Description: Goat polyclonal to Spike protein of Middle East respiratory Syndrome coronavirus. Coronaviruses access host cells by membrane fusion, a process mediated by specific fusion or “spike” proteins on the virion, often activated by cellular proteases.

Description: Recombinant human monoclonal antibody recognizing the SARS-CoV-2 Spike RBD glycoprotein. This antibody cross-reacts with the Spike protein from the SARS-CoV virus.

Description: Recombinant human monoclonal antibody recognizing the SARS-CoV-2 Spike RBD glycoprotein. This antibody cross-reacts with the Spike protein from the SARS-CoV virus.

Description: Coronavirus disease 2019 (COVID-19), formerly known as 2019-nCoV acute respiratory disease, is an infectious disease caused by SARS-CoV-2, a virus closely related to the SARS virus (1). The disease is the cause of the 2019–20 coronavirus outbreak (2). The structure of 2019-nCoV consists of the following: a Spike protein (S), hemagglutinin-esterease dimer (HE), a membrane glycoprotein (M), an envelope protein (E) a nucleoclapid protein (N) and RNA. Coronavirus invades cells through Spike (S) glycoproteins, a class I fusion protein. It is the major viral surface protein that coronavirus uses to bind to the human cell surface receptor. It also mediates the fusion of host and viral cell membrane, allowing the virus to enter human cells and begin infection (3). The spike protein is the major target for neutralizing antibodies and vaccine development (4). The protein modeling suggests that there is strong interaction between Spike protein receptor-binding domain and its host receptor angiotensin-converting enzyme 2 (ACE2), which regulate both the cross-species and human-to-human transmissions of COVID-19 (5). The recent study has shown that the SARS-CoV-2 spike protein binds ACE2 with higher affinity than SARS-CoV spike protein (6).

Description: Coronavirus disease 2019 (COVID-19), formerly known as 2019-nCoV acute respiratory disease, is an infectious disease caused by SARS-CoV-2, a virus closely related to the SARS virus (1). The disease is the cause of the 2019–20 coronavirus outbreak (2). The structure of 2019-nCoV consists of the following: a Spike protein (S), hemagglutinin-esterease dimer (HE), a membrane glycoprotein (M), an envelope protein (E) a nucleoclapid protein (N) and RNA. Coronavirus invades cells through Spike (S) glycoproteins, a class I fusion protein. It is the major viral surface protein that coronavirus uses to bind to the human cell surface receptor. It also mediates the fusion of host and viral cell membrane, allowing the virus to enter human cells and begin infection (3). The spike protein is the major target for neutralizing antibodies and vaccine development (4). The protein modeling suggests that there is strong interaction between Spike protein receptor-binding domain and its host receptor angiotensin-converting enzyme 2 (ACE2), which regulate both the cross-species and human-to-human transmissions of COVID-19 (5). The recent study has shown that the SARS-CoV-2 spike protein binds ACE2 with higher affinity than SARS-CoV spike protein (6).

Description: Coronavirus disease 2019 (COVID-19), formerly known as 2019-nCoV acute respiratory disease, is an infectious disease caused by SARS-CoV-2, a virus closely related to the SARS virus (1). The disease is the cause of the 2019–20 coronavirus outbreak (2). The structure of 2019-nCoV consists of the following: a Spike protein (S), hemagglutinin-esterease dimer (HE), a membrane glycoprotein (M), an envelope protein (E) a nucleoclapid protein (N) and RNA. Coronavirus invades cells through Spike (S) glycoproteins, a class I fusion protein. It is the major viral surface protein that coronavirus uses to bind to the human cell surface receptor. It also mediates the fusion of host and viral cell membrane, allowing the virus to enter human cells and begin infection (3). The spike protein is the major target for neutralizing antibodies and vaccine development (4). The protein modeling suggests that there is strong interaction between Spike protein receptor-binding domain and its host receptor angiotensin-converting enzyme 2 (ACE2), which regulate both the cross-species and human-to-human transmissions of COVID-19 (5). The recent study has shown that the SARS-CoV-2 spike protein binds ACE2 with higher affinity than SARS-CoV spike protein (6).

Description: Coronavirus disease 2019 (COVID-19), formerly known as 2019-nCoV acute respiratory disease, is an infectious disease caused by SARS-CoV-2, a virus closely related to the SARS virus (1). The disease is the cause of the 2019–20 coronavirus outbreak (2). The structure of 2019-nCoV consists of the following: a Spike protein (S), hemagglutinin-esterease dimer (HE), a membrane glycoprotein (M), an envelope protein (E) a nucleoclapid protein (N) and RNA. Coronavirus invades cells through Spike (S) glycoproteins, a class I fusion protein. It is the major viral surface protein that coronavirus uses to bind to the human cell surface receptor. It also mediates the fusion of host and viral cell membrane, allowing the virus to enter human cells and begin infection (3). The spike protein is the major target for neutralizing antibodies and vaccine development (4). The protein modeling suggests that there is strong interaction between Spike protein receptor-binding domain and its host receptor angiotensin-converting enzyme 2 (ACE2), which regulate both the cross-species and human-to-human transmissions of COVID-19 (5). The recent study has shown that the SARS-CoV-2 spike protein binds ACE2 with higher affinity than SARS-CoV spike protein (6).

