Abstract:
:The hepatitis B virus (HBV) is a major cause of hepatocellular carcinoma (HCC), partly driven by viral integration and specific oncogenic HBV variants. However, the biological significance of HBV genomes within lymphoid cells (i.e., peripheral blood mononuclear cells, PBMCs) is unclear. Here, we collected available plasma, PBMC, liver, and tumor from 52 chronic HBV (CHB) carriers: 32 with HCC, 19 without HCC, and one with dendritic cell sarcoma, DCS. Using highly sensitive sequencing techniques, next generation sequencing, and AluPCR, we demonstrate that viral genomes (i.e., HBV DNA, RNA, and cccDNA), oncogenic variants, and HBV-host integration are often found in all sample types collected from 52 patients (including lymphoid cells and a DCS tumor). Viral integration was recurrently identified (n = 90 such hits) in genes associated with oncogenic consequences in lymphoid and liver cells. Further, HBV genomes increased in PBMCs derived from 7 additional (treated or untreated) CHB carriers after extracellular mitogen stimulation. Our study shows novel HBV molecular data and replication not only liver, but also within 63.8% of lymphoid cells analysed (including a representative lymphoid cell malignancy), that was enhanced in ex vivo stimulated PBMC.
journal_name
Cancer Lettjournal_title
Cancer lettersauthors
Lau KC,Joshi SS,Gao S,Giles E,Swidinsky K,van Marle G,Bathe OF,Urbanski SJ,Terrault NA,Burak KW,Osiowy C,Coffin CSdoi
10.1016/j.canlet.2020.03.022subject
Has Abstractpub_date
2020-06-28 00:00:00pages
39-47eissn
0304-3835issn
1872-7980pii
S0304-3835(20)30155-5journal_volume
480pub_type
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