Persistent poliovirus infection in mouse motoneurons

Destombes, J.; Couderc, Thérèse; Thiesson, D.; Girard, Sophie; Wilt, Susan G.; Blondel, B

doi:10.1128/jvi.71.2.1621-1628.1997

Cited by 40 publications

(25 citation statements)

References 32 publications

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“…The Ala67Thr mutation has also been found to facilitate increased resistance against poliovirusinduced cell lysis and apoptosis [Pavio et al, 2000;Gosselin et al, 2003]. The delayed course of poliovirusinduced cytolysis may thus have implications for development of persistent infections within the CNS [Destombes et al, 1997].…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, poliovirus receptor mutants, including the Ala67Thr mutation, can be selected during persistent infection of human neuroblastoma cells [Pavio et al, 2000] and these mutants have been found to increase resistance to cell lysis [Pavio et al, 2000] and reduce apoptosis [Gosselin et al, 2003]. It has been also reported that PV can persist in human fetal brain cells [Pavio et al, 2000] and in mouse spinal cord for at least 12 months after onset of paralysis [Destombes et al, 1997].…”

Section: Introductionmentioning

confidence: 99%

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Ala67Thr mutation in the poliovirus receptor CD155 is a potential risk factor for vaccine and wild‐type paralytic poliomyelitis

Kindberg

Fiore

et al. 2009

Journal of Medical Virology

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Poliovirus infections can be asymptomatic or cause severe paralysis. Why some individuals develop paralytic poliomyelitis is unknown, but a role for host genetic factors has been suggested. To investigate if a polymorphism, Ala67Thr, in the poliovirus receptor, which has been found to facilitate increased resistance against poliovirus-induced cell lysis and apoptosis, is associated with increased risk of paralytic poliomyelitis, poliovirus receptor genotyping was undertaken among Italian subjects with vaccine-associated (n = 9), or with wild-type paralytic poliomyelitis (n = 6), and control subjects (n = 71), using RFLP-PCR and pyrosequencing. Heterozygous poliovirus receptor Ala67Thr genotype was found in 13.3% of the patients with paresis and in 8.5% of the controls (Odds Ratio = 1.667). The frequency of Ala67Thr among the controls is in agreement with earlier published data. It is concluded that the Ala67Thr mutation in the poliovirus receptor is a possible risk factor for the development of vaccine-associated or paralytic poliomyelitis associated with wild-type virus.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Ala67Thr mutation in the poliovirus receptor CD155 is a potential risk factor for vaccine and wild‐type paralytic poliomyelitis

Kindberg

Fiore

et al. 2009

Journal of Medical Virology

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“…The carrier state of FMDV, for example, has been defined by the presence of infectious virus in oropharyngeal fluids of infected animals for 28 or more days after infection (23). Other picornaviruses that are known to establish long-term persistence include the human pathogens poliovirus (PV), rhinovirus (RV), and coxsackievirus (CV) and the animal pathogens encephalomyocarditis virus (EMCV) and Theiler's murine encephalomyelitis virus (TMEV) (24,25,(27)(28)(29). Despite the significance of persistent infections and their implications for the control of picornaviruses, little is known about the mechanisms underlying establishment, maintenance, and potential recrudescence of persistent picornaviral infections.…”

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confidence: 99%

Persistent Infection and Transmission of Senecavirus A from Carrier Sows to Contact Piglets

