Accelerate viral infection therapies and vaccine discoveries
Kits, reagents and services to accelerate virology research
Viral diseases include everything from human influenza, commonly known as the flu, human immunodeficiency virus (HIV) and Zika to the recent severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) which caused the coronavirus disease 2019 outbreak (COVID-19).
Due to the diversity and complexity of viral diseases, vaccine development and anti-viral therapeutic discovery can be long and complex processes.
Now more than ever, researchers working on viral diseases needs solutions to accelererate timelines for bringing antiviral therapies and vaccines to market. PerkinElmer | Cisbio offers a large product portfolio and tools for virology research.
Discover our reagents, kits and services for virology research in the video below. They provide easy-to-use, rapid and cost-effective solutions to scientists working on viral diseases. For years, renown companies and academic labs have been relying on these solutions for the discovery of antiviral agents targeting the binding, integration, replication, and assembly steps of the viral life cycle.
Monitoring antiviral humoral response
The humoral immune response, also known as the antibody-mediated immune response, targets pathogens circulating in extracellular fluids (lymph or the blood). It involves B-cells that recognize antigens of pathogens. The secretion of soluble antibodies by the antibody-secreting plasma cells causes the destruction of extracellular microorganisms, preventing the spread of intracellular infections. Immunization can be attained through this humoral response.
Every step of the humoral response can be monitored, offering multiple solutions to support antiviral therapies and vaccines discovery.
Vaccination and immunity are closley linked to inflammation. Cytokines, inflammatory pathways, and inflammatory mediators are the hallmarks of those processes. During infection, multiple pathways like NFKB, JAK-STAT and, MAP Kinase are activated to contribute to cell stimulation. IL-6, IL1β, TNFα and the different IFN (-γ, -α, -β), among others, can be at the origin of the activation of these pathways and so represent an opportunity to be investigated for monitoring immunity through inflammation. Furthermore, multiple studies have emerged demonstrating that in some cases, such as Covid19, these secretions become abnormal and critically high. This phenomenon is known as a cytokine storm.
Studying T-Cells and B-Cells following their activation after antigen presentation represents considerable potential for tackling viral diseases, especially where the immune response either fails to protect or clear disease. Having a deeper look into ZAP-70 and BTK pathways can be of high interest when studying T-cell and B-cell activation respectively.
The humoral response can be split into 4 stages:
- 1 The virus enters the body and infects the cells. Dendritic cells (DCs) and NK cells are the first cells to respond to the antigens. They co-stimulate each other
- 2 DCs recruit adaptive immunity cells and present them with viral antigens
- 3 T-cells differentiate into helper T-cells
- 4 B-cells differentiate into memory cells and antibody-secreting cells. The antibodies are released and circulate through the body, binding to antigens. This final stage allows for the development of immunity.
In the case of vaccination, harmless antigens replace the actual virus to trigger the humoral response. The outcome is the creation of antibodies against a future possible infection of the diseases targeted by the vaccination.
Monitoring and disrupting the viral life cycle
Different therapeutic approaches can be applied to monitor and/or disrupt the viral life cycle. As described in the figure below, several steps in the virus replication cycle are protein-protein interactions (PPIs) events: the virus binds to the cytoplasm, the nucleus of the host cell, and interacts with DNA. Multiple PPI strategies are used by researchers to target different steps of the virus life cycle, from attachment and integration to assembly, as described in the article
“Disrupting protein-protein interactions in the viral life cycle: the contribution of tr-FRET“.
Ultimately, as a result of the viral infection, some infected cells may die from apoptosis or plasmolysis triggered by excess viral particles. Investigating cytotoxicity and cellular death can be of interest when researching antiviral drugs. Hallmarks of this type of cellular death are the apoptotic caspase pathway and DNA fragmentation. Cleaved PARP, considering its essential role in the apoptosis process, can be of interest to researchers trying to monitor apoptotic events. Equally, Phospho-H2AX as a specific marker of double-stranded DNA breaks, represents a good target to monitor the fragmentation of the DNA of host cells.
The viral life cycle can be split into 6 steps
- 1 Attachment and entry: The virus uses capsid attachment proteins to bind itself to specific receptors of the host cells membrane. It then enters via endocytosis.
- 2 Uncoating: The virus capsid and/or the viral envelop disassemble to release the genetic material and viral proteins
- 3 Integration: The viral genome is integrated inside the host cell genome via DNA binding protein interactions
- 4 Replication: The virus replicates itself extensively through the synthesis of its different components
- 5 Assembly: Newly synthesized genome and proteins are assembled to form new virus particles
- 6 Release: The viruses are now mature and are released, ready to invade or attack new cells.
- A As a result of the viral infection, some infected cells may die.