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Recombination in human herpesvirus-8 strains from Uganda and evolution of the K15 gene

MRC Virology Unit, Church Street, Glasgow G11 5JR, UK¹
Molecular Virology Group, Department of Medical Microbiology and Genitourinary Medicine, The University of Liverpool, Liverpool L69 3GA, UK²
Uganda Cancer Institute, Old Mulago Hospital, PO Box 3935, Kampala, Uganda³
Department of Statistics, University of Oxford, 1 South Parks Road, Oxford OX1 3TG, UK⁴

Author for correspondence: Andrew Davison. Fax +44 141 337 2236. e-mail a.davison{at}vir.gla.ac.uk

Human herpesvirus-8 (HHV-8) is believed to be the aetiological agent of Kaposi’s sarcoma (KS). KS accounts for half the reported cancer cases in Uganda, and occurs in endemic and epidemic [human immunodeficiency virus (HIV)-associated] forms. We confirmed a high prevalence (74%) of HHV-8 antibodies in 114 HIV-negative Ugandan blood donors, and characterized the genomes of HHV-8 strains present in 30 adult Ugandan KS patients. Phylogenetic analysis of the uniquely variable K1 gene indicated that the majority of KS patients were infected by the B subtype of HHV-8, several by the A5 subtype, and one by a variant of the C subtype. Sequence analysis of nine strains at several other genome loci spaced out across the genome indicated that five are recombinants between subtypes when considered independently of previously published definitions of parental (unrecombined) genotypes. When previously published parental genotypes were taken into account, seven of the nine strains appeared to be recombinants. Analysis of the K15 gene, which exists in HHV-8 in two highly diverged alleles, indicated that the P allele predominates, with only a single strain bearing the M allele. Divergence between the M allele in the latter strain and that in the previously sequenced BC1 strain is at least as great as that between representatives of the P allele. This indicates that introduction of the M allele into extant HHV-8 subtypes did not occur by a single, relatively recent recombination event as was concluded from a previous study in which very limited variation in the M allele was reported.

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