Talk:Abnormal Development - Polio Virus

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On this website the Discussion Tab or "talk pages" for a topic has been used for several purposes: References - recent and historic that relates to the topic Additional topic information - currently prepared in draft format Links - to related webpages Topic page - an edit history as used on other Wiki sites Lecture/Practical - student feedback Student Projects - online project discussions. Links: Pubmed Most Recent | Reference Tutorial | Journal Searches Glossary Links Glossary: A | B | C | D | E | F | G | H | I | J | K | L | M | N | O | P | Q | R | S | T | U | V | W | X | Y | Z | Numbers | Symbols | Term Link Cite this page: Hill, M.A. (2024, May 5) Embryology Abnormal Development - Polio Virus. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Abnormal_Development_-_Polio_Virus

2011

A statistical model of the international spread of wild poliovirus in Africa used to predict and prevent outbreaks

PLoS Med. 2011 Oct;8(10):e1001109. Epub 2011 Oct 18.

O'Reilly KM, Chauvin C, Aylward RB, Maher C, Okiror S, Wolff C, Nshmirimana D, Donnelly CA, Grassly NC.Source Medical Research Council Centre for Outbreak Analysis and Modelling, Department of Infectious Disease Epidemiology, School of Public Health, Imperial College London, London, United Kingdom.

Abstract

BACKGROUND: Outbreaks of poliomyelitis in African countries that were previously free of wild-type poliovirus cost the Global PolioEradication Initiative US$850 million during 2003-2009, and have limited the ability of the program to focus on endemic countries. A quantitative understanding of the factors that predict the distribution and timing of outbreaks will enable their prevention and facilitate the completion of global eradication.

METHODS AND FINDINGS: Children with poliomyelitis in Africa from 1 January 2003 to 31 December 2010 were identified through routine surveillance of cases of acute flaccid paralysis, and separate outbreaks associated with importation of wild-type poliovirus were defined using the genetic relatedness of these viruses in the VP1/2A region. Potential explanatory variables were examined for their association with the number, size, and duration of poliomyelitis outbreaks in 6-mo periods using multivariable regression analysis. The predictive ability of 6-mo-ahead forecasts of poliomyelitis outbreaks in each country based on the regression model was assessed. A total of 142 genetically distinct outbreaks of poliomyelitis were recorded in 25 African countries, resulting in 1-228 cases (median of two cases). The estimated number of people arriving from infected countries and <5-y childhood mortality were independently associated with the number of outbreaks. Immunisation coverage based on the reported vaccination history of children with non-polio acute flaccid paralysis was associated with the duration and size of each outbreak, as well as the number of outbreaks. Six-month-ahead forecasts of the number of outbreaks in a country or region changed over time and had a predictive ability of 82%.

CONCLUSIONS: Outbreaks of poliomyelitis resulted primarily from continued transmission in Nigeria and the poor immunisation status of populations in neighbouring countries. From 1 January 2010 to 30 June 2011, reduced transmission in Nigeria and increased incidence in reinfected countries in west and central Africa have changed the geographical risk of polio outbreaks, and will require careful immunisation planning to limit onward spread. Please see later in the article for the Editors' Summary.

PMID 22028632

Intestinal microbiota promote enteric virus replication and systemic pathogenesis

Science. 2011 Oct 14;334(6053):249-52.

Kuss SK, Best GT, Etheredge CA, Pruijssers AJ, Frierson JM, Hooper LV, Dermody TS, Pfeiffer JK.Source Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

Abstract

Intestinal bacteria aid host health and limit bacterial pathogen colonization. However, the influence of bacteria on enteric viruses is largely unknown. We depleted the intestinal microbiota of mice with antibiotics before inoculation with poliovirus, an enteric virus. Antibiotic-treated mice were less susceptible to poliovirus disease and supported minimal viral replication in the intestine. Exposure to bacteria or their N-acetylglucosamine-containing surface polysaccharides, including lipopolysaccharide and peptidoglycan, enhanced poliovirus infectivity. We found that poliovirus binds lipopolysaccharide, and exposure of poliovirus to bacteria enhanced host cell association and infection. The pathogenesis of reovirus, an unrelated enteric virus, also was more severe in the presence of intestinal microbes. These results suggest that antibiotic-mediated microbiota depletion diminishes enteric virus infection and that enteric viruses exploit intestinal microbes for replication and transmission. Comment in Science. 2011 Oct 14;334(6053):168.PMID 21998395

The TLR3/TICAM-1 Pathway Is Mandatory for Innate Immune Responses to Poliovirus Infection

J Immunol. 2011 Oct 12.

