HTLV1 VIS Detail Information

> This page shows VIS [6016919] detail information, including site information (chromosome, GRCh38 location, disease, sample, etc) and literature information.

Site Information

DVID	6016919
VISID	TVIS44007704
Chromosome	chr4
GRCh38 Location	123081713
Disease	Leukemia-Lymphoma, Adult T-Cell
Sample	Nontumor
Virus Reference Genome	Not given
Target Gene	AFG2A

Literature Information

PubMed PMID	24735963
Year	2014 Jun 19;123(25):3925-31
Journal	Blood
Title	The role of HTLV-1 clonality, proviral structure, and genomic integration site in adult T-cell leukemia/lymphoma.
Author	Cook LB,Melamed A,Niederer H,Valganon M,Laydon D,Foroni L,Taylor GP,Matsuoka M,Bangham CR
Evidence	Adult T-cell leukemia/lymphoma (ATL) occurs in approximately 5% of human T-lymphotropic virus type 1 (HTLV-1)-infected individuals and is conventionally thought to be a monoclonal disease in which a single HTLV-1(+) T-cell clone progressively outcompetes others and undergoes malignant transformation. Here, using a sensitive high-throughput method, we quantified clonality in 197 ATL cases, identified genomic characteristics of the proviral integration sites in malignant and nonmalignant clones, and investigated the proviral features (genomic structure and 5' long terminal repeat methylation) that determine its capacity to express the HTLV-1 oncoprotein Tax. Of the dominant, presumed malignant clones, 91% contained a single provirus. The genomic characteristics of the integration sites in the ATL clones resembled those of the frequent low-abundance clones (present in both ATL cases and carriers) and not those of the intermediate-abundance clones observed in 24% of ATL cases, suggesting that oligoclonal proliferation per se does not cause malignant transformation. Gene ontology analysis revealed an association in 6% of cases between ATL and integration near host genes in 3 functional categories, including genes previously implicated in hematologic malignancies. In all cases of HTLV-1 infection, regardless of ATL, there was evidence of preferential survival of the provirus in vivo in acrocentric chromosomes (13, 14, 15, 21, and 22).