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Cellular life cycle of poliovirus

(1) First, poliovirus binds to the cell surface macromolecule CD155, which functions as the receptor. (2) Uncoating the viral RNA is mediated by receptor-dependent destabilization of the virus capsid. (3) Cleavage of the viral protein VPg is performed by a cellular phosphodiesterase, and translation of the viral RNA occurs by a cap-independent (IRES-mediated) mechanism. (4) Proteolytic processing of the viral polyprotein yields mature structural and non-structural proteins. (5) The positive-sense RNA serves as the template for complementary negative-strand synthesis, thereby producing a double-stranded RNA (replicative form, RF). (6) Initiation of many positive strands from a single negative strand produces the partially single-stranded replicative intermediate (RI). (7) The newly synthesized positive-sense RNA molecules can either serve as templates for translation or (8) associate with capsid precursors to undergo encapsidation and induce the maturation cleavage of VP0, which ultimately generates progeny virions. (9) Lysis of the infected cell results in release of infectious progeny virions. (Source: De Jesus NH. Epidemics to eradication: the modern history of poliomyelitis. Virol J 2007;4:70. Creative Commons Attribution [CC BY] license,

Associated Disorders

  • Aseptic meningitis
  • Bulbar polio
  • Bulbospinal polio
  • Infantile paralysis
  • Nonparalytic polio
  • Paralytic polio
  • Polioencephalitis
  • Post-polio progressive muscular atrophy
  • Post-polio syndrome
  • Spinal paralytic polio