Oshiumi H, Okamoto M, Fujii K, Kawanishi T, Matsumoto M, Koike S, Seya T.Source Department of Microbiology and Immunology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan.

Abstract

Cytoplasmic and endosomal RNA sensors recognize RNA virus infection and signals to protect host cells by inducing type I IFN. The cytoplasmic RNA sensors, retinoic acid inducible gene I/melanoma differentiation-associated gene 5, actually play pivotal roles in sensingvirus replication. IFN-β promoter stimulator-1 (IPS-1) is their common adaptor for IFN-inducing signaling. Toll/IL-1R homology domain-containing adaptor molecule 1 (TICAM-1), also known as TRIF, is the adaptor for TLR3 that recognizes viral dsRNA in the early endosome in dendritic cells and macrophages. Poliovirus (PV) belongs to the Picornaviridae, and melanoma differentiation-associated gene 5 reportedly detects replication of picornaviruses, leading to the induction of type I IFN. In this study, we present evidence that the TLR3/TICAM-1 pathway governs IFN induction and host protection against PV infection. Using human PVR transgenic (PVRtg) mice, as well as IPS-1(-/-) and TICAM-1(-/-) mice, we found that TICAM-1 is essential for antiviral responses that suppress PV infection. TICAM-1(-/-) mice in the PVRtg background became markedly susceptible to PV, and their survival rates were decreased compared with wild-type or IPS-1(-/-) mice. Similarly, serum and organ IFN levels were markedly reduced in TICAM-1(-/-)/PVRtg mice, particularly in the spleen and spinal cord. The sources of type I IFN were CD8α(+)/CD11c(+) splenic dendritic cells and macrophages, where the TICAM-1 pathway was more crucial for PV-derived IFN induction than was the IPS-1 pathway in ex vivo and in vitro analyses. These data indicate that the TLR3/TICAM-1 pathway functions are dominant in host protection and innate immune responses against PV infection.

PMID 21998457

Japanese vaccinations and practices, with particular attention to polio and pertussis

Travel Med Infect Dis. 2011 Jul;9(4):169-75. Epub 2010 Jun 3.

Nakano T.

Source Mie National Hospital, 357 Ozato-Kubota, Tsu, Mie 514-0125, Japan.

Abstract

This article introduces Japanese vaccinations and practices, focusing on polio and pertussis. Japan is one of the few industrialized countries still using live attenuated oral poliovirus vaccine (OPV). Current status of vaccine-associated paralytic poliomyelitis in Japan is discussed. This review is intended to encourage early conversion of OPV to inactivated poliovirus vaccine (IPV) for the routine vaccination as soon as possible. The other topic pertains to the results of a study designed to evaluate the safety and immunogenicity of the Japanese DPT vaccine in adults when administered at the dose of 0.2ml (2/5th of the ordinary dose). In Japan, there is no system for providing advice to adults on vaccination once the childhood schedule is completed. The author, however, wishes to propose here that if the currently approved DPT vaccine can be better utilized as Tdap, we may improve the means for disease prophylaxis.

Copyright © 2010 Elsevier Ltd. All rights reserved.

PMID 21995861

N Engl J Med. 2011 Oct 6;365(14):1355; author reply 1355.

Vaccine-derived poliomyelitis 12 years after infection

MacLennan CA, Huissoon AP, Kumararatne DS.Comment on

N Engl J Med. 2011 Jun 16;364(24):2316-23.

"DeVries et al. (June 16 issue)1 describe a patient with vaccine-derived poliomyelitis. We were unable to clear chronic, asymptomatic, neurovirulent poliovirus infection in a similarly antibody-deficient patient despite the use of antiviral therapy, breast milk, and oral immune globulin.2 In our patient, the mean IgG trough levels were 1000 mg per deciliter, and paralysis did not develop during an estimated 29 years of poliovirus infection. Neutralizing antibodies against his own poliovirus isolates were detected in his replacement immune globulin by the National Institute for Biological Standards and Control.3 In the patient described by DeVries et al., the IgG trough levels were 438 and 648 mg per deciliter before the onset of paralysis, and the immune globulin–replacement product had recently been changed. Since immunity to enteroviruses is primarily antibody-mediated,4 adequate immune globulin replacement is key for the prevention of paralysis in immunodeficient poliovirus carriers. Where possible, replacement immune globulin should be tested for antiviral activity against poliovirus isolates from such carriers until new antiviral agents that can cure this condition are available."

http://www.nejm.org/doi/full/10.1056/NEJMc1108814

PMID 21991972