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Adv Exp Med Biol. 2018;1045:209-226. doi: 10.1007/978-981-10-7230-7_10.

Chromosomal Integration by Human Herpesviruses 6A and 6B.

Author information

1
Division of Infectious and Immune Diseases, CHU de Québec Research Center, QC, Quebec, Canada. Louis.Flamand@crchul.ulaval.ca.
2
Department of Microbiology, Infectious Disease and Immunology, Faculty of Medicine, Université Laval, QC, Quebec, Canada. Louis.Flamand@crchul.ulaval.ca.

Abstract

Upon infection and depending on the infected cell type, human herpesvirus 6A (HHV-6A) and 6B (HHV-6B) can replicate or enter a state of latency. HHV-6A and HHV-6B can integrate their genomes into host chromosomes as one way to establish latency. Viral integration takes place near the subtelomeric/telomeric junction of chromosomes. When HHV-6 infection and integration occur in gametes, the virus can be genetically transmitted. Inherited chromosomally integrated HHV-6 (iciHHV-6)-positive individuals carry one integrated HHV-6 copy per somatic cell. The prevalence of iciHHV-6+ individuals varies between 0.6% and 2%, depending on the geographical region sampled. In this chapter, the mechanisms leading to viral integration and reactivation from latency, as well as some of the biological and medical consequences associated with iciHHV-6, were discussed.

KEYWORDS:

Chromosomal integration; Chromosomes; HHV-6; Telomeres; Telomeric motifs; iciHHV-6

PMID:
29896669
DOI:
10.1007/978-981-10-7230-7_10
[Indexed for MEDLINE]

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