Description: Coronavirus disease 2019 (COVID-19), formerly known as 2019-nCoV acute respiratory disease, is an infectious disease caused by SARS-CoV-2, a virus closely related to the SARS virus (1). The disease is the cause of the 2019–20 coronavirus outbreak (2). The structure of 2019-nCoV consists of the following: a Spike protein (S), hemagglutinin-esterease dimer (HE), a membrane glycoprotein (M), an envelope protein (E) a nucleoclapid protein (N) and RNA. Coronavirus invades cells through Spike (S) glycoproteins, a class I fusion protein. It is the major viral surface protein that coronavirus uses to bind to the human cell surface receptor. It also mediates the fusion of host and viral cell membrane, allowing the virus to enter human cells and begin infection (3). The spike protein is the major target for neutralizing antibodies and vaccine development (4). The protein modeling suggests that there is strong interaction between Spike protein receptor-binding domain and its host receptor angiotensin-converting enzyme 2 (ACE2), which regulate both the cross-species and human-to-human transmissions of COVID-19 (5). The recent study has shown that the SARS-CoV-2 spike protein binds ACE2 with higher affinity than SARS-CoV spike protein (6).

Description: In September of 2020 a new lineage of SARS-CoV-2, known as B.1.1.7 and named as Alpha variant, was discovered in the United Kingdom. This lineage developed 14 lineage-specific amino acid replacements and 3 deletions. These changes caused an increase in transmission of Alpha variant (B.1.1.7 lineage) by at least 50%, leading to increased disease severity and higher death rates. The effectiveness of COVID19 vaccines are not affected by the Alpha variant. One of the mutations associated with this lineage is a N501Y in the spike protein of the virus. It is believed that this mutation is able to increase the spike protein's affinity for the host ACE2 receptor and it has been associated with increased infectivity and virulence. B.1.1.7 viruses have also been shown to have a P681H mutation in the cleavage site of spike protein. This location is one of the residues that make up the furin proteolytic cleavage site between S1 and S2 in spike protein.

Description: In September of 2020 a new lineage of SARS-CoV-2, known as B.1.1.7 and named as Alpha variant, was discovered in the United Kingdom. This lineage developed 14 lineage-specific amino acid replacements and 3 deletions. These changes caused an increase in transmission of Alpha variant (B.1.1.7 lineage) by at least 50%, leading to increased disease severity and higher death rates. The effectiveness of COVID19 vaccines are not affected by the Alpha variant. One of the mutations associated with this lineage is a N501Y in the spike protein of the virus. It is believed that this mutation is able to increase the spike protein's affinity for the host ACE2 receptor and it has been associated with increased infectivity and virulence. B.1.1.7 viruses have also been shown to have a P681H mutation in the cleavage site of spike protein. This location is one of the residues that make up the furin proteolytic cleavage site between S1 and S2 in spike protein.

Description: In September of 2020 a new lineage of SARS-CoV-2, known as B.1.1.7 and named as Alpha variant, was discovered in the United Kingdom. This lineage developed 14 lineage-specific amino acid replacements and 3 deletions. These changes caused an increase in transmission of Alpha variant (B.1.1.7 lineage) by at least 50%, leading to increased disease severity and higher death rates. The effectiveness of COVID19 vaccines are not affected by the Alpha variant. One of the mutations associated with this lineage is a N501Y in the spike protein of the virus. It is believed that this mutation is able to increase the spike protein's affinity for the host ACE2 receptor and it has been associated with increased infectivity and virulence. B.1.1.7 viruses have also been shown to have a P681H mutation in the cleavage site of spike protein. This location is one of the residues that make up the furin proteolytic cleavage site between S1 and S2 in spike protein.

Description: In September of 2020 a new lineage of SARS-CoV-2, known as B.1.1.7 and named as Alpha variant, was discovered in the United Kingdom. This lineage developed 14 lineage-specific amino acid replacements and 3 deletions. These changes caused an increase in transmission of Alpha variant (B.1.1.7 lineage) by at least 50%, leading to increased disease severity and higher death rates. The effectiveness of COVID19 vaccines are not affected by the Alpha variant. One of the mutations associated with this lineage is a N501Y in the spike protein of the virus. It is believed that this mutation is able to increase the spike protein's affinity for the host ACE2 receptor and it has been associated with increased infectivity and virulence. B.1.1.7 viruses have also been shown to have a P681H mutation in the cleavage site of spike protein. This location is one of the residues that make up the furin proteolytic cleavage site between S1 and S2 in spike protein.

