B-cell receptor (BCR) and antibodies recognizing Norovirus GI.1 and GII.4 VP1 virus-like particles (BCR/Ab (NoV GI.1/GII.4))

The B-cell receptor (BCR) and resulting antibodies recognizing Norovirus GI.1 and GII.4 VP1 virus-like particles (VLPs) are critical components of the adaptive immune response against Norovirus, the leading cause of acute viral gastroenteritis worldwide (Ramani et al., 2016, Nature Reviews Gastroenterology & Hepatology). The VP1 protein is the major structural component of the Norovirus capsid, and when expressed recombinantly, it self-assembles into VLPs that morphologically and antigenically resemble the native virus (Atmar et al., 2011, NEJM). These VLPs serve as the primary antigenic target in vaccine development, specifically designed to engage BCRs on B-lymphocytes. Upon engagement, these B cells differentiate into plasma cells that secrete neutralizing antibodies capable of blocking the interaction between the virus and host cell receptors, such as histo-blood group antigens (HBGAs) (Lindesmith et al., 2011, Journal of Virology). Therapeutic strategies, such as the bivalent VLP vaccine TAK-214 (HIL-214), aim to elicit a robust and durable antibody response against the most prevalent Norovirus genotypes, GI.1 and GII.4 (Bernstein et al., 2015, Journal of Infectious Diseases). Monitoring the efficacy of these interventions typically involves measuring HBGA-blocking antibody titers, which serve as a correlate of protection against infection and clinical disease.

Other names

Norovirus-specific B-cell receptorAnti-Norovirus VP1 antibodiesGI.1 and GII.4 VLP-reactive immunoglobulinsNorovirus neutralizing antibodies

Vaccine-mediated activation of B-cell receptors leads to the clonal expansion of B cells and the secretion of high-affinity neutralizing antibodies. These antibodies specifically target the VP1 capsid protein of Norovirus GI.1 and GII.4 strains, preventing the virus from binding to histo-blood group antigens (HBGAs) on the surface of host enterocytes, thereby neutralizing the infection (Lindesmith et al., 2011, Journal of Virology).