the angiotensin-converting enzyme 2 (ACE2) as a receptor for cell entry 41, which is the same receptor that the SARS coronavirus uses for entry 42. For both viruses, the coronavirus binds to ACE2 through its S protein on the virion, where after fusion of the viral membrane and cell membrane will occur. Subsequently, the RNA virus will replicate its genome inside the cell, and ultimately make new virions that will be secreted to infect other cells. The coincidence of SARS and 2019-nCoV using ACE2 receptor opens up the possibility of using the extensive research studied on SARS entry and applying it to 2019-nCoV. Based on the SARS literature, several potential blocking strategies could be considered, which were shown to be effective in preventing infection in SARS models.

    LitCovid-PD-MONDO

    However, there is another strategy to pursue in this scenario that does not rely on targeting the viral glycoprotein directly. In this strategy, a neutralizing effect could be obtained by targeting the viral receptor protein on the cell surface, thereby blocking the virus from binding to it and gaining entry. Fortunately, scientists have already uncovered the identity of the viral receptor in cell culture. A recent pre-print publication found that the 2019-nCoV uses the angiotensin-converting enzyme 2 (ACE2) as a receptor for cell entry 41, which is the same receptor that the SARS coronavirus uses for entry 42. For both viruses, the coronavirus binds to ACE2 through its S protein on the virion, where after fusion of the viral membrane and cell membrane will occur. Subsequently, the RNA virus will replicate its genome inside the cell, and ultimately make new virions that will be secreted to infect other cells. The coincidence of SARS and 2019-nCoV using ACE2 receptor opens up the possibility of using the extensive research studied on SARS entry and applying it to 2019-nCoV. Based on the SARS literature, several potential blocking strategies could be considered, which were shown to be effective in preventing infection in SARS models.

    LitCovid-PD-CLO

    However, there is another strategy to pursue in this scenario that does not rely on targeting the viral glycoprotein directly. In this strategy, a neutralizing effect could be obtained by targeting the viral receptor protein on the cell surface, thereby blocking the virus from binding to it and gaining entry. Fortunately, scientists have already uncovered the identity of the viral receptor in cell culture. A recent pre-print publication found that the 2019-nCoV uses the angiotensin-converting enzyme 2 (ACE2) as a receptor for cell entry 41, which is the same receptor that the SARS coronavirus uses for entry 42. For both viruses, the coronavirus binds to ACE2 through its S protein on the virion, where after fusion of the viral membrane and cell membrane will occur. Subsequently, the RNA virus will replicate its genome inside the cell, and ultimately make new virions that will be secreted to infect other cells. The coincidence of SARS and 2019-nCoV using ACE2 receptor opens up the possibility of using the extensive research studied on SARS entry and applying it to 2019-nCoV. Based on the SARS literature, several potential blocking strategies could be considered, which were shown to be effective in preventing infection in SARS models.

    LitCovid-PD-CHEBI

    However, there is another strategy to pursue in this scenario that does not rely on targeting the viral glycoprotein directly. In this strategy, a neutralizing effect could be obtained by targeting the viral receptor protein on the cell surface, thereby blocking the virus from binding to it and gaining entry. Fortunately, scientists have already uncovered the identity of the viral receptor in cell culture. A recent pre-print publication found that the 2019-nCoV uses the angiotensin-converting enzyme 2 (ACE2) as a receptor for cell entry 41, which is the same receptor that the SARS coronavirus uses for entry 42. For both viruses, the coronavirus binds to ACE2 through its S protein on the virion, where after fusion of the viral membrane and cell membrane will occur. Subsequently, the RNA virus will replicate its genome inside the cell, and ultimately make new virions that will be secreted to infect other cells. The coincidence of SARS and 2019-nCoV using ACE2 receptor opens up the possibility of using the extensive research studied on SARS entry and applying it to 2019-nCoV. Based on the SARS literature, several potential blocking strategies could be considered, which were shown to be effective in preventing infection in SARS models.

    LitCovid-sentences

    However, there is another strategy to pursue in this scenario that does not rely on targeting the viral glycoprotein directly. In this strategy, a neutralizing effect could be obtained by targeting the viral receptor protein on the cell surface, thereby blocking the virus from binding to it and gaining entry. Fortunately, scientists have already uncovered the identity of the viral receptor in cell culture. A recent pre-print publication found that the 2019-nCoV uses the angiotensin-converting enzyme 2 (ACE2) as a receptor for cell entry 41, which is the same receptor that the SARS coronavirus uses for entry 42. For both viruses, the coronavirus binds to ACE2 through its S protein on the virion, where after fusion of the viral membrane and cell membrane will occur. Subsequently, the RNA virus will replicate its genome inside the cell, and ultimately make new virions that will be secreted to infect other cells. The coincidence of SARS and 2019-nCoV using ACE2 receptor opens up the possibility of using the extensive research studied on SARS entry and applying it to 2019-nCoV. Based on the SARS literature, several potential blocking strategies could be considered, which were shown to be effective in preventing infection in SARS models.