Description: In September of 2020 a new lineage of SARS-CoV-2, known as B.1.1.7 and named as Alpha variant, was discovered in the United Kingdom. This lineage developed 14 lineage-specific amino acid replacements and 3 deletions. These changes caused an increase in transmission of Alpha variant (B.1.1.7 lineage) by at least 50%, leading to increased disease severity and higher death rates. The effectiveness of COVID19 vaccines are not affected by the Alpha variant. One of the mutations associated with this lineage is a N501Y in the spike protein of the virus. It is believed that this mutation is able to increase the spike protein's affinity for the host ACE2 receptor and it has been associated with increased infectivity and virulence. B.1.1.7 viruses have also been shown to have a P681H mutation in the cleavage site of spike protein. This location is one of the residues that make up the furin proteolytic cleavage site between S1 and S2 in spike protein.

Description: In September of 2020 a new lineage of SARS-CoV-2, known as B.1.1.7 and named as Alpha variant, was discovered in the United Kingdom. This lineage developed 14 lineage-specific amino acid replacements and 3 deletions. These changes caused an increase in transmission of Alpha variant (B.1.1.7 lineage) by at least 50%, leading to increased disease severity and higher death rates. The effectiveness of COVID19 vaccines are not affected by the Alpha variant. One of the mutations associated with this lineage is a N501Y in the spike protein of the virus. It is believed that this mutation is able to increase the spike protein's affinity for the host ACE2 receptor and it has been associated with increased infectivity and virulence. B.1.1.7 viruses have also been shown to have a P681H mutation in the cleavage site of spike protein. This location is one of the residues that make up the furin proteolytic cleavage site between S1 and S2 in spike protein.

Description: SARS-CoV Spike Antibody: A novel coronavirus has been identified as the causative agent of SARS (Severe Acute Respiratory Syndrome). Coronaviruses are a major cause of upper respiratory diseases in humans. The genomes of these viruses are positive-stranded RNA approximately 27-31kb in length. SARS infection can be mediated by the binding of the viral spike protein, a glycosylated 139 kDa protein and the major surface antigen of the virus, to the angiotensin-converting enzyme 2 (ACE2) on target cells. This binding can be blocked by a soluble form of ACE2.

Description: SARS-CoV Spike Antibody: A novel coronavirus has been identified as the causative agent of SARS (Severe Acute Respiratory Syndrome). Coronaviruses are a major cause of upper respiratory diseases in humans. The genomes of these viruses are positive-stranded RNA approximately 27-31kb in length. SARS infection can be mediated by the binding of the viral spike protein, a glycosylated 139 kDa protein and the major surface antigen of the virus, to the angiotensin-converting enzyme 2 (ACE2) on target cells. This binding can be blocked by a soluble form of ACE2.

Description: SARS-CoV Spike Antibody: A novel coronavirus has recently been identified as the causative agent of SARS (Severe Acute Respiratory Syndrome). Coronaviruses are a major cause of upper respiratory diseases in humans. The genomes of these viruses are positive-stranded RNA approximately 27-31kb in length. SARS infection can be mediated by the binding of the viral spike protein, a glycosylated 139 kDa protein and the major surface antigen of the virus, to the angiotensin-converting enzyme 2 (ACE2) on target cells. This binding can be blocked by a soluble form of ACE2.

Description: SARS-CoV Spike Antibody: A novel coronavirus has recently been identified as the causative agent of SARS (Severe Acute Respiratory Syndrome). Coronaviruses are a major cause of upper respiratory diseases in humans. The genomes of these viruses are positive-stranded RNA approximately 27-31kb in length. SARS infection can be mediated by the binding of the viral spike protein, a glycosylated 139 kDa protein and the major surface antigen of the virus, to the angiotensin-converting enzyme 2 (ACE2) on target cells. This binding can be blocked by a soluble form of ACE2.

Description: SARS Spike Antibody: A novel coronavirus has recently been identified as the causative agent of SARS (Severe Acute Respiratory Syndrome). Coronaviruses are a major cause of upper respiratory diseases in humans. The genomes of these viruses are positive-stranded RNA approximately 27-31kb in length. SARS infection can be mediated by the binding of the viral spike protein, a glycosylated 139 kDa protein and the major surface antigen of the virus, to the angiotensin-converting enzyme 2 (ACE2) on target cells. This binding can be blocked by a soluble form of ACE2.

Description: SARS Spike Antibody: A novel coronavirus has recently been identified as the causative agent of SARS (Severe Acute Respiratory Syndrome). Coronaviruses are a major cause of upper respiratory diseases in humans. The genomes of these viruses are positive-stranded RNA approximately 27-31kb in length. SARS infection can be mediated by the binding of the viral spike protein, a glycosylated 139 kDa protein and the major surface antigen of the virus, to the angiotensin-converting enzyme 2 (ACE2) on target cells. This binding can be blocked by a soluble form of ACE2.

Description: SARS-CoV Spike antibody: A novel coronavirus has recently been identified as the causative agent of SARS (Severe Acute Respiratory Syndrome). Coronaviruses are a major cause of upper respiratory diseases in humans. The genomes of these viruses are positive-stranded RNA approximately 27-31kb in length. SARS infection can be mediated by the binding of the viral spike protein, a glycosylated 139 kDa protein and the major surface antigen of the virus, to the angiotensin-converting enzyme 2 (ACE2) on target cells. This binding can be blocked by a soluble form of ACE2.