Multiple effects govern endogenous retrovirus survival patterns in human gene introns

Louie N Van De Lagemaat,Dixie L Mager,Patrik Medstrand

doi:10.1186/gb-2006-7-9-r86

Louie N Van De Lagemaat, Dixie L Mager + Show 1 more

Open Access

https://doi.org/10.1186/gb-2006-7-9-r86

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Abstract

An analysis of human endogenous retrovirus families suggests suppression of splicing among young intronic retroviruses oriented antisense to gene transcription.

Highlights

Endogenous retroviruses (ERVs) and solitary long terminal repeats (LTRs) have a significant antisense bias when located in gene introns, suggesting strong negative selective pressure on such elements oriented in the same transcriptional direction as the enclosing gene
Mutagenic early transposon (ETn) ERVs are oppositely oriented to overall genomic ETns To begin our analysis of mechanisms contributing to ERV orientation bias, we reasoned that, if this bias is a consequence of detrimental impact by sense-oriented insertions, we would expect a predominant sense orientation among insertions with known detrimental effects
While no mutagenic or disease-causing ERV insertions are known in humans, significant numbers have been studied in the mouse and have been reviewed recently [5]

Summary

Introduction

Endogenous retroviruses (ERVs) and solitary long terminal repeats (LTRs) have a significant antisense bias when located in gene introns, suggesting strong negative selective pressure on such elements oriented in the same transcriptional direction as the enclosing gene. Any orientation biases observed for endogenous retroviral elements must reflect the forces of selection In support of this premise is a recent study by Bushman's group that was the first to directly compare genomic insertion patterns of exogenous avian leukosis virus after infection in vitro with patterns of fixed endogenous elements of the same family [17]. The antisense bias exhibited by fixed ERVs/LTRs in genes suggests that retroviral elements found in the same transcriptional orientation within a gene are much more likely to have a negative effect. The mechanisms underlying these detrimental effects have not been analyzed in depth

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