Two Clusters of HIV-1 Infection, Rural Idaho, USA, 2008

of 54°C, and 45 amplifi cation cycles. PCR blanks containing all reagents except for DNA and extraction blanks were included in every PCR set. Results of the amplifi cation reactions are listed in the Table. All accompanied extraction and PCR controls remained free of amplifi cation products. All amplicons resulting from suicide PCRs were sequenced. Amplicons resulting from the use of primer pairs YP14F/YP13R and pst-F/pst-R matched the reference sequence to 100% (GenBank accession no. AL109969.1). Amplicons resulting from the use of primer pair PCP-F/PCP-R matched this reference sequence to only 97.78%. This deviation is because of a 2-bp insertion (2 Ts, positions 8531 and 8532, GenBank accession no. AL109969.1) at Y. pestis strain CO92 plasmid pPCP1. The sequences obtained from 3 persons’ remains showed in the pPCP1 sequence section between nucleotide positions 8528–8532 only 3 Ts instead of 5 Ts described for Y. pestis strain CO92 plasmid pPCP1 (GenBank accession no. AL109969.1). The sequences found in this study were deposited in GenBank under accession nos. HQ290521–HQ290523. To conclude, the successful recovery of several Y. pestis plasmid pPCP1 DNA sequences in skeletal fi nds from the mass burial site excavated in Manching-Pichl suggests that these persons died of plague. Moreover, our fi ndings constitute a molecularly supported confi rmation for the presence of Y. pestis, the etiologic agent of plague, in late medieval (1250–1500 CE) southern Germany. In future studies, we will attempt to recover chromosomal Y. pestis DNA from the mass grave skeletal remains to obtain clues as to the specifi c Y. pestis strain and the microbiology of past plague in Europe.