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Journal of Clinical Microbiology, December 1999, p. 3928-3933, Vol. 37, No. 12
0095-1137/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Molecular Epidemiology and Genetic Diversity of Echovirus Type 30 (E30): Genotypes Correlate with Temporal Dynamics of E30 Isolation

M. Steven Oberste,1,* Kaija Maher,1 Margery L. Kennett,2 Janice J. Campbell,3 Michael S. Carpenter,3 David Schnurr,4 and Mark A. Pallansch1

Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia1; Victorian Infectious Diseases Reference Laboratory, North Melbourne, Victoria, Australia2; National Centre for Enteroviruses, Halifax, Nova Scotia, Canada3 and Viral and Rickettsial Disease Laboratory, California Department of Health Services, Berkeley, California4

Received 25 May 1999/Returned for modification 22 July 1999/Accepted 16 September 1999

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.

* Corresponding author. Mailing address: Centers for Disease Control and Prevention, 1600 Clifton Rd. NE, Mailstop G-17, Atlanta, GA 30333. Phone: (404) 639-2751. Fax: (404) 639-4011. E-mail: mbo2{at}cdc.gov.

Journal of Clinical Microbiology, December 1999, p. 3928-3933, Vol. 37, No. 12
0095-1137/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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