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1.
Frontiers in medicine ; 9, 2022.
Article in English | EuropePMC | ID: covidwho-1981003

ABSTRACT

Several vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have been approved for controlling the coronavirus disease 2019 (COVID-19) pandemic worldwide. Antibody response is essential to understand the immune response to different viral targets after vaccination with different vaccine platforms. Thus, the main aim of this study was to describe how vaccination with two distinct SARS-CoV-2 vaccine preparations elicit IgG antibody specific responses against two antigenically relevant SARS-CoV-2 viral proteins: the receptor-binding domain (RBD) and the full-length spike (S). To do so, SARS-CoV-2 protein specific in-house enzyme-linked immunosorbent assays (ELISAs) were standardized and tested against serum samples collected from 89 adults, recipients of either a single-dose of the Spike-encoding mRNA-based Pfizer/BioNTech (Pf-BNT) (70%, 62/89) or the Spike-encoding-Adenovirus-5-based CanSino Biologics Inc. (CSBIO) (30%, 27/89) in Merida, Mexico. Overall, we identified an IgG seroconversion rate of 88% (68/78) in all vaccinees after more than 25 days post-vaccination (dpv). Anti-RBD IgG-specific responses ranged from 90% (46/51) in the Pf-BNT vaccine at 25 dpv to 74% (20/27) in the CSBIO vaccine at 42 dpv. Compared to the S, the RBD IgG reactivity was significantly higher in both Pf-BNT (p < 0.004) and CSBIO (p < 0.003) vaccinees. Interestingly, in more than 50% of vaccine recipients, with no history of COVID-19 infection, antibodies against the nucleocapsid (N) protein were detected. Thus, participants were grouped either as naïve or pre-exposed vaccinees. Seroconversion rates after 25 and more dpv varies between 100% in Pf-BNT (22/22) and 75% (9/12) in CSBIO pre-exposed vaccinees, and 89% (26/29) and 73% (11/15) in Pf-BNT and CSBIO naïve vaccine recipients, respectively. In summary, observed seroconversion rates varied depending on the type of vaccine, previous infection with SARS-CoV-2, and the target viral antigen. Our results indicate that both vaccine preparations can induce detectable levels of IgG against the RBD or Spike in both naïve and SARS-CoV-2 pre-exposed vaccinees. Our study provides valuable and novel information about the serodiagnosis and the antibody response to vaccines in Mexico.

2.
Non-conventional in English | [Unspecified Source], Grey literature | ID: grc-750512

ABSTRACT

Severe Acute Respiratory Syndrome Coronavirus -2 (SARS-CoV-2) emerged in late 2019 and has spread worldwide resulting in the Coronavirus Disease 2019 (COVID-19) pandemic. Although animal models have been evaluated for SARS-CoV-2 infection, none have recapitulated the severe lung disease phenotypes seen in hospitalized human cases. Here, we evaluate heterozygous transgenic mice expressing the human ACE2 receptor driven by the epithelial cell cytokeratin-18 gene promoter (K18-hACE2) as a model of SARS-CoV-2 infection. Intranasal inoculation of SARS-CoV-2 in K18-hACE2 mice results in high levels of viral infection in lung tissues with additional spread to other organs. Remarkably, a decline in pulmonary function, as measured by static and dynamic tests of respiratory capacity, occurs 4 days after peak viral titer and correlates with an inflammatory response marked by infiltration into the lung of monocytes, neutrophils, and activated T cells resulting in pneumonia. Cytokine profiling and RNA sequencing analysis of SARS-CoV-2-infected lung tissues show a massively upregulated innate immune response with prominent signatures of NF-kB-dependent, type I and II interferon signaling, and leukocyte activation pathways. Thus, the K18-hACE2 model of SARS-CoV-2 infection recapitulates many features of severe COVID-19 infection in humans and can be used to define the mechanistic basis of lung disease and test immune and antiviral-based countermeasures.

4.
Nat Immunol ; 21(11): 1327-1335, 2020 11.
Article in English | MEDLINE | ID: covidwho-728991

ABSTRACT

Although animal models have been evaluated for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, none have fully recapitulated the lung disease phenotypes seen in humans who have been hospitalized. Here, we evaluate transgenic mice expressing the human angiotensin I-converting enzyme 2 (ACE2) receptor driven by the cytokeratin-18 (K18) gene promoter (K18-hACE2) as a model of SARS-CoV-2 infection. Intranasal inoculation of SARS-CoV-2 in K18-hACE2 mice results in high levels of viral infection in lungs, with spread to other organs. A decline in pulmonary function occurs 4 days after peak viral titer and correlates with infiltration of monocytes, neutrophils and activated T cells. SARS-CoV-2-infected lung tissues show a massively upregulated innate immune response with signatures of nuclear factor-κB-dependent, type I and II interferon signaling, and leukocyte activation pathways. Thus, the K18-hACE2 model of SARS-CoV-2 infection shares many features of severe COVID-19 infection and can be used to define the basis of lung disease and test immune and antiviral-based countermeasures.


Subject(s)
Betacoronavirus/immunology , Coronavirus Infections/pathology , Immunity, Innate/immunology , Peptidyl-Dipeptidase A/genetics , Pneumonia, Viral/pathology , Pneumonia/pathology , Angiotensin-Converting Enzyme 2 , Animals , COVID-19 , Chlorocebus aethiops , Coronavirus Infections/immunology , Disease Models, Animal , Female , Humans , Interferon Type I/immunology , Interferon-gamma/immunology , Keratin-18/genetics , Leukocytes/immunology , Lymphocyte Activation/immunology , Male , Mice , Mice, Transgenic , Monocytes/immunology , NF-kappa B/immunology , Neutrophil Infiltration/immunology , Neutrophils/immunology , Pandemics , Pneumonia/genetics , Pneumonia/virology , Pneumonia, Viral/immunology , Promoter Regions, Genetic/genetics , SARS-CoV-2 , T-Lymphocytes/immunology , Vero Cells , Virus Replication/immunology
5.
bioRxiv ; 2020 Jul 10.
Article in English | MEDLINE | ID: covidwho-665969

ABSTRACT

Severe Acute Respiratory Syndrome Coronavirus -2 (SARS-CoV-2) emerged in late 2019 and has spread worldwide resulting in the Coronavirus Disease 2019 (COVID-19) pandemic. Although animal models have been evaluated for SARS-CoV-2 infection, none have recapitulated the severe lung disease phenotypes seen in hospitalized human cases. Here, we evaluate heterozygous transgenic mice expressing the human ACE2 receptor driven by the epithelial cell cytokeratin-18 gene promoter (K18-hACE2) as a model of SARS-CoV-2 infection. Intranasal inoculation of SARS-CoV-2 in K18-hACE2 mice results in high levels of viral infection in lung tissues with additional spread to other organs. Remarkably, a decline in pulmonary function, as measured by static and dynamic tests of respiratory capacity, occurs 4 days after peak viral titer and correlates with an inflammatory response marked by infiltration into the lung of monocytes, neutrophils, and activated T cells resulting in pneumonia. Cytokine profiling and RNA sequencing analysis of SARS-CoV-2-infected lung tissues show a massively upregulated innate immune response with prominent signatures of NF-kB-dependent, type I and II interferon signaling, and leukocyte activation pathways. Thus, the K18-hACE2 model of SARS-CoV-2 infection recapitulates many features of severe COVID-19 infection in humans and can be used to define the mechanistic basis of lung disease and test immune and antiviral-based countermeasures.

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