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Open AccessArticle

Viral Proteins U41 and U70 of Human Herpesvirus 6A Are Dispensable for Telomere Integration

Institut für Virologie, Freie Universität Berlin, Robert von Ostertag-Straße 7-13, 14163 Berlin, Germany
Institute for Molecular Infection Biology, Julius-Maximilians-Universität Wϋrzburg, Josef-Schneider-Straße 2, 97080 Wϋrzburg, Germany
Molecular Biology and Biophysics, UConn Health, 263 Farmington Avenue, Farmington, CT 06030-3205, USA
Department of Microbiology and Immunology, CHU de Québec, Université Laval, Quebec, QC G1V 4G2, Canada
Authors to whom correspondence should be addressed.
Viruses 2018, 10(11), 656;
Received: 19 September 2018 / Revised: 16 November 2018 / Accepted: 17 November 2018 / Published: 21 November 2018
(This article belongs to the Section Animal Viruses)
PDF [1919 KB, uploaded 21 November 2018]


Human herpesvirus-6A and -6B (HHV-6A and -6B) are two closely related betaherpesviruses that infect humans. Upon primary infection they establish a life-long infection termed latency, where the virus genome is integrated into the telomeres of latently infected cells. Intriguingly, HHV-6A/B can integrate into germ cells, leading to individuals with inherited chromosomally-integrated HHV-6 (iciHHV-6), who have the HHV-6 genome in every cell. It is known that telomeric repeats flanking the virus genome are essential for integration; however, the protein factors mediating integration remain enigmatic. We have previously shown that the putative viral integrase U94 is not essential for telomere integration; thus, we set out to assess the contribution of potential viral recombination proteins U41 and U70 towards integration. We could show that U70 enhances dsDNA break repair via a homology-directed mechanism using a reporter cell line. We then engineered cells to produce shRNAs targeting both U41 and U70 to inhibit their expression during infection. Using these cells in our HHV-6A in vitro integration assay, we could show that U41/U70 were dispensable for telomere integration. Furthermore, additional inhibition of the cellular recombinase Rad51 suggested that it was also not essential, indicating that other cellular and/or viral factors must mediate telomere integration. View Full-Text
Keywords: human herpesvirus 6A; HHV-6A; telomere integration; latency; recombination human herpesvirus 6A; HHV-6A; telomere integration; latency; recombination

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Wight, D.J.; Wallaschek, N.; Sanyal, A.; Weller, S.K.; Flamand, L.; Kaufer, B.B. Viral Proteins U41 and U70 of Human Herpesvirus 6A Are Dispensable for Telomere Integration. Viruses 2018, 10, 656.

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