Human endogenous retroviruses and tumors / 白血病·淋巴瘤

Viral etiology of tumor has been studied for a century.Seven human tumor viruses were identified over the past half century.The complexity and regularity of the pathogenic mechanisms of human tumor viruses have been elucidated preliminarily.Human genome sequencing indicated that 8 ％ of human genes were composed of human endogenous retroviruses (HERVs).Owing to the findings that adult T-cell leukemia virus (HTLV) can cause human adult T-cell leukemia and animal exogenous and HERVs can induce tumors and malignant diseases,the relationship between HERVs and human tumors has attracted much attention receutly.Here this article discusses the association of the expression of HERVs with leukemia and solid tumors progression,which may be an important aspect of tumor virology.

Transposable Elements: No More 'Junk DNA'

Since the advent of whole-genome sequencing, transposable elements (TEs), just thought to be 'junk' DNA, have been noticed because of their numerous copies in various eukaryotic genomes. Many studies about TEs have been conducted to discover their functions in their host genomes. Based on the results of those studies, it has been generally accepted that they have a function to cause genomic and genetic variations. However, their infinite functions are not fully elucidated. Through various mechanisms, including de novo TE insertions, TE insertion-mediated deletions, and recombination events, they manipulate their host genomes. In this review, we focus on Alu, L1, human endogenous retrovirus, and short interspersed element/variable number of tandem repeats/Alu (SVA) elements and discuss how they have affected primate genomes, especially the human and chimpanzee genomes, since their divergence.

Identification of a Novel Intronic Transcript Containing 11q13.5 HERV-W gag Sequence / 天津医药

Objective:To identify the novel intronic transcripts containing 11q13.5 HERV-W gag sequence, and explore the modulation of the transcripts on the alternative splicing of host gene PTD015. Methods:Half-nested PCR and touchdown PCR were used to amplify the target transcripts. The transcripts were cloned and sequenced. The plasmids inserted with the target transcripts were transfected into JEG3 cells and the alternative spliced mRNA levels of PTD015 were measured with real time PCR. Results:A 1 739 bp novel intronic transcript containing 755 bp 11q13.5 HERV-W gag sequence, 527 bp 5′ long terminal repeat and 457 bp sequence on the 5′-end of 11q13.5 HERV-W was identified. The intronic antisense transcripts significantly down-regulated the alternative spliced mRNA levels of PTD015. Conclusion:The intronic antisense transcripts originating from the second intron of gene PTD015 could modulate the alternative splicing of the host gene PTD015.