In August 2025, the World Health Organization (WHO) reported that Israel detected nine circulating vaccine-derived poliovirus type 1 (cVDPV1) samples at seven environmental monitoring sites in Jerusalem and central regions. Although no paralytic cases have been reported, WHO has classified this event as an ongoing community transmission outbreak and included it within the prolonged Public Health Emergency of International Concern (PHEIC) framework since 2014. Polio has long been a major cause of childhood disability. While wild poliovirus has been nearly eradicated, the emergence of vaccine-derived viruses highlights that immunization gaps can allow the virus to "resurge."
Figure 1. WHO Report on Poliovirus Detection in Israel
Virus Overview
Poliovirus belongs to the Picornaviridae family, genus Enterovirus. It is a non-enveloped, single-stranded positive-sense RNA virus, approximately 30 nm in diameter. Its 7.5 kb genome is translated into a polyprotein via an IRES, which is then cleaved by viral proteases into structural and non-structural proteins. The structural proteins, consisting of VP1, VP2, VP3, and VP4 capsid proteins, form an icosahedral structure. Non-structural proteins regulate replication, translation suppression, and immune evasion.
Figure 2. Enterovirus Structure (From Viralzone)
| Category |
Protein |
Function |
| Capsid Proteins |
VP1 |
Located at the vertices of the icosahedral capsid, VP1 binds to the host receptor PVR, mediating viral attachment and entry. Binding induces conformational changes in the capsid, exposing structures that facilitate genome entry into the host cell. Entry mechanisms vary by cell type, and the virus can disrupt endothelial barriers, increasing permeability and aiding spread to the central nervous system. |
| VP2 / VP3 |
Primarily stabilize the capsid and maintain particle integrity during assembly. Their conformational changes affect infection efficiency and immune recognition. |
| VP4 |
Located on the inner capsid surface, VP4 is exposed along with the VP1 N-terminus upon receptor binding, forming a pore. When triggered by receptor binding, VP4 inserts into the cell membrane, facilitating RNA release. |
| Non-Structural Proteins |
2A |
A viral protease that cleaves its own polyprotein and various host proteins, inhibiting host mRNA translation, nuclear-cytoplasmic transport, and IFN pathways, thus giving viral RNA a translational advantage. |
| 2B |
A viral pore-forming protein that forms pores in the endoplasmic reticulum, releasing Ca²⁺ to promote membrane transport and replication complex formation. |
| 2C |
Binds and reshapes intracellular membranes, exhibiting RNA-binding and NTPase activity. It may interact with VP3, aiding in assembly and RNA encapsidation. |
| 3A |
Localizes the replication complex to membrane vesicles. 3A inhibits ER-to-Golgi transport, disrupts Golgi structure, reduces MHC and IFN receptor expression, and recruits ACBD3 and PI4KB to promote replication membrane formation. |
| 3B |
Serves as a replication primer by covalently binding to the RNA 5' end, providing a starting point for 3D polymerase to initiate RNA synthesis. |
| 3C |
Cleaves the viral polyprotein and degrades host factors (e.g., PABP), inhibiting cellular translation and interfering with immune responses. |
| 3D |
An RNA-dependent RNA polymerase directly responsible for genome replication. Its high error rate leads to diverse viral populations, accelerating adaptation to environmental and immune pressures and contributing to the emergence of vaccine-derived strains. |
Figure 3. Virus Replication Cycle (From Viralzone)
After extensive replication in the gut, the virus can enter the bloodstream and, in rare cases, invade the central nervous system, destroying anterior horn motor neurons and causing acute flaccid paralysis. Most infections are asymptomatic, but approximately 1 in 200 cases result in paralysis, with 5–10% of these cases leading to death due to respiratory muscle paralysis.
Polio is a highly contagious disease primarily affecting children under 5, potentially causing permanent paralysis or death. Vaccines are the primary defense against polio. Oral polio vaccine (OPV), in rare cases, can mutate and spread in under-immunized populations, forming cVDPV.
| Phase |
Vaccine/Strategy |
Features and Progress |
Key Impact |
| Early (1950s–2015) |
IPV (Inactivated Vaccine) and OPV (Trivalent Live Attenuated Vaccine) |
IPV: Safe, does not cause vaccine-related viruses, but offers limited mucosal immunity.
OPV: Easy to administer orally, strong herd immunity, but carries cVDPV risk. |
Established the foundation for global polio control, significantly reducing cases. |
| Since 2016 |
Trivalent OPV → Bivalent OPV (Type 2 removed) + IPV |
Due to cVDPV2 risks, global withdrawal of trivalent OPV; IPV integrated into routine programs. |
Reduced risk of type 2-related cVDPV outbreaks. |
| Recent (2020s) |
IPV as primary routine, nOPV2 for emergency use |
IPV: Becoming the mainstay of routine vaccination.
nOPV2: Higher genetic stability, used in nearly 2 billion emergency doses globally, significantly curbing cVDPV2 outbreaks. |
Enhanced safety and outbreak control. |
Israel's outbreak, though without clinical cases, underscores that maintaining high, uniform vaccination coverage is the only way to eradicate polio completely. The combined use of IPV and nOPV offers a viable path to polio elimination, but immunization gaps could allow the virus to resurge.
abinScience is a France-based biotechnology company focused on developing and producing high-quality research reagents. We are dedicated to providing innovative, reliable tools and technical solutions for global life science researchers. Below is a list of poliovirus-related proteins and antibodies offered by abinScience:
| Type |
Catalog Number |
Product Name |
| Protein |
VK703012 |
Recombinant Poliovirus type 1 VP0/Capsid protein VP0 Protein, N-His |
| VK674012 |
Recombinant Poliovirus type 1 VP1/Capsid protein VP1 Protein, N-His |
| VK644012 |
Recombinant Poliovirus type 1 VP3/Capsid protein VP3 Protein, N-His |
| Antibody |
VK557010 |
InVivoMAb Anti-Poliovirus Capsid protein VP1 (C3) |
| VK557020 |
InVivoMAb Anti-Poliovirus Capsid protein VP1 (19B) |
| VK703014 |
Anti-Poliovirus type 1 VP0/Capsid protein VP0 Polyclonal Antibody |
| VK674014 |
Anti-Poliovirus type 1 VP1/Capsid protein VP1 Polyclonal Antibody |
| VK644014 |
Anti-Poliovirus type 1 VP3/Capsid protein VP3 Polyclonal Antibody |
| VK557013 |
Anti-Poliovirus Capsid protein VP3 Nanobody (7A) |
References
- World Health Organization. Disease Outbreak News; Circulating vaccine-derived poliovirus type 1 in Israel. 20 August 2025.
- WHO factsheet on Poliomyelitis.
- GPEI. Updates on nOPV development and use.
