Two or more mutations in the VP1 and VP2 capsid protein genes are likely required for poliovirus to establish persistent infection in HEp-2 cells.
Multiple VP1/VP2 mutations required for poliovirus persistence in vitro; leaves open in vivo relevance and clinical implications.
Poliovirus mutants were selected during the persistent infection of human neuroblastoma cells. These viruses could establish secondary persistent infections in HEp-2 nonneural cells. We report the identification of a region of the genome of a persistent virus (S11) that was sufficient to confer to a recombinant virus the phenotype that causes persistent infection in HEp-2 cells. This region, between nucleotides 1148 and 3481, contained 11 missense mutations mapping exclusively in the genes of capsid proteins VP1 and VP2. Because recombinant viruses carrying only one of these two mutated genes were not able to cause persistent infection, it seems very probable that two or more mutations in these genes are required for expression of the phenotype that causes persistent infection.
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Cálvez et al. (1993) studied this question.
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