The progress of the Polio Eradication Initiative: what prospects for eradicating measles? (9/1057)

Although various attempts have been made to eradicate infectious diseases, only smallpox has been eradicated to date. Polio is targeted for eradication in 2000 and already planning has begun for the eradication of measles. However, before we commit to a measles eradication effort, we must examine the lessons to be learned from polio eradication. Of particular importance is the debate over whether resources should be invested in 'horizontal' or 'vertical' programmes. The outcome of these debates will have a very deep and lasting impact on global health development in years to come. Collaboration between targeted programmes and the primary health care sector through polio and measles eradication efforts will help bring about the necessary balance between goal-oriented programmes, which are subject to quality control and can be evaluated by measurable outcomes, and broader efforts to build up sustainable health infrastructure.  (+info)

Induction of mucosal immunity by inactivated poliovirus vaccine is dependent on previous mucosal contact with live virus. (10/1057)

The inactivated poliovirus vaccine (IPV) is used for protection against poliomyelitis in The Netherlands. It is not clear, however, whether IPV vaccination can lead to priming of the mucosal immune system and the induction of IgA. It has been demonstrated that IPV vaccination is able to induce strong memory IgA responses in the serum of persons who have been naturally exposed to wild-type poliovirus. This has led to the hypothesis that IPV vaccination is able to induce poliovirus-specific IgA at mucosal sites in persons who have been previously primed with live poliovirus at mucosal sites. To test this hypothesis, the kinetics of the IgA response in serum and saliva after IPV vaccination were examined in persons previously vaccinated with oral poliovirus vaccine (OPV) or IPV. ELISA and enzyme-linked immunospot assays were used for the detection of poliovirus-specific IgA responses. In addition, B cell populations were separated on the basis of the expression of mucosal (alpha4beta7 integrin) and peripheral homing receptors (L-selectin). Parenteral IPV vaccination was able to boost systemic and mucosal IgA responses in previously OPV-vaccinated persons only. None of the previously vaccinated IPV recipients responded with the production of IgA in saliva. In agreement with this finding, a large percentage of the poliovirus-specific IgA-producing lymphocytes detected in previous OPV recipients expressed the alpha4beta7 integrin. It is concluded that IPV vaccination alone is insufficient to induce a mucosal IgA response against poliovirus. In mucosally (OPV-) primed individuals, however, booster vaccination with IPV leads to a strong mucosal IgA response.  (+info)

Wild poliovirus circulation among healthy children immunized with oral polio vaccine in Antananarivo, Madagascar. (11/1057)

From July 1995 to December 1996, 3185 stool specimens from healthy children aged 6-59 months attending 6 dispensaries in the Antananarivo area were examined for poliovirus. The children had been routinely immunized according to the Expanded Programme on Immunization (EPI) schedule and received the last dose of oral polio vaccine (OPV) more than 1 month before stool collection. 99.4% of the children were immunized with at least 3 doses of OPV. HEp-2 cell culture revealed virus infections in 192 stools (6.0%), including 9 poliovirus (0.3%) and 183 nonpolio enterovirus isolates (5.7%). Infections occurred throughout the year, but incidence was higher during the hot and rainy season (P=0.01). Using a neutralization test with monoclonal antibodies and PCR-RFLP in two genomic regions coding for the VP1 capsid and RNA polymerase, 4 wild polioviruses (3 type 1 and 1 type 3) and 5 vaccine-related polioviruses (2 Sabin 1-like variants, 1 Sabin 2-like and 2 Sabin 3-like) strains were identified. The wild polioviruses were isolated at the beginning and the end of the dry season. Similar RFLP patterns were observed for the 3 wild type 1 polioviruses. Comparison of partial genomic sequences in the VP1/2 A region of 1 of the wild type 1 isolates with 2 wild type strains isolated in Antananarivo in 1992 and 1993 showed a divergence of at least 10% between the strains, suggesting at least two different pathways of transmission during this period. Our findings demonstrate that immunization with 3 doses of OPV did not prevent intestinal carriage of wild poliovirus strains, and that there is a risk of wild poliovirus transmission to susceptible children in the area. Multiple strategies are required to improve immunization coverage in Madagascar.  (+info)

