MOUSE ANTI-ENTEROVIRUS 71 VP1 (3658)
Mouse anti Enterovirus 71 VP1 (3658) antibody is specific for EV71 VP1 and has been developed for use in ELISA and immunofluorescence. These monoclonal antibodies have been developed to meet the need for highly reactive and specific EV71 antibodies for the future development of serological assays.
PRODUCT DETAILS – MOUSE ANTI-ENTEROVIRUS 71 VP1 ANTIBODY (3658)
- Mouse anti Enterovirus 71 VP1 (3658). Specific for the VP1 of Enterovirus type 71. Does not cross react with related viruses including Coxsackie A9, Coxsackie B2, ECHO 30, EV70 and Polio, type 2.
- Purified preparations consist of >90% pure mouse monoclonal antibody purified from ascites fluid or culture medium by protein A chromatography or sequential differential precipitations.
- Presented in PBS pH7.2 with 0.1% sodium azide.
- For use in ELISA and immunofluorescence.
- Can be used with Goat anti mouse IgG HRP and PanBlock ELISA Blocking Buffer.
Enteroviruses (EV) are single-stranded RNA viruses belonging to the Picornaviridae family and are the smallest, non-enveloped viruses known to infect both humans and animals. They are common seasonal viruses that are associated with a variety of diseases. Enterovirus 71 (EV71) has been identified as one of the main causative agents responsible for large outbreaks of hand, foot, and mouth disease (HFMD) across the Asia-Pacific region. Other members of the genus Enterovirus cause HFMD, including coxsackieviruses A16, A6, A5, A7, A9, A10, B2, and B5, but EV71 is linked to severe complications, including brainstem encephalitis, aseptic meningitis, and pulmonary edema (Caine et al., 2016). As yet, no effective EV-specific antiviral treatments are available, and vaccines are available only against polioviruses. Ongoing experience with EV71 outbreaks in the Asia-Pacific region has demonstrated that co-infections with other EV and indeed viruses belonging to other families, is common and raises the possibility that some co-infections can increase the severity of disease and change the clinical presentation.
These viruses are spread primarily through the fecal–oral route, but some species can be spread through respiratory secretions (e.g., EV-D68 and rhinovirus). The average incubation period for enteroviral contagious is from 3 – 10 to 30 days. The virus, after replicating and breaking the gastrointestinal tract barrier, is transmitted via the blood stream to every organ of the body. EV shows tropism towards organs like the heart, skin, and in particular the central nervous system. It has been observed that infected people excrete large quantities of the virus in faeces for a period of even 16 weeks. Most human enterovirus infections are either asymptomatic or result in mild disease. Periodically, enteroviruses are associated with outbreaks of more serious disease, resulting in considerable morbidity and occasionally in significant mortality.
The VP1 capsid gene is considered to be an ideal target for typing enterovirus because of variability of the region. Phylogenetic analysis of VP1 gene sequences also correlates well with serotyping in serum neutralization assays (Muehlenbachs et al., 2015). A domain has also been identified on the EV71 VP1 capsid protein which is critical for receptor attachment and necessary for the stability of infectious virions. It includes a group of positively charged amino acids near the 5-fold vertices of the capsid protein. EV71 receptors are believed to increase the ability of the virus to become neurotropic and so increase the severity of the disease it causes (Caine et al., 2016). This region is therefore an ideal target for the development of neutralising antibodies and anti-viral drugs.
- Enterovirus surveillance guidelines. Guidelines for enterovirus surveillance in support of the Polio Eradication Initiative. World Health Organization 2015.
- Jia et al. (2017). Effective in vivo therapeutic IgG antibody against VP3 of enterovirus 71 with receptor-competing activity. Sci Rep. 7:46402.
- Wells, AI and Coyne, CB (2019). Enteroviruses: A Gut-Wrenching Game of Entry, Detection, and Evasion. Viruses 2019, 11(5), 460.
- Caine et al. (2016). A Single Mutation in the VP1 of Enterovirus 71 Is Responsible for Increased Virulence and Neurotropism in Adult Interferon-Deficient Mice. J Virol. 90(19):8592-604.
- Muehlenbachs et al. (2015). Tissue tropism, pathology and pathogenesis of enterovirus infection. J Pathol. 235(2):217-28.
- Factsheet about enteroviruses. European Centre for Disease Prevention and Control (ECDC), 2010.