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. 2000 Mar;38(3):945-52.
doi: 10.1128/JCM.38.3.945-952.2000.

Resolution of the pathways of poliovirus type 1 transmission during an outbreak

L M Shulman  1 , R Handsher, C F Yang, S J Yang, J Manor, A Vonsover, Z Grossman, M Pallansch, E Mendelson, O M Kew
Affiliations

Resolution of the pathways of poliovirus type 1 transmission during an outbreak

L M Shulman et al. J Clin Microbiol. 2000 Mar.

Abstract

An outbreak of poliomyelitis with 20 cases occurred in Israel, Gaza, and the West Bank from October 1987 to October 1988. The wild type 1 poliovirus associated with the outbreak was most closely related to viruses found in the Nile Delta. The epidemiologic links among patients involved in the outbreak and patients with community-acquired infections during the outbreak were inferred from the evolutionary relationships among isolates of the outbreak virus. Complete VP1 sequences (906 nucleotides) were determined for 12 clinical and 4 sewage isolates. A total of 58 nucleotide differences were found among the 16 isolates; 74% of all substitutions were synonymous third-position transitions. An evolutionary tree, representing both the pathways of VP1 sequence evolution and the inferred chains of virus transmission during the outbreak, was constructed under the assumption that each substitution had occurred only once. The combined epidemiologic and molecular data suggest that a single founder strain was introduced into Israel from the vicinity of Gaza in the fall of 1987. Poliovirus circulation was apparently localized to southern communities during the winter and spread north by the following summer into the Hadera subdistrict of Israel, where it radiated via multiple chains of transmission into other communities in northern Israel and the West Bank. The close sequence matches (>99%) between clinical and sewage isolates from the same communities confirm the utility of environmental sampling as a tool for monitoring wild poliovirus circulation.

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Figures

FIG. 1
FIG. 1
Geographic distribution of patients with clinical cases of polio and sewage samples associated with isolates of wild type 1 poliovirus (indicated by closed circles) from the 1987-1988 Israel outbreak. Gray arrows trace the main pathways of poliovirus transmission during the outbreak inferred from the epidemiologic record and the sequence relationships among poliovirus isolates. The dashed arrow indicates the proposed pathway of transmission from Egypt to Gaza and from Gaza to Rahat in the fall of 1987; the dashed line connecting Kfar Kasem and Rahat indicates linkage between the 1987 cases in these communities, but the direction of the pathway of transmission is uncertain. The dashed ellipse encloses communities in the Hadera subdistrict where the majority of polio cases occurred in 1988.
FIG. 2
FIG. 2
Tree summarizing sequence relatedness across the interval of nts 3296 to 3445 (VP1/2A region) among 9 clinical isolates from the 1987-1988 Israel outbreak, 43 wild type 1 poliovirus isolates from the Middle East and other regions of the world (usually from cases that had occurred within 5 years of the Israel outbreak), the Sabin 1 vaccine strain, and a representative Sabin 1 vaccine-derived clinical isolate (8219/USA88). Isolates are identified by laboratory number, three-letter country code, and year of isolation. Country abbreviations: AZB, Azerbaijan; BRA, Brazil; CHN, China; EGY, Egypt; ETH, Ethiopia; GEO, Georgia; GRE, Greece; GUT; Guatemala; IND, India; INO, Indonesia; ISR, Israel; JOR, Jordan; KUW, Kuwait; MMR, Myanmar; NIE, Nigeria; OMA, Oman; PAK, Pakistan; PER: Peru; PHL, Philippines; POR, Portugal; SAA, Saudi Arabia; SEN, Senegal; SOA, South Africa; TOG, Togo; TUN, Tunisia; TUR, Turkey; UAE, United Arab Emirates; USA, United States; VEN, Venezuela; VTN, Vietnam (31). Wild poliovirus genotypes within each serotype are identified by a four-letter code; the first two letters indicate eight compass points (NO, NE, EA, SE, SO, SW, WE, NW) or central (CE), and the last two letters indicate continents (AF [Africa], AS [Asia], EU [Europe], NA [North America], SA [South America]). When more than one type 1 genotype has been endemic to a region, the individual genotypes are distinguished by a letter suffix (e.g., SEAS-A). Sabin vaccine strain-related isolates are identified as Sab.
FIG. 3
FIG. 3
VP1 nucleotide (A) and amino acid (B) sequence alignment of the Sabin 1 reference strain and the 1987 isolate, Rahat-A. Sabin 1 strain nucleotide positions are numbered as described by Nomoto et al. (21); those of the Rahat-A isolate are numbered similarly for comparability. Capsid amino acid positions are indicated by a four-digit number: the first digit identifies the virion protein, and the next three digits specify residue position (e.g., 1001 indicates residue 1 of VP1). Boldface letters identify residues that encode or form NAg I (nts 2750 to 2785; amino acids 1091 to 1102), NAg II (nts 3140 to 3157; amino acids 1221 to 1226), and NAg III (nts 3338 to 3355; amino acids 1287 to 1292) (16).
FIG. 4
FIG. 4
Tree summarizing evolutionary relationships among outbreak isolates based upon differences in VP1 nucleotide sequences. The branch structure of the tree was constructed under the assumption that each substitution occurred only once, and the tree was rooted to three 1987 isolates, Rahat-A, Gaza-A, and Kfar Kasem-A. Vertical branches are scaled to the number of nucleotide differences between VP1 sequences. The VP1 nucleotide substitutions that encode amino acid changes (A2514G, N1012S; G2537A, A1020T; T2538C, M1020T; A2678G, I1067V; G2798A, V1107M; G2891A, V1138I; G2957A, V1160I; G3132A, R1218K; C3141T, S1221L; C3144T, A1222V; C3150T, S1224L) are underlined. Dates shown are the dates on which the samples were taken. The direction of the substitutions above the node between Rahat-A and Rahat-B, representing the sequence of the hypothetical founder virus, is unambiguous. The direction below the node considers three alternative lineages connecting each 1987 isolate to the hypothetical founder.
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References

    1. Afif H, Sutter R W, Fontaine R E, Kew O M, Pallansch M A, Goyal M K, Cochi S L. Outbreak of poliomyelitis in Gizan, Saudi Arabia: co-circulation of wild type 1 polioviruses from three separate origins. J Infect Dis. 1997;175(Suppl. 1):S71–S75. - PubMed
    1. Alexander J P, Jr, Alemu W, Kilpatrick D, Kebede S, Yang C-F, Beyene H, Kew O M. Poliomyelitis in Ethiopia: virologic links to poliomyelitis cases in the Indian subcontinent. Pediatr Infect Dis J. 1996;15:629–631. - PubMed
    1. Centers for Disease Control and Prevention. Virologic surveillance and progress toward poliomyelitis eradication—Eastern Mediterranean Region, 1995–September 1998. Morbid Mortal Weekly Rep. 1998;47:1001–1005. - PubMed
    1. Crainic R, Couillin P, Blondel B, Cabau N, Boue A, Horodniceanu F. Natural variation of poliovirus neutralization epitopes. Infect Immun. 1983;41:1217–1225. - PMC - PubMed
    1. Dahling D R, Berg G, Berman D. BGM, a continuous cell line more sensitive than primary rhesus and African green kidney cells for the recovery of viruses from water. Health Lab Sci. 1974;11:275–282. - PubMed

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