HIV-1 infection has been rare in Estonia. In 2000, an explosive epidemic among injecting drug users was detected in the Eastern border region, resulting in 3603 newly reported cases by the end of 2003. The molecular epidemiology of the outbreak was studied to establish whether the Estonian epidemic is linked to the epidemics in Eastern Europe. Over 200 newly infected individuals were prospectively sampled from June 2000 to March 2002 in a geographically representative way, with known dates of diagnosis and information of probable route of transmission. Viral regions coding for two viral gene regions were directly sequenced from plasma viral RNA and phylogenetically analyzed. In addition, a larger region coding for the entire env gene was sequenced from one sample and studied for indications of possible recombinant structure. The Estonian HIV outbreak was found to be caused by simultaneous introduction of two strains: a minor subtype A strain very similar to the Eastern European subtype A strain (approximately 8% of cases), and a second major strain (77%) found to be most closely related to the CRF06-cpx strain, previously described only from African countries. The variability in the two clusters was very low, suggesting point source introductions. Ten percent of cases seemed to be newly generated recombinants of the A and CRF06-cpx strains. Analysis of viral diversification over time revealed a rate of change within the V3 region of 0.83%/year for the CRF06-cpx strain, consistent with findings from other subtypes. Due to the relatively frequently found novel recombinant forms, the Estonian HIV-1 epidemic may allow studies of coinfection and intersubtype recombination in detail.

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 1084 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.

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The aim of this study was to report on the epidemiology of HIV infection in Estonia and to molecularly characterize Estonian HIV-1 variants. Epidemiological data were obtained from the Estonian National HIV/AIDS Database. In 1995-1996 blood samples were collected from 54 of the 65 HIV-infected individuals that had been diagnosed at that time. The V3 domain of the env gene was directly sequenced from peripheral blood mononuclear cells of 49 of these 54 individuals and the sequences used for phylogenetic analyses. At the end of 1999 Estonia reported 96 diagnosed HIV cases; 46 (48%) were homosexual or bisexual men and 31 (32%) were presumed to have been infected heterosexually. Importantly, only four individuals were likely to have become infected through intravenous drug use. Forty-three individuals (45%) were presumed to have been infected outside of Estonia, whereas 38 (40%) were likely to have become infected in Estonia. As expected, a majority of the investigated individuals (80%) were found to carry subtype B virus. Infections with subtypes A, C, D, G, and CRF02_AG were also documented. The dominance of subtype B was restricted to homosexual and bisexual men. Thus, subtype B infections were documented in 33 of 34 (97%) homosexual and bisexual men, but only 6 of 15 (40%) individuals with other probable routes of infection. Thirty of the 39 subtype B sequences were joined in a tight sequence cluster that also included sequences from neighboring Russia and Lithuania. This pattern suggests a local spread of HIV-1 among homosexual and bisexual men within the region. The results from the phylogenetic analyses agreed well with other epidemiological information. In conclusion, Estonia remains a country with a low prevalence of HIV infection. A majority of the identified cases are homosexual or bisexual men, whereas HIV infection among intravenous drug users is rare. A large proportion of the homosexual and bisexual men carried closely related subtype B variants. The sequences have been deposited in GenBank under accession numbers AF286538-AF286586.

Human immunodeficiency virus (HIV)-1 transmitted drug resistance in the drug-naïve population is of growing relevance in Estonia, where the number of antiretroviral (ARV) treatment-experienced subjects has been exponentially increasing during the last 10 y. The aim of this study was to estimate the rate of transmitted drug resistance among newly diagnosed subjects in Estonia in 2008. Genotypic resistance testing for viral genomic RNA was conducted for 201 subjects tested HIV-positive between 1 April and 30 November 2008. Of 145 genotyped viral strains in newly diagnosed patients, 123 were CRF06_cpx, 2 were subtype A1 and 3 were subtype B; in 17 cases viral sequences revealed recombinant structures similar to CRF06_cpx, subtype A1 and CRF02_AG. Resistance mutations were found in 8 (5.5%) virus strains, and 3 strains were resistant to at least 2 ARV classes. A total of 2.8% of sequences harboured mutations indicating nucleoside/nucleotide reverse transcriptase inhibitor resistance (M41L, M184V, M184I, T215C and T215D), 2.1% non-nucleoside reverse transcriptase inhibitor resistance (K103N, P225H) and 2.8% protease inhibitor resistance (M46I, L90M). These data suggest the need to extend genotypic HIV-1 drug resistance testing to newly diagnosed HIV-positive subjects to prevent potential ARV treatment failure.