EV71 VP1 Specific Neutra™ Antibody Products

Enterovirus 71 (EV71) is a small, non-enveloped virus that belongs to the Picornaviridae family, primarily responsible for hand, foot, and mouth disease (HFMD), especially in young children. It is also associated with severe neurological complications, such as encephalitis and meningitis. EV71 is transmitted through respiratory droplets, the fecal-oral route, and direct contact. The virus features a genome of single-stranded RNA and an icosahedral capsid. The viral capsid contains four major viral structural proteins: VP1, VP2, VP3, and VP4. EV71 infects host cells by attaching to different receptors on the cell surface and initiating multiple consecutive steps.

Fig. 1 Structure and genome of EV71.^{1, 3}

The Important Neurovirulence Determinant of EV71: VP1

VP1, a capsid subunit protein, contributes to the pathogenicity and stability of the EV71 virus, helping it persist in the gastrointestinal tract. As part of the viral capsid, VP1 is involved in host cell attachment and entry by interacting with cell surface receptors, initiating infection. VP1 facilitates the viral uncoating process, allowing the release of the RNA genome into the host cell cytoplasm, where replication occurs. During maturation, VP1 assembles into the viral capsid, enabling the virus to form infectious particles. The structural features of VP1 also contribute to immune evasion by regulating host immune responses. Its involvement in neurovirulence is particularly significant, as mutations in VP1 are linked to increased pathogenicity in the central nervous system.

EV71 VP1 Signaling Pathway

EV71 VP1 regulates several key signaling pathways involved in viral replication and immune modulation. VP1 can alter host cell apoptosis and autophagy processes via the mTOR signaling pathway to enhance viral replication. VP1 can also upregulate the expression of ERICH3, ZC3H13 and modulate interferon signaling, helping EV71 manipulate host cell machinery for efficient replication and immune evasion, contributing to the virus's pathogenicity and neurovirulence. VP1 interacts with host cell proteins to activate pathways like the MAPK and NF-κB pathways, which influence inflammatory responses and cellular stress responses. By targeting these proteins and pathways, VP1 enhances viral persistence and spread.

Anti-EV71 VP1 Neutralizing Antibodies

Neutralizing antibodies targeting EV71 VP1 protein block the virus's ability to bind to host cell receptors, preventing viral entry and replication. These antibodies primarily recognize epitopes on VP1's surface, which are essential for viral attachment. Research has shown that such antibodies can provide protective immunity against EV71 infection. For example, a single neutralizing monoclonal antibody (mAb) against the GH loop of EV71 VP1 was found to inhibit viral attachment and internalization during viral entry as well as subsequent uncoating and RNA release, and the mechanism was shown to be interference with the binding of EV71 to its key receptors, including heparan sulfate, SCARB2, and PSGL-1.

Fig. 2 Characterization of EV71-neutralizing mAbs.^2,3

With years of expertise in antibody research, Creative Biolabs offers highly specific and sensitive anti-EV71 VP1 neutralizing antibodies, designed to support and enhance your diverse research needs.

REFERENCES

1. Yee, Pinn Tsin Isabel, and Chit Laa Poh. "Development of novel vaccines against enterovirus-71." Viruses 8.1 (2015): 1.
2. Arthur Huang, Kuan-Ying, et al. "Epitope-associated and specificity-focused features of EV71-neutralizing antibody repertoires from plasmablasts of infected children." Nature communications 8.1 (2017): 762.
3. Distributed under Open Access license CC BY 4.0, without modification.