[Source: Journal of Virology, full page: (LINK). Abstract, edited.]
A cluster of paralytic poliomyelitis cases due to transmission of slightly diverged Sabin-2 vaccine virus
Ekaterina A. Korotkova a,b, Anatoly P. Gmyl b, Maria L. Yakovenko a,b, Olga E. Ivanova b, Tatyana P. Eremeeva b, Liubov I. Kozlovskaya b, Armen K. Shakaryan b, Galina Y. Lipskaya a, Irina L. Parshina c, Nataliya V. Loginovskikh d, Nadezhda S. Morozova e and Vadim I. Agol a,b#
Author Affiliations: aA. N. Belozersky Institute of Physical-Chemical Biology, M. V. Lomonosov Moscow State University, Moscow 119899, Russia; bM. P. Chumakov Institute of Poliomyelitis and Viral Encephalitides, Moscow 142782, Russia; cCenter for Hygiene and Epidemiology in the Altai Region, Barnaul 656049, Russia; dCenter for Hygiene and Epidemiology in the Omsk Region, Omsk 644116, Russia; eFederal Center of Hygiene and Epidemiology, Russian Federal Service for Surveillance on Consumer Rights Protection and Human Wellbeing, Moscow 117105, Russia
Four cases of acute flaccid paralysis caused by slightly evolved (Sabin-like) vaccine polioviruses of serotype 2 were registered in July-August, 2010 in an orphanage of Biysk (Altai Region, Russia). The Biysk cluster of vaccine-associated paralytic poliomyelitis (VAPP) had several uncommon, if not unique, features (1). Until this outbreak, Sabin-like viruses (in distinction with more markedly evolved vaccine-derived polioviruses, VDPV) were reported to cause only sporadic cases of VAPP. Consequently, VAPP were not considered to require outbreak-type responses. However, the Biysk outbreak completely blurred the borderline between Sabin-like viruses and VDPV in epidemiological terms (2). The outbreak demonstrated a very high disease/infection ratio, apparently exceeding even that reported for wild polioviruses. The viral genome structures did not provide any substantial hints as to the underlying reason(s) for such pathogenicity (3). The replacement of intestinal poliovirus lineages by other Sabin-like lineages during short intervals after the disease onsets was observed in two patients. Again, the sequences of the respective genomes provided no clues to explain these events (4). The polioviruses isolated from the patients and their contacts demonstrated a striking heterogeneity as well as rapid and uneven evolution of the whole genomes and their parts, apparently due to extensive interpersonal contacts in a relatively small closed community, multiple bottlenecking and recombination. Altogether, the results demonstrate several new aspects of pathogenicity, epidemiology, and evolution of vaccine-related polioviruses and underscore several serious gaps in understanding these problems.
The oral poliovirus vaccine largely contributed to the nearly complete disappearance of poliovirus-caused poliomyelitis. Being generally safe, it can, in some cases, result in a paralytic disease. Two types of such outcomes are distinguished: caused by slightly diverged (Sabin-like) viruses, on the one hand, and by significantly diverged VDPVs, on the other. This classification is based on the number of mutations in the viral genome region encoding a viral structural protein. Until now, only sporadic poliomyelitis cases due to Sabin-like polioviruses were described, and, in distinction with the VDPV-triggered outbreaks, they did not require broad-scale epidemiological responses. Here, an unusual outbreak of poliomyelitis caused by a Sabin-like virus is reported, which had an exceptionally high disease/infection ratio. This outbreak blurred the borderline between Sabin-like polioviruses and VDPV both in pathogenicity and kind of responses required as well as underscores important gaps in understanding pathogenicity, epidemiology, and evolution of vaccine-derived polioviruses.
#To whom inquiries regarding the paper should be addressed: M. P. Chumakov Institute of Poliomyelitis and Viral Encephalitides, Moscow 142782, Russia; email@example.com.
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Keywords: Research; Abstracts; Poliomyelitis; Vaccines.