Plain language summary of Pfizer-BioNTech BNT162b2 COVID-19 vaccine safety in participants 16 years or older and protection against COVID-19 in participants 12 years or older

What is this summary about?This is a summary of an article about part of a clinical study for the BNT162b2 COVID-19 vaccine, also called the Pfizer-BioNTech vaccine. The article was published in the New England Journal of Medicine in September 2021. The part of the study described in the article began in July 2020 and is ongoing. This means that the final results may be different from the results included in this summary.What happened in this study?The participants in this study received 2 injections of either the BNT162b2 vaccine or a placebo, 21 days apart. The placebo looked like the BNT162b2 vaccine but had no active vaccine in it. None of the trial participants or study teams knew who received vaccine or placebo.What were the results?Most of the reactions to the injections were mild or moderate and lasted for a short period of time. The most common reactions were pain at the injection site, extreme tiredness (fatigue), and headache. These reactions usually happened in the first 7 days after receiving a vaccine dose. A small number of participants had severe reactions to the vaccine.Compared to participants who received the placebo, participants who received the BNT162b2 vaccine were much less likely to become ill if they were infected with the virus that causes COVID-19. The vaccine also had very good efficacy at preventing severe COVID-19.Participants in South Africa who received the BNT162b2 vaccine were less likely to become ill after infection with the beta variant of the virus compared to participants who received the placebo. The beta variant was very common in South Africa when the study was taking place.

Risk aversion impacts on need for transparency and traceability pre- and post-pandemic

The need for transparency and traceability of product information has increased due to the increased attention towards food contamination in both the United States and China. Examining this need is vital to companies considering business decisions involving product development, supply chain management, and marketing tactics. To address this need, companies must understand the underlying motivators. Through MANOVA analysis, this paper studies how risk aversion impacts consumers’ need for transparency and traceability concerning product information both before and after the COVID-19 pandemic. Results obtained pre-COVID-19 indicate that high-risk-averse individuals have an increased need for transparency and traceability. Post-COVID-19, results indicate no difference between high- and low-risk-averse individuals. Study 1 (pre-pandemic) results suggest that firms need to consider risk related to their product when increasing transparency and traceability. Study 2 (post-pandemic) results indicate that firms should create a generalised approach to improve transparency and traceability. The pandemic minimised the impact of risk aversion on the need for transparency and traceability. © 2022 Kedge Business School.

INVESTIGATING CONSERVED SEQUENCE in the SARS-CoV-2 GENOME AS NOVEL VACCINE IMMUNOGEN

Background: It is imperative to investigate novel, broadly conserved coronavirus immunogens as new SARS-CoV-2 variants of concern are continually emerging. The goal of this study was to generate a broadly protective long-term vaccine candidate against potential new variants of SARS-CoV-2 and novel, outbreak coronaviruses. The vaccine immunogen spanned portions of the highly conserved RNA replication machinery (nsp12 and nsp13) (CoV.Con). The vaccine was packaged into a rhesus adenoviral vector (RhAd52.CoV.Con) with the goal of generating robust long-lived CD8+ T-cell responses. Methods: The CoV.Con immunogen was generated by aligning coronavirus sequences to determine the most conserved region. ACE2 carrier and BALB/c mice were immunized intramuscularly with 109 RhAd52.CoV.Con and boosted four weeks later. Splenocytes were harvested four weeks after boost. Cellular immunity was determined through ELIspot and intracellular cytokine stain (ICS). BALB/c mice were primed and boosted with RhAd52.CoV.Con. Four weeks post boost mice were challenged intranasally with mouse adapted SARS-CoV-2. Protection was measured by weight loss and plaque assay. Results: Four weeks post RhAd52.CoV.Con boost immunization, ACE2 carrier and BALB/c mice developed cellular immunity as shown by ELIspot (Fig 1a) and ICS. ACE2 carrier mice cellular immunity showed bias toward nsp12 while BALB/c mice showed nsp13 preference. BALB/c mice were primed and boosted with RhAd52.CoV.Con. Four weeks after boost mice were challenged with mouse adapted SARS-CoV-2. RhAd52.CoV.Con was compared against and combined with a suboptimal dose of RhAd52.S.pp at 4 and 8 weeks post injection. Protection against weight loss (Fig 1b) and viral load (Fig 1c) was minimal although increased RhAd52.S.pp protection was observed from 4 to 8 weeks post immunization. Increased RhAd52.S.pp protection corresponded to increased spike antibody binding and neutralizing titers. Conclusion: Our work investigates a highly conserved coronavirus immunogen, CoV.Con, demonstrating immunogenicity in two mouse strains. While RhAd52. CoV.Con protection in the mouse model was minimal it demonstrates a schema for generating coronavirus immunogens that can protect against multiple different viruses. This work takes the first steps towards generating a long-lived broadly protective T-cell coronavirus vaccine.

Pulmonary fibroproliferative response in old mice that survive acute lung injury by mouse-adapted sars-cov-2

RATIONALE While SARS-CoV-2 viral infection, acute lung injury, and inflammation resolve in a timely manner in most individuals, there is growing clinical evidence of long-term sequelae of COVID-19 in some patients, particularly in vulnerable populations. We established a mouse model of SARS-CoV-2 infection using a mouseadapted virus and a standard laboratory strain of mice that displays age-dependent disease severity. In comparison to young BALB/c mice, old BALB/c mice display increased morbidity and mortality when infected with SARS-CoV-2 MA-10, and most succumb to acute infection or reach the criteria for humane euthanasia within 7 days of infection. We examined the lung pathology of older BALB/c mice that survive acute infection to determine the potential long-term pulmonary manifestations of COVID-19 in vulnerable populations such as the elderly.METHODS Mice were randomized and assigned to specific harvest days spanning 30 days prior to the start of the experiment. BALB/cAnNHsd mice were intranasally infected with SARS-CoV-2 MA-10 and clinical signs of disease were monitored, including weight loss and lung function via whole body plethysmography. At each time point, animals were sacrificed and lung lobes were collected for viral titer and histopathological analyses. Lung viral titers of the caudal right lobe were determined by plaque assay. Histopathology of the left lobe was assessed utilizing formalin-fixed, paraffin-embedded specimens.RESULTSIn comparison to 10-week-old BALB/c mice, 1-year-old BALB/c mice were highly susceptible to SARS-CoV-2 MA-10, displaying high morbidity and mortality, even requiring a lower viral dose than young BALB/c mice to yield similar kinetics of weight loss and clinical signs. In some experiments, survival of older mice was low as ∼15% at day 7. For older mice surviving to days 15 and 30 post infection, acute lung injury resolved but there were regionally extensive consolidated areas containing proliferative smooth muscle actin-positive fibroblasts, collagen accumulation, and admixed immune cells with formation of tertiary lymphoid organs. Mice displaying this pulmonary fibroproliferative response did not have detectable levels of virus in the lung.CONCLUSIONSThis mouse adapted SARS-CoV-2 model reveals a response in older mice surviving acute lung injury with robust chronic inflammation and tissue remodeling resulting in pulmonary fibrosis despite viral clearance of the tissue. This offers a model to investigate mediators driving the fibroproliferative and inflammatory responses that may be a COVID-19 sequela and cause persistent pulmonary dysfunction in some vulnerable patients such as the elderly.