Maggioli

Fernandes

Joshi

et al. 2019

J Virol

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Senecavirus A (SVA) is a picornavirus that causes acute vesicular disease (VD), that is clinically indistinguishable from foot-and-mouth disease (FMD), in pigs. Notably, SVA RNA has been detected in lymphoid tissues of infected animals several weeks following resolution of the clinical disease, suggesting that the virus may persist in select host tissues. Here, we investigated the occurrence of persistent SVA infection and the contribution of stressors (transportation, immunosuppression, or parturition) to acute disease and recrudescence from persistent SVA infection. Our results show that transportation stress leads to a slight increase in disease severity following infection. During persistence, transportation, immunosuppression, and parturition stressors did not lead to overt/recrudescent clinical disease, but intermittent viremia and virus shedding were detected up to day 60 postinfection (p.i.) in all treatment groups following stress stimulation. Notably, real-time PCR and in situ hybridization (ISH) assays confirmed that the tonsil harbors SVA RNA during the persistent phase of infection. Immunofluorescence assays (IFA) specific for double-stranded RNA (dsRNA) demonstrated the presence of double-stranded viral RNA in tonsillar cells. Most importantly, infectious SVA was isolated from the tonsil of two animals on day 60 p.i., confirming the occurrence of carrier animals following SVA infection. These findings were supported by the fact that contact piglets (11/44) born to persistently infected sows were infected by SVA, demonstrating successful transmission of the virus from carrier sows to contact piglets. Results here confirm the establishment of persistent infection by SVA and demonstrate successful transmission of the virus from persistently infected animals. IMPORTANCE Persistent viral infections have significant implications for disease control strategies. Previous studies demonstrated the persistence of SVA RNA in the tonsil of experimentally or naturally infected animals long after resolution of the clinical disease. Here, we showed that SVA establishes persistent infection in SVA-infected animals, with the tonsil serving as one of the sites of virus persistence. Importantly, persistently infected carrier animals shedding SVA in oral and nasal secretions or feces can serve as sources of infection to other susceptible animals, as evidenced by successful transmission of SVA from persistently infected sows to contact piglets. These findings unveil an important aspect of SVA infection biology, suggesting that persistently infected pigs may function as reservoirs for SVA.

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“…In vitro, the possible role of poliovirus receptor mutations has been documented in neuroblastoma cells persistently infected with PV. 50 Experimental studies in mice have shown that PV may cause persistent infection and paralysis upon immunosuppression, 51 that infection can be traced to motor neurons, 52 and that hindered replication of the PV genome possibly contributes to PV persistence in the CNS. 53 Genomic changes in persistent PV isolates (especially in the 5 0untranslated region (5 0 -UTR) and VP1 region) have been reported in immunodeficient individuals who are chronic carriers of the virus.…”

Section: Persistent Poliovirus Infection In Vitro and In Vivomentioning

confidence: 99%

Post-poliomyelitis syndrome as a possible viral disease

Baj

Colombo

Headley³

et al. 2015

International Journal of Infectious Diseases

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This review summarizes current concepts on post-polio syndrome (PPS), a condition that may arise in polio survivors after partial or complete functional recovery followed by a prolonged interval of stable neurological function. PPS affects 15-20 million people worldwide. Epidemiological data are reported, together with the pathogenic pathways that possibly lead to the progressive degeneration and loss of neuromuscular motor units. As a consequence of PPS, polio survivors experience new weakness, generalized fatigue, atrophy of previously unaffected muscles, and a physical decline that may culminate in the loss of independent life. Emphasis is given to the possible pathogenic role of persistent poliovirus infection and chronic inflammation. These factors could contribute to the neurological and physical decline in polio survivors. A perspective is then given on novel anti-poliovirus compounds and monoclonal antibodies that have been developed to contribute to the final phases of polio eradication. These agents could also be useful for the treatment or prevention of PPS. Some of these compounds/antibodies are in early clinical development. Finally, current clinical trials for PPS are reported. In this area, the intravenous infusion of normal human immunoglobulins appears both feasible and promising.

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Persistent poliovirus infection in mouse motoneurons

Cited by 40 publications

References 32 publications

Ala67Thr mutation in the poliovirus receptor CD155 is a potential risk factor for vaccine and wild‐type paralytic poliomyelitis

Ala67Thr mutation in the poliovirus receptor CD155 is a potential risk factor for vaccine and wild‐type paralytic poliomyelitis

Persistent Infection and Transmission of Senecavirus A from Carrier Sows to Contact Piglets

Post-poliomyelitis syndrome as a possible viral disease

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