Human Herpesviruses: Diversity and Disease

Dear Colleagues,

Human herpesviruses are ancient vertebrate pathogens, of which nine types infect humans. Some are associated with cancers (Epstein–Barr virus—EBV, Kaposi’s sarcoma herpesvirus), while others cause diseases typically thought of as childhood infections (varicella-zoster virus—VZV, human herpesvirus 7). They all share the lytic–latent life cycle that allows them to cause primary infection before becoming latent and go on to periodically reactivate throughout the human life course, with the potential to infect new hosts. Cytomegalovirus (CMV), herpes simplex virus-1 and EBV are particular problems for solid-organ transplant recipients, especially in the first 100 days, because of the profound immune suppression required to prevent organ rejection. Novel herpesvirus–disease associations, processes and mechanisms continue to show how much there still is to learn about herpesviruses and our health. For example, recent studies have suggested a link between Alzheimer’s disease and human herpesviruses 6A, 6B and 7 ¹.

Deep sequencing and population surveys of herpesvirus diversity have revealed the high degree of recombination that has shaped CMV genomes ^2,3, as well as the complexity of drug resistance within some transplant recipients who may be infected with two or more drug-resistant strains ⁴. Virus genomics has also revealed the unusual history of many human herpesviruses, from ancient host-switching events between hominin species ⁵ to the origins of some of Europe’s most common chromosomally integrated HHV6 lineages before the last Ice Age ⁶ and the surprisingly recent last common ancestor of currently circulating VZV lineages ⁷.

For this Special Issue of Pathogens, we invite you to submit either an original research article or a review on emerging aspects of human herpesvirus diversity and disease. These may include topics such as new genomic methods for sequencing human herpesviruses, the problem of anti-viral drug resistance, the contribution of viral diversity to virus or host phenotypes, or new insights into how human herpesviruses cause disease. We look forward to your contribution.

References

1. Readhead, B. et al. Multiscale Analysis of Independent Alzheimer’s Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus. Neuron 99, 64–82.e7 (2018).
2. Lassalle, F. et al. Islands of linkage in an ocean of pervasive recombination reveals two-speed evolution of human cytomegalovirus genomes. Virus Evol. 2, (2016).
3. Sijmons, S. et al. High-Throughput Analysis of Human Cytomegalovirus Genome Diversity Highlights the Widespread Occurrence of Gene-Disrupting Mutations and Pervasive Recombination. J. Virol. 89, 7673–7695 (2015).
4. Cudini, J. et al. Human cytomegalovirus haplotype reconstruction reveals high diversity due to superinfection and evidence of within-host recombination. Proc. Natl. Acad. Sci. 201818130 (2019). doi:10.1073/pnas.1818130116
5. Underdown, S. J., Kumar, K. & Houldcroft, C. Network analysis of the hominin origin of Herpes Simplex virus 2 from fossil data. Virus Evol. 3, (2017).
6. Zhang, E. et al. Inherited Chromosomally Integrated Human Herpesvirus 6 Genomes Are Ancient, Intact, and Potentially Able To Reactivate from Telomeres. J. Virol. 91, e01137-17 (2017).
7. Weinert, L. A. et al. Rates of vaccine evolution show strong effects of latency: implications for varicella zoster virus epidemiology. Mol. Biol. Evol. 32, 1020–8 (2015).

Dr. Charlotte Houldcroft
Guest Editor

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• Host–pathogen interactions
• Genomics
• Herpesviruses