Lineages of varicella-zoster virus

Relationships among varicella-zoster virus (VZV; Human herpesvirus 3) genome sequences were examined to evaluate descent of strains, structures of lineages and incidence of recombination events. Eighteen complete, published genome sequences were aligned and 494 single nucleotide polymorphisms (SNPs) extracted, each as two alleles. At 281 SNPs, a single sequence differed from all the others. Distributions of the remaining 213 SNPs indicated that the sequences fell into five groups, which coincided with previously recognized phylogenetic groupings, termed E1, E2, J, M1 and M2. The 213-SNP set was divisible into 104 SNPs that were specific to a single group, and 109 cross-group SNPs that defined relationships among groups. This last set was evaluated by criteria of continuities in relationships between groups and breaks in such patterns, to identify crossover points and ascribe them to lineages. For the 99 cross-group SNPs in the genome's long unique region, it was seen that the E2 and M2 groups were almost completely distinct in their SNP alleles, and the E1 group was derived from a recombinant of E2 and M2. A valid phylogenetic tree could thus be constructed for the four E2 and two M2 strains. There was no substantive evidence for recombination within the E2 group or the E1 group (ten strains). The J and M1 groups each contained only one strain, and both were interpreted as having substantial distinct histories plus possible recombinant elements from the E2 and M2 lineages. The view of VZV recombination and phylogeny reached represents a major clarification of deep relationships among VZV lineages

Chronic Viral Infection and Primary Central Nervous System Malignancy

Primary central nervous system (CNS) tumors cause significant morbidity and mortality in both adults and children. While some of the genetic and molecular mechanisms of neuro-oncogenesis are known, much less is known about possible epigenetic contributions to disease pathophysiology. Over the last several decades, chronic viral infections have been associated with a number of human malignancies. In primary CNS malignancies, two families of viruses, namely polyomavirus and herpesvirus, have been detected with varied frequencies in a number of pediatric and adult histological tumor subtypes. However, establishing a link between chronic viral infection and primary CNS malignancy has been an area of considerable controversy, due in part to variations in detection frequencies and methodologies used among researchers. Since a latent viral neurotropism can be seen with a variety of viruses and a widespread seropositivity exists among the population, it has been difficult to establish an association between viral infection and CNS malignancy based on epidemiology alone. While direct evidence of a role of viruses in neuro-oncogenesis in humans is lacking, a more plausible hypothesis of neuro-oncomodulation has been proposed. The overall goals of this review are to summarize the many human investigations that have studied viral infection in primary CNS tumors, discuss potential neuro-oncomodulatory mechanisms of viral-associated CNS disease and propose future research directions to establish a more firm association between chronic viral infections and primary CNS malignancies

Evolutionary relationships of virion glycoprotein genes in the S regions of alphaherpesvirus genomes

The short region in the genome of herpes simplex virus type 1 contains a contiguous array of five genes (US4, US5, US6, US7 and US8) which encode known or proposed virion-surface glycoprotein species. Counterparts for certain of these have been described in the genomes of other alphaherpesviruses, namely herpes simplex virus type 2, pseudorabies virus and varicellazoster virus. Within each of the US4-, US6- and US7related sets, the amino acid sequences are most conserved in a region containing several cysteine residues. Comparisons in this region among the three sets were carried out by first aligning three cysteine residues which were very similarly placed in each set, and a number of other similarities were then visible. It was concluded that the US4, US6 and US7 sets of genes are related, and thus have evolved by duplication and divergence. The US8-related sequences are distinct from the US4, US6 and US7 sequences, although possible signs of a distant relationship were detected. The US8 set contains two clusters ofcysteine residues, and the sequences around these show some similarity, which was interpreted as evidence for occurrence of an intramolecular duplication event

Lineage structures in the genome sequences of three Epstein-Barr virus strains

Whole genome sequences for three Epstein-Barr virus strains (B95-8, GD1 and AG876) were aligned and compared. In addition to known variable loci (including type-specific alleles for the EBNA2, EBNA3A, EBNA3B and EBNA3C genes, plus the EBNA1 and LMP1 genes), seven large-scale regions of lower-level diversity were identified with strains at each in two major groupings. All three possible patterns of strain associations were represented across the seven loci. Tree-building studies supported the existence of two distinct lineages in each case, and occurrence of recombination between lineages therefore has to be invoked to account for the observed genotypes of virus strains

Integrating Reptilian Herpesviruses into the Family Herpesviridae

The phylogeny of reptilian herpesviruses (HVs) relative to mammalian and avian HVs was investigated by using available gene sequences and by alignment of encoded amino acid sequences and derivation of trees by maximum-likelihood and Bayesian methods. Phylogenetic loci were obtained for green turtle HV (GTHV) primarily on the basis of DNA polymerase (POL) and DNA binding protein sequences, and for lung-eye-trachea disease-associated HV (LETV) primarily from its glycoprotein B sequence; both have nodes on the branch leading to recognized species in the Alphaherpesvirinae subfamily and should be regarded as new members of that subfamily. A similar but less well defined locus was obtained for an iguanid HV based on a partial POL sequence. On the basis of short POL sequences (around 60 amino acid residues), it appeared likely that GTHV and LETV belong to a private clade and that three HVs of gerrhosaurs (plated lizards) are associated with the iguanid HV. Based on phylogenetic branching patterns for mammalian HV lineages that mirror those of host lineages, we estimated a date for the HV tree's root of around 400 million years ago. Estimated dates for branching events in the development of reptilian, avian, and mammalian Alphaherpesvirinae lineages could plausibly be accounted for in part but not completely by ancient coevolution of these virus lines with reptilian lineages and with the development of birds and mammals from reptilian progenitors