Current data indicate that poliovirus genomes or fragments remain present in the CNS of post-polio syndrome patients decades after acute paralysis, potentially driving chronic inflammation.
Establishing a pathogenetic link between poliovirus persistence and post-polio syndrome could lead to the development of etiologic therapies aimed at virus eradication.
The three poliovirus serotypes (PVs) cause acute paralytic poliomyelitis. Decades after being hit by polio, survivors may develop a condition known as post-polio syndrome (PPS). PPS is characterized by extreme fatigue, progressing muscular weakness and chronic pain. The pathogenesis is unclear and, thus, empirical therapies are employed. PVs are known to be able to persist in infected host cells both in vitro and in vivo. The understanding of PV genomes has made it possible to set up sensitive and specific molecular tests capable of detecting minute amounts of virus in samples from PPS patients. Current data indicate that complete PV genomes (or genomic fragments) remain present, decades after acute paralysis, in the CNS of these patients. Virus persistence is hypothesized to bring about chronic inflammation, immune-mediated injury and decreased expression of neurotrophic factors. Establishing a pathogenetic link between PV persistence and PPS would be extremely relevant to the development of an etiologic therapy aimed at virus eradication.
Baj et al. (2007) conducted a review in Post-polio syndrome (PPS). Poliovirus persistence was evaluated. Current data indicate that poliovirus genomes or fragments remain present in the CNS of post-polio syndrome patients decades after acute paralysis, potentially driving chronic inflammation.
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