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Updated: Oct 23, 2025

Amplification, Next-generation Sequencing, and Genomic DNA Mapping of Retroviral Integration Sites
Published on: March 22, 2016
[Human herpesviruses HHV-6 and chromosomal integration: pathological and medical associated consequences]
Frédéric Trempe1, Guillaume Morissette1, Annie Gravel1
1Centre hospitalier universitaire de Québec, université Laval, faculté de médecine, centre de recherche en rhumatologie et immunologie, T1-49, 2705, boulevard Laurier, Québec, Canada.
Abstract:
Herpesviruses are extremely well adapted to their hosts and cause persistent infections that span over decades. Typically, these viruses establish latency by maintaining their viral genomes as extrachromosomal episomes and restricting their gene expression to a minimum. Human herpesvirus 6 (HHV-6) is perhaps one of the most well-adapted human herpesvirus with a prevalence approaching 100%. Unlike any other human herpesviruses, HHV-6 has developed the ability to integrate its genome into the host chromosomes by targeting the telomeric region. Whether integration represents a true mode of latency for this virus or whether is constitutes a viral dead-end remains uncertain. The present review aims to familiarize the readers with the concept of viral integration and delineates the various biological, pathological and medical consequences associated with HHV-6 chromosomal integration.
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