Background: Persistent poliovirus (PV) infection has been reported frequently in individuals with B lymphocyte deficiency (and low or absent serum immunoglobulins). The origin of PPS is poorly understood, but inflammation in meninges, spinal cord and muscles has been noticed (Semino-Mora & Dalakas, 1998). Inflammatory infiltrates suggest: persistent PV infection, autoimmune attack on CNS targets, increased vulnerability of CNS to further infections. The possibility of persistent PV infection was investigated in a cohort of PPS patients. Methods: Patients were diagnosed according to EFNS criteria: PPS cases (n=112), stable polio cases (n=15). Family members of PPS patients (n=50) and non-polio controls (n=57) were also investigated. Specimens: cerebrospinal fluid, peripheral blood leukocytes, assorted live cells (duodenal mucosa, skeletal muscle, peripheral nerve). Samples were co-cultured with PVsusceptible cell lines, then poliovirus-specific RT-PCR assays were performed. Results: Poliovirus genome was detected in 93/112 (83%) PPS patients, 4/15 (27%) stable polio cases, 2/107 (2%) controls. Type 1 poliovirus was found most frequently (59%), followed by type 2 (13%) and type 3 (11%). Some cases could not be typed. Epithelial cell lines infected with PV from PPS patients produced PV capsid proteins and enhanced levels of the chemokine MCP-1. Serum immunoglobulin levels were measured in cases and controls. IgG1, IgG2, IgG4 and IgA were significantly reduced in PPS cases and their family members. IgM levels and titers of poliovirus neutralizing antibodies were not significantly different among PPS cases and controls. Conclusions: Low-level PV activity was detected at high frequency in PPS patients decades after the acute attack and might play a pathogenetic role. PV infection is not transmitted by PPS patients to their family members, a relevant finding for public health. Effective treatments for PPS are missing (Koopman et al., 2011). In order to avoid PPS or block its progression, identification of individuals with chronic PV infection might lead to treatment with intravenous human IgG preparations, antiviral drugs, anti-PV antibodies. Antiviral treatments are under development and may hold the potential for eradicating chronic PV infection.

Persistence of poliovirus genome in polio survivors diagnosed with post-polio syndrome

BAJ, ANDREINA
Primo
;
BONO, GIORGIO GIOVANNI;TONIOLO, ANTONIO
Ultimo
2014-01-01

Abstract

Background: Persistent poliovirus (PV) infection has been reported frequently in individuals with B lymphocyte deficiency (and low or absent serum immunoglobulins). The origin of PPS is poorly understood, but inflammation in meninges, spinal cord and muscles has been noticed (Semino-Mora & Dalakas, 1998). Inflammatory infiltrates suggest: persistent PV infection, autoimmune attack on CNS targets, increased vulnerability of CNS to further infections. The possibility of persistent PV infection was investigated in a cohort of PPS patients. Methods: Patients were diagnosed according to EFNS criteria: PPS cases (n=112), stable polio cases (n=15). Family members of PPS patients (n=50) and non-polio controls (n=57) were also investigated. Specimens: cerebrospinal fluid, peripheral blood leukocytes, assorted live cells (duodenal mucosa, skeletal muscle, peripheral nerve). Samples were co-cultured with PVsusceptible cell lines, then poliovirus-specific RT-PCR assays were performed. Results: Poliovirus genome was detected in 93/112 (83%) PPS patients, 4/15 (27%) stable polio cases, 2/107 (2%) controls. Type 1 poliovirus was found most frequently (59%), followed by type 2 (13%) and type 3 (11%). Some cases could not be typed. Epithelial cell lines infected with PV from PPS patients produced PV capsid proteins and enhanced levels of the chemokine MCP-1. Serum immunoglobulin levels were measured in cases and controls. IgG1, IgG2, IgG4 and IgA were significantly reduced in PPS cases and their family members. IgM levels and titers of poliovirus neutralizing antibodies were not significantly different among PPS cases and controls. Conclusions: Low-level PV activity was detected at high frequency in PPS patients decades after the acute attack and might play a pathogenetic role. PV infection is not transmitted by PPS patients to their family members, a relevant finding for public health. Effective treatments for PPS are missing (Koopman et al., 2011). In order to avoid PPS or block its progression, identification of individuals with chronic PV infection might lead to treatment with intravenous human IgG preparations, antiviral drugs, anti-PV antibodies. Antiviral treatments are under development and may hold the potential for eradicating chronic PV infection.
2014
Baj, Andreina; Colombo, M.; Maccari, G.; Nauti, A.; Bono, GIORGIO GIOVANNI; Roivainen, M.; Toniolo, Antonio
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11383/1918920
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