Progress toward poliomyelitis eradication--South East Asia Region, 1997-1998. (12/1057)

In 1988, the World Health Assembly resolved to eradicate poliomyelitis by 2000. To achieve this goal, in 1994 World Health Organization (WHO) South East Asia Region (SEAR) member countries accelerated implementation of polio eradication strategies. In 1994, Thailand became the region's first country to initiate National Immunization Days (NIDs), followed by Bangladesh, Bhutan, India, Indonesia, and Sri Lanka (1995); Myanmar and Nepal (1996); and Democratic People's Republic (DPR) of Korea and Maldives (1997). This report summarizes the progress in achieving routine and supplemental vaccination coverage and surveillance for cases of acute flaccid paralysis (AFP) and the impact of these activities on polio eradication in the region.  (+info)

Progress toward poliomyelitis eradication--Nigeria, 1996-1998. (13/1057)

In 1988, the World Health Assembly resolved to eradicate poliomyelitis globally by 2000. In the African Region of the World Health Organization (WHO), eradication efforts were accelerated following supporting resolutions by WHO's Regional Committee for Africa in 1995 and the Organization of African Unity in 1996. Nigeria, the most populous country in Africa and part of a densely populated West African area extending from Nigeria to Cote D'Ivoire, is critically important to the global polio eradication initiative. This report summarizes 1) the success of National Immunization Days (NIDs); 2) the establishment of acute flaccid paralysis (AFP) surveillance; and 3) accelerated efforts to meet the 2000 target, including mopping-up planned for later in 1999.  (+info)

WHO responds to major polio outbreak in Angola.(14/1057)

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Molecular epidemiology of poliovirus infection in Tunisia. (15/1057)

This report is an overview of poliomyelitis surveillance in Tunisia from 1991 to 1996. In all, 2088 stool specimens, collected from 152 acute flaccid paralysis (AFP) cases and from 1747 of their healthy contacts were investigated. Virus isolation was done systematically in RD and HEp-2C cell lines and isolated viruses were typed by sero-neutralisation as polioviruses or non-polio enteroviruses. Poliovirus isolates were analysed systematically for their wild or vaccine-related origin by two methods--one based on antigenic differences and one on genetic differences between strains. All type 2 polioviruses were vaccine-related and most wild viruses belonged to polio serotype 3. Wild polio type 3 viruses were detected in 1991 and 1992 in six cases of paralytic polio. A silent circulation of wild polio 1 and wild polio 3 was detected in 1994. No wild virus was detected in Tunisia from 1995 onwards. Wild polioviruses were sequenced and compared with Tunisian wild strains isolated during the 1980s, as well as other genotypes from the international database. These investigations revealed a single Tunisian polio 3 genotype that has been circulating from 1985 to 1994 and two different polio 1 genotypes. These results reflect effective control strategies within the country and contribute to the improvement of the polio eradication programme effectiveness at national and global levels.  (+info)

The GDVII strain of Theiler's virus spreads via axonal transport. (16/1057)

Following intracerebral inoculation, the DA strain of Theiler's virus sequentially infects neurons in the gray matter and glial cells in the white matter of the spinal cord. It persists in the latter throughout the life of the animal. Several observations suggest that the virus spreads from the gray to the white matter by axonal transport. In contrast, the neurovirulent GDVII strain causes a fatal encephalitis with lytic infection of neurons. It does not infect the white matter of the spinal cord efficiently and does not persist in survivors. The inability of this virus to infect the white matter could be due to a defect in axonal transport. Using footpad inoculations, we showed that the GDVII strain is, in fact, transported in axons. Transport was prevented by sectioning the sciatic nerve. The kinetics of transport and experiments using colchicine suggested that the virus uses microtubule-associated fast axonal transport. Our results show that a cardiovirus can spread by fast axonal transport and suggest that the inability of the GDVII strain to infect the white matter is not due to a defect in axonal transport.  (+info)