Sequential changes in hepatitis A virus genotype distribution in Estonia during 1994 to 2001
Hepatitis A virus (HAV) isolates from a large outbreak and from non‐outbreak cases in Estonia were characterized by sequencing the aminoterminal VP1 region. From January 1998 to December 1999, a total of 1,084 cases of hepatitis A were reported to the Harjumaa‐Tallinn and Ida‐Virumaa Health Protecti...
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Veröffentlicht in: | Journal of medical virology 2003-06, Vol.70 (2), p.187-193 |
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Sprache: | eng |
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Zusammenfassung: | Hepatitis A virus (HAV) isolates from a large outbreak and from non‐outbreak cases in Estonia were characterized by sequencing the aminoterminal VP1 region. From January 1998 to December 1999, a total of 1,084 cases of hepatitis A were reported to the Harjumaa‐Tallinn and Ida‐Virumaa Health Protection Services in Estonia. The attack rate was highest among males aged 15–29. Initial cases were noted to be associated with injecting drug use. IgM anti‐HAV positive sera were available from 107 hospitalized outbreak cases and from 68 patients sampled during 1994 to 2001. HAV RNA was detected in 42% of sera from 1994–1996 and in 88% of sera from 1998–2001. It was possible to obtain HAV sequences from 83 outbreak and 29 background cases. The outbreak strain was represented by five different sequences, all belonging to subtype IIIA. During the outbreak, this IIIA strain also spread into the general population. All available non‐outbreak isolates from 1994 to 2001 but one belonged to genotype IA and formed distinct clusters as compared to isolates from other parts of the world. One subtype IIIA isolate from 1995 was unrelated to the outbreak strain. Subtype IA had been dominating in Estonia during 1994–2001, but the outbreak strain from 1998 to 1999 was IIIA. This subtype was encountered previously in addicts in Sweden during the 1980s and in Norway at the end of the 1990s. This study supports the use of limited sequencing within the aminoterminal VP1 region for studying the molecular epidemiology of hepatitis A. J. Med. Virol. 70: 187–193, 2003. © 2003 Wiley‐Liss, Inc. |
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ISSN: | 0146-6615 1096-9071 |
DOI: | 10.1002/jmv.10377 |