Genome sequence of a pathogenic isolate of monkey B virus (species Macacine herpesvirus 1)

Abstract

The only genome sequence for monkey B virus (BV; species Macacine herpesvirus 1) is that of an attenuated vaccine strain originally isolated from a rhesus monkey (BVrh). Here we report the genome sequence of a virulent BV strain isolated from a cynomolgus macaque (BVcy). The overall genome organization is the same, although sequence differences exist. The greatest sequence divergence is located in non-coding areas of the long and short repeat regions. Like BVrh, BVcy has duplicated Ori elements and lacks an ORF corresponding to the μ34.5 gene of herpes simplex virus. Nine of ten miRNAs and the majority of ORFs are conserved between BVrh and BVcy. The most divergent genes are several membrane-associated proteins and those encoding immediate early proteins.

Genome sequence variation among isolates of monkey B virus ( Macacine alphaherpesvirus 1) from captive macaques

“…Since repeats were found in all these BV genomes but some were not identified in the BVcy E90-136 genome. (Ohsawa et al, 2014). We therefore re-examined these areas of the E90-136 genome by PCR using Deep Vent pol/betaine and high T m primers.…”

“…(Ohsawa et al, 2014; Simon et al, 1993) Since E2490 and the cynomolgus BV isolate viruses are different BV genotypes (BVrh & BVcy, resp. ), comparison of these genome sequences provides little insight regarding the degree of sequence variation within or between BV genotypes.…”

Sequence of the ateline alphaherpesvirus 1 (HVA1) genome

“…Phylogenetic analyses separate these viruses into three distinct clades (human/ape, Old World monkey and New World monkey viruses), suggesting that these viruses have co-evolved with their hosts [2, 3]. Complete genome sequences have been determined for all of the primate alphaherpesviruses except HVA1 [9–14]. With the exception of HVS1, the primate alphaherpesviruses all have type E genomes and have the same overall genetic arrangement: unique long (U L ) and unique short (U S ) regions flanked by inverted repeat regions (R L and R S , respectively).…”

B Virus (Macacine Herpesvirus 1) Divergence: Variations in Glycoprotein D from Clinical and Laboratory Isolates Diversify Virus Entry Strategies

“…Postmortem examinations reveal focal neuronal lesions occasionally seen in parietal neurons, but far more often in the brainstem and cervical spinal cord, which are primary sites of virus recovery (5-11). The molecular basis for the differences in neurovirulence between HSV and B virus in humans remains a mystery despite the fact that specific molecular differences between these two viruses have been identified (12)(13)(14)(15)(16)(17)(18)(19).B virus is genetically and immunologically closely related to HSV, and some aspects of cell entry and cell-to-cell transmission of B virus and HSV are conserved (14,(20)(21)(22)(23). The specific interactions of glycoprotein D (gD) with cognate cellular receptors, viz., herpesvirus entry mediator (HVEM), nectin-1, and nectin-2, as well as one of the several isoforms of 3-O-sulfated heparan …”

“…Postmortem examinations reveal focal neuronal lesions occasionally seen in parietal neurons, but far more often in the brainstem and cervical spinal cord, which are primary sites of virus recovery (5-11). The molecular basis for the differences in neurovirulence between HSV and B virus in humans remains a mystery despite the fact that specific molecular differences between these two viruses have been identified (12)(13)(14)(15)(16)(17)(18)(19).…”