Overview
While the COVID-19 global pandemic continues to evolve, BD Biosciences stands strong to support critical scientific research to better understand and ultimately battle the COVID-19 outbreak. Now more than ever, BD Biosciences is committed to being your scientific partner of choice and providing you with the tools and support required to enable your COVID-19 research. We provide a comprehensive portfolio of research tools to facilitate discovery in the following areas of COVID-19 research:
Viral immune response
Cytokine analysis
Vaccine research
Biomarkers and therapeutics
Navigate this site to learn more about BD Biosciences’ solutions and their applications in COVID-19 research. All products mentioned on these pages are for research use only, except for the BD FACSLyric™ Flow Cytometer, which is a combined-function flow cytometer for both IVD and research use. Its use in COVID-19 is for research purposes only.
For information on the comprehensive COVID-19 response efforts from BD—including product availability, status of BD operations and business continuity planning—visit bd.com/COVID-19.
Biology of SARS-CoV-2
COVID-19, or coronavirus disease 2019, is caused by the SARS-CoV-2 virus (severe acute respiratory syndrome coronavirus 2). SARS-CoV-2 is a novel virus belonging to the coronavirus family, which includes strains responsible for the common cold as well as the viruses responsible for SARS and MERS. It is genetically related to the coronavirus responsible for the SARS outbreak in 2003.
SARS-CoV-2 is an enveloped single-stranded RNA virus of the Coronaviridae family. Its genome encodes 29 proteins involved in the infection, replication and virion assembly process. Key structural proteins of the virus include the spike (S) glycoprotein, the envelope (E) protein and the matrix (M) transmembrane glycoprotein.1 Initial infection is believed to take place in nasal epithelial cells, which are rich in ACE-2 receptors.
Viral entry also depends on cathepsin B/L activity and protease activity of TMPRSS2. These receptors are found distributed throughout epithelial cells of the respiratory and gastrointestinal tract. The S protein from SARS-CoV-2 enables cellular receptor binding, membrane fusion and hemagglutinin activity. The S protein contains a receptor binding domain (RBD), which is the most variable region of its genome. The RBD binds the human angiotensin-converting enzyme 2 (ACE-2) initiating viral uptake in human cells by endocytosis. The E and M proteins collaborate for viral envelope formation.1
Before entering a cell, SARS-CoV-2 needs to recognize and bind surface receptors such as ACE-2. From there, a cascade of sequential events take place to ensure successful viral infection and replication.2 The life cycle of SARS-CoV-2 includes the following:
SARS-CoV-2 binds to ACE-2 receptor
SARS-CoV-2 is endocytosed
SARS-CoV-2 fuses with a vesicle and viral RNA is released
SARS-CoV-2 RNA is translated into proteins
New SARS-CoV-2 virions are assembled
New SARS-CoV-2 virions are released
Types of immune responses to SARS-CoV-2
SARS-CoV-2 infection induces a multistep response from the host immune system:
First-line defense by the innate immune system with natural killer (NK) cells, macrophage activation and multinucleated giant cell formation
Proinflammatory cytokine and chemokine activation
Antigen presenting cells engulf and process SARS-CoV-2 antigens
T helper cells are activated by SARS-CoV-2 antigen
Cytotoxic T cells and B cells are cross activated by T helper cells
Immunological memory is formed for SARS-CoV-2
When the immune system fails to control its immune defense response properly, severe forms of COVID-19 develop.
Three major phases have been described in COVID-19 disease:
Viremia phase
Acute (pneumonia) phase
Recovery phase
Severe forms of SARS-CoV-2 induced COVID-19 are associated with increased release of pro-inflammatory cytokines (e.g., IL-6, Il-2, GM-CSF), also known as cytokine storm syndrome, hypercytokinemia or cytokine release syndrome, along with weak production of type I interferons (IFN-Is).3, 4
References
- Shang J, Wan Y, Luo C, et al. Cell entry mechanisms of SARS-CoV-2. Proc Natl Acad Sci U S A. 2020;117(21):11727-11734. doi:10.1073/pnas.2003138117
- Callaway E. The race for coronavirus vaccines. Nature. 2020;580(7805):576-577. doi: 10.1038/d41586-020-01221-y
- Sa Ribero M, Jouvenet N, Dreux M, Nisole S. Interplay between SARS-CoV-2 and the type I interferon response. PLoS Pathog. 2020;16(7):e1008737. doi:10.1371/journal.ppat.1008737
- Blanco-Melo D, Nilsson-Payant BE, Liu WC, et al. Imbalanced host response to SARS-CoV-2 drives development of COVID-19. Cell. 2020;181(5):1036-1045.e9. doi:10.1016/j.cell.2020.04.026
