Abstract
Herpes simplex virus type 1 (HSV-1) and varicella zoster virus (VZV) are closely related viruses causing lifelong infections. They are typically associated with mucocutaneous or skin lesions, but may also cause severe neurological or ophthalmic diseases, possibly due to viral- and/or host-genetic factors. Although these viruses are well characterized, genome-wide evolutionary studies have hitherto only been presented for VZV. Here, we present a genome-wide study on HSV-1. We also compared the evolutionary characteristics of HSV-1 with those for VZV. We demonstrate that, in contrast to VZV for which only a few ancient recombination events have been suggested, all HSV-1 genomes contain mosaic patterns of segments with different evolutionary origins. Thus, recombination seems to occur extremely frequent for HSV-1. We conclude by proposing a timescale for HSV-1 evolution, and by discussing putative underlying mechanisms for why these otherwise biologically similar viruses have such striking evolutionary differences.
Highlights
Human alpha-herpesviruses comprise three members, herpes simplex virus (HSV) 1 and 2 and varicella zoster virus (VZV)
The genetic distance between the most distantly related Herpes simplex virus type 1 (HSV-1) strains ranged from approximately 0.4% to 1.7%, and the most distantly related VZV strains ranged from approximately 0.1% to 0.5%
The second network (Fig. 1C) includes only strains which were sequenced in this study, and where no recombination crossovers were detected in the US7– US8 region
Summary
Human alpha-herpesviruses comprise three members, herpes simplex virus (HSV) 1 and 2 and varicella zoster virus (VZV) These viruses have a wide host cell range and an efficient and rapid reproductive cell cycle [1]. All three viruses have the capacity to establish life-long infections with latency/persistency in sensory neurons, and may induce vesicular lesions during reactivation; HSV-1 and HSV-2 in form of oral or genital ulcers while VZV cause herpes zoster. These viruses may cause severe complications from the visual and nervous systems. Genetic markers of virulence among circulating strains are largely unknown, but are suggested to be involved in the pathogenesis [3,4,5]
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