Poliovirus tropism and attenuation are determined after internal ribosome entry
Open accessAbstract
Poliovirus replication is limited to a few organs, including the brain and spinal cord. This restricted tropism may be a consequence of organ-specific differences in translation initiation by the poliovirus internal ribosome entry site (IRES). A C-to-U mutation at base 472 in the IRES of the Sabin type 3 poliovirus vaccine strain, known to attenuate neurovirulence, may further restrict tropism by eliminating viral replication in the CNS. To determine the relationship between IRES-mediated translation and poliovirus tropism, recombinant human adenoviruses were used to express bicistronic mRNAs in murine organs. The IRESs of poliovirus, the cardiotropic coxsackievirus B3 (CVB3), and the hepatotropic hepatitis C virus (HCV) mediate translation in many organs, including those that do not support viral replication. A translation defect associated with the Sabin type 3 IRES was observed in all organs examined. Poliovirus type 1 and recombinant polioviruses dependent on the IRES of CVB3 or HCV replicate in the CNS of mice and cause paralysis. Although the type 3 Sabin strain is an effective vaccine, polioviruses with a U at base 472 of the IRES cause paralysis in newborn mice. Tropism of wild-type and vaccine strains of poliovirus is therefore determined after internal ribosome entry.
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DomV forms part of the internal ribosome entry site (IRES), and destabilizing this structure is thought to reduce the efficiency of translation initiation.
“DomV forms part of the internal ribosome entry site (IRES), and it is thought that destabilizing this structure reduces the efficiency of translation initiation (Kauder and Racaniello, 2004, Macadam et al., 1994, Svitkin et al., 1990).”
From Engineering the Live-Attenuated Polio Vaccine to Prevent Reversion to Virulence (2020) · cites this paper as Kauder and Racaniello, 2004
The Introduction identifies the poliovirus IRES as a site of translation initiation, and the section on vaccine-strain IRES mutations reports that C472U decreases IRES-dependent translation. Our copy does not identify DomV or say that destabilizing its structure causes that decrease, so the structural mechanism is not supported by this source. (LLM, conf=0.85)
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- Authors
- Kauder, S. E., & Racaniello, V. R.
- Affiliations
- Columbia University (US)
- Corresponding author
- Racaniello, Vincent R.
- Venue
- Journal of Clinical Investigation
- Published
- 2004-06-15
- Volume
- 113
- Issue
- 12
- Pages
- 1743-1753
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC420511
- OpenAlex
- W4251222835
- Cited by
- 83
- References
- 59
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2023: 5 · 2022: 7 · 2021: 3 · 2020: 6 · 2019: 5 · 2018: 4 · 2017: 1 · 2016: 2 · 2015: 3 · 2014: 3 · 2013: 1
- FWCI
- 4.58
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ai020017-08, AI20017, AI07161)
- National Institute of Allergy and Infectious Diseases (T32AI07161, R01 AI20017, T32AI007161)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Viral Infections and Immunology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA and protein synthesis mechanisms
- Health Sciences › Medicine › Epidemiology › Virology and Viral Diseases
- Keywords
- poliovirus, internal ribosome entry site, viral tropism, neurovirulence, IRES-mediated translation, coxsackievirus B3, hepatitis C virus, paralysis
- MeSH terms
- Adenoviridae, Animals, Cell Line, Humans, Mice, Inbred C57BL, Nucleic Acid Conformation, Poliomyelitis, Poliovirus Vaccine, Oral, Regulatory Sequences, Nucleic Acid, Ribosomes, RNA, Viral, Protein Biosynthesis, Virus Replication, Survival Rate, Hepacivirus, Poliovirus, 5' Untranslated Regions, Enterovirus B, Human, Mice
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