Intranasal delivery of NS1-deleted influenza virus vectored COVID-19 vaccine restrains the SARS-CoV-2 inflammatory response (Hamster Lung RNA-seq Data)

The emergence of SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus-2) variants and “anatomical escape” characteristics threaten the effectiveness of current coronavirus disease (COVID-19) vaccines. There is an urgent need to understand the immunological mechanism of broad-spectrum respiratory tract protection to guide broader vaccines development. In this study, we investigated immune responses induced by an NS1-deleted influenza virus vectored intranasal COVID-19 vaccine (dNS1-RBD) which provides broad-spectrum protection against SARS-CoV-2 variants. Intranasal delivery of dNS1-RBD induced innate immunity, trained immunity and tissue-resident memory T cells covering the upper and lower respiratory tract. It restrained the inflammatory response by suppressing early phase viral load post SARS-CoV-2 challenge and attenuating pro-inflammatory cytokine (IL-6, IL-1B, and IFN-γ) levels, thereby reducing excess immune-induced tissue injury compared with the control group. By inducing local cellular immunity and trained immunity, intranasal delivery of NS1-deleted influenza virus vectored vaccine represents a broad-spectrum COVID-19 vaccine strategy to reduce disease burden. To investigate the immune response, pathological process caused by SARS-CoV-2 Beta variants infection in Golden Hamster lung. Golden hamsters were vaccinated with dNS1-RBD vaccine at day0 and day 14, and 2 months later the vccinated hamster were challenged with SARS-CoV-2 Beta varians together with control group hamster. Then the lung samples were collected at 0, 1, 3, 5 post infection to sequence for the RNA-seq data, then performed gene expression analysis using data obtained from RNA-seq. Comparative gene expression analysis and enrichment analysis analysis of lung RNA-seq data of control group and vaccinated group at different time point (day 0, 1, 3, 5) post SARS-CoV-2 Beta Virus challenge.