Cover image for Vol. 37 Issue 6

Edited By: Andrew Moore

Online ISSN: 1521-1878

Google Hangout Summary

On September 19th BioEssays hosted its first live Google Hangout event. This Hangout discussed the role of endogenous retroviruses in placental evolution and potential pathogenicity to their hosts, and was chaired by David Haig (Harvard University, USA) and Andrew Moore (BioEssays), with Edward Chuong (University of Utah, USA) and George Kassiotis (MRC, Mill Hill, UK) as presenters. Read more ...

To watch a recording of this one hour event, please go to our You Tube channel.

The hangout notes/slides from the presenters can be accessed here: Edward Chuong's notes and George Kassiotis' slides.

The event was initiated following the publication of these articles in BioEssays:

Genomic vagabonds: Endogenous retroviruses and placental evolution (comment on DOI 10.1002/bies.201300059)
David Haig, BioEssays Volume 35, Issue 10, pages 845-846.

Retroviruses facilitate the rapid evolution of the mammalian placenta
Edward Chuong, BioEssays Volume 35, Issue 10, pages 853-861.

conflict, co-option, endogenous retroviruses, evolution, evolvability, placenta, regulatory evolution

Endogenous retroviruses (ERVs) are methylated in somatic tissues, but are transcriptionally active in the hypomethylated placenta. Therefore, placental cells are exposed to an abundance of rapidly evolving mutations. Recurrent ERV co-option may be driven by parent-offspring conflict, and suggests a mechanism underlying the extensive evolutionary diversification of the eutherian placenta.

Are human endogenous retroviruses pathogenic? An Approach to testing the hypothesis
George R. Young, Jonathan P. Stoye and George Kassiotis, BioEssays Volume 35, Issue 9, pages 794-803.

autoimmunity, cancer, endogenous retrovirus, integrations, mutagenesis, pathogenesis

The human genome contains numerous and repetitive human endogenous retroviruses (HERVs), relics of ancestral infection. Their mere presence in the genome, as well as distinct nucleic acid intermediates of retroviral replication and proteins produced by intact open reading frames may cause or contribute to pathology through the mechanism depicted.