Journal of Clinical Epigenetics Open Access

  • ISSN: 2472-1158
  • Journal h-index: 10
  • Average acceptance to publication time (5-7 days)
  • Average article processing time (30-45 days) Less than 5 volumes 30 days
    8 - 9 volumes 40 days
    10 and more volumes 45 days

Abstract

Identification of distribution of human endogenous retroviruses K (HML-2) by PCR-based target enrichment sequencing

Bei Xue

Human endogenous retroviruses (HERVs), suspected to be transposition-defective, are more likely to reshape the transcriptional network of the human genome by regulatory elements distributed in their long terminal repeats (LTRs). HERV-K (HML-2), the most preserved group with the least accumulation of mutations, has been documented to be involved in tumorigenesis and autoimmune diseases. Because of the high sequence similarity between different HERV-Ks, current methods have limitations in providing genome-wide mapping specific for HERV-K (HML-2), a major barrier in delineating HERV-K (HML-2) function. While trying to acquire itemized appropriation data of HERV-K (HML-2), we used a PCR-based objective advancement sequencing convention for HERV-K (HML-2) (PTESHK) loci, which maps the nearness of reference loci, yet additionally distinguishes non-reference loci, empowering assurance of the genome-wide dissemination of HERV-K (HML-2) loci. Here we report on the genomic information got from three people (3 imitates each). We distinguished an aggregate of 978 loci utilizing this technique, including 30 new reference loci and 5 non-reference loci. Among the 3 people in our examination, 14 polymorphic HERV-K (HML-2) loci were recognized, and solo-LTR330 and N6p21.32 were distinguished as polymorphic just because. Strikingly, PTESHK gives a way to deal with the ID of the genome-wide dispersion of HERV-K (HML-2) and can be utilized for the distinguishing proof of polymorphic loci. Since the reconciliation polymorphism of HERV-K (HML-2) is associated to be unified with the purposes behind their pathogenicity, PTESHK can enhance other developing methods in getting to polymorphic HERV-K (HML-2) components in malignancy and immune system illnesses.