Molecular epidemiology and genetic diversity of echovirus type 30 (E30): genotypes correlate with temporal dynamics of E30 isolation

Abstract

Echovirus type 30 (E30) (genus, Enterovirus; family, Picornaviridae) has caused large outbreaks of aseptic meningitis in many regions of the world in the last 40 years. U.S. enterovirus surveillance data for the period 1961 to 1998 indicated that the annual proportion of E30 isolations relative to total enterovirus isolations has fluctuated widely, from a low of 0% in 1966 to a high of 42% in 1998. Peaks of E30 isolations occurred in the years 1968 to 1969, 1981 to 1984, 1990 to 1993, and 1997 to 1998, coincident with large nationwide outbreaks of E30-associated aseptic meningitis. Analysis of the complete VP1 sequence (876 nucleotides) of 136 E30 strains isolated in geographically dispersed regions of the United States and nine other countries between 1956 and 1998 indicated that the currently circulating E30 strains are genetically distinct from those isolated 30 to 40 years ago. Phylogenetic reconstruction demonstrated the existence of at least four distinct genetic groups, three of which have not been isolated in North America since 1981. Two of the three groups disappeared during periods when E30 was isolated infrequently. All North American E30 strains isolated after 1988 were closely related to one another, and all post-1993 isolates were of the same lineage within this group. Surveillance data indicate that E30 causes large national outbreaks of 2- to 4-year durations, separated by periods of relative quiescence. Our results show that shifts in the overall genetic diversity of E30 and the predominant genetic type correlate temporally with the dynamics of E30 isolation. The sequence data also provide a basis for the application of molecular techniques for future epidemiologic investigations of E30 disease.

FIG. 1

Frequency of E30 isolation in the United States between 1961 and 1998. E30 isolations are expressed as a proportion of total EV isolations for a given year, as reported to the CDC by state and territorial public health laboratories through the U.S. EV surveillance program.

FIG. 2

Phylogram depicting the phylogenetic relationships among 136 E30 strains isolated between 1956 and 1998. U.S. and Canadian isolates are listed by state or province (by their postal abbreviations), year of isolation (last two numbers of year), and laboratory identifier; all others are listed by country, year (last two numbers of year), and laboratory identifier, using World Health Organization-standard three-letter country codes: AUS, Australia; COL, Colombia; DEU, Germany; MEX, Mexico; PHL, Philippines; TRT, Trinidad and Tobago; and UNK, United Kingdom. All Australian isolates were from Victoria. Phylogenetic reconstruction was performed by using the neighbor-joining method with a maximum likelihood distance matrix (8). Branch lengths were calculated by the maximum likelihood method by using the Puzzle program (28). E21 was included as the outgroup, but the tree is unrooted. Numbers adjacent to nodes represent percent bootstrap support for the clusters to the right of the node for major genetic groups and for clusters of at least five members with greater than 80% bootstrap support. Major genetic groups and the years in which they have been observed are shown.