@article{mbs:/content/journal/jgv/10.1099/jgv.0.000502, author = "Wallaschek, Nina and Gravel, Annie and Flamand, Louis and Kaufer, Benedikt B.", title = "The putative U94 integrase is dispensable for human herpesvirus 6 (HHV-6) chromosomal integration", journal= "Journal of General Virology", year = "2016", volume = "97", number = "8", pages = "1899-1903", doi = "https://doi.org/10.1099/jgv.0.000502", url = "https://www.microbiologyresearch.org/content/journal/jgv/10.1099/jgv.0.000502", publisher = "Microbiology Society", issn = "1465-2099", type = "Journal Article", keywords = "integration", keywords = "telomeres", keywords = "U94", keywords = "integrase", keywords = "latency", keywords = "Human herpesvirus 6", abstract = "Human herpesvirus 6 (HHV-6) can integrate its genome into the telomeres of host chromosomes and is present in the germline of about 1 % of the human population. HHV-6 encodes a putative integrase U94 that possesses all molecular functions required for recombination including DNA-binding, ATPase, helicase and nuclease activity, and was hypothesized by many researchers to facilitate integration ever since the discovery of HHV-6 integration. However, analysis of U94 in the virus context has been hampered by the lack of reverse-genetic systems and efficient integration assays. Here, we addressed the role of U94 and the cellular recombinase Rad51 in HHV-6 integration. Surprisingly, we could demonstrate that HHV-6 efficiently integrated in the absence of U94 using a new quantitative integration assay. Additional inhibition of the cellular recombinase Rad51 had only a minor impact on virus integration. Our results shed light on this complex integration mechanism that includes factors beyond U94 and Rad51.", }