Study provides new insight into the immune pathogenesis of FMDV
Researchers at the Pirbright Institute and the Roslin Institute have discovered how foot-and-mouth disease virus (FMDV) interacts with immune cells in lymphoid tissues, helping the virus to persist in animals such as African buffalo. Their findings are reported in PLoS Pathogens.
In studies in mice, they found that FMDV binds to follicular dendritic cells, which are essential for presenting the virus to the immune system so that it can prevent disease.
Follicular dendritic cells are only found in lymphoid tissues, such as lymph nodes and the spleen. These tissues are part of the adaptive immune response which allows the immune system to mount a specific response and have ‘memory’ of it so it can recognise a subsequent infection.
Researchers also found that FMDV binds to a receptor known as CR2/CR1 on the follicular dendritic cells. This receptor is important in the adaptive immune response and this research demonstrated that it was essential for trapping and retaining the virus, which in turn leads to a better, and longer-lived immune response.
The scientists consider this helps the virus to persist in animals such as African buffalo and allows these animals to become carriers of the disease, which in turn poses a risk to other susceptible livestock.
Professor Bryan Charleston, Director of The Pirbright Institute and Head of the Viral Immunology group said: “This research helps to bridge the knowledge gap of how the immune system deals with FMDV infection in large animals. Our extensive work in African buffalo, a natural host of the disease, allowed us to predict why and how persistence may occur and then test this theory in a small animal model. This has given us new insights into the immune responses to FMDV and could provide clues about how to increase vaccine protection longevity.”
Article: Gordon, L., Mabbott, N., Wells, J., Kulik, L., Juleff, N., Charleston, B., Perez-Martin, E. (2022). Foot-and-mouth disease virus localisation on follicular dendritic cells and sustained induction of neutralising antibodies is dependent on binding to complement receptors (CR2/CR1). PLoS Pathogens, 18(5), e1009942, doi: 10.1371/journal.ppat.1009942
[SOURCE: Pirbright Institute\Roslin Institute]