Abstract
Background
Human endogenous retroviruses (HERVs) are genetic elements in the human genome, which
resulted from ancient retroviral germline infections. HERVs have strong transcriptional
promoters and enhancers that affect a cell's transcriptome. They also encode proteins
that can exert effects in human cells. This review examines how our increased understanding
of HERVs have led to their potential use as biomarkers and immunologic targets.
Material and methods
PubMed/Medline, Embase, Web of Science, and Cochrane databases were used in a systematic
search to identify all articles studying the potential impact of HERVs on surgical
diseases. The search included studies that involved clinical patient samples in diseases
including cancer, inflammatory conditions, and autoimmune disease. Articles focused
on conditions not routinely managed by surgeons were excluded.
Results
Eighty six articles met inclusion and quality criteria for this review and were included.
Breast cancer and melanoma have robust evidence regarding the use of HERVs as potential
tumor markers and immunologic targets. Reported evidence of the activity of HERVs
in colorectal cancer, pancreatic cancer, hepatocellular cancer, prostate and ovarian
cancer, germ cell tumors as well as idiopathic pulmonary hypertension, and the inflammatory
response in burns was also reviewed.
Conclusions
Increasingly convincing evidence indicates that HERVs may play a role in solid organ
malignancy and present important biomarkers or immunologic targets in multiple cancers.
Innovative investigation of HERVs is a valuable focus of translational research and
can deepen our understanding of cellular physiology and the effects of endogenous
retroviruses on human biology. As strategies for treatment continue to focus on genome-based
interventions, understanding the impact of endogenous retroviruses on human disease
will be critical.
Keywords
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Article info
Publication history
Published online: March 29, 2019
Accepted:
February 4,
2019
Received in revised form:
December 22,
2018
Received:
October 28,
2018
Identification
Copyright
© 2019 Elsevier Inc. All rights reserved.