ERVS

Endogenous retroviruses (ERVs) are remnants of ancient retroviral infections that became part of the host genome and are inherited through generations. They originate when retroviruses integrate their DNA into germ cells, allowing the inserted sequences to be transmitted to offspring. Over evolutionary time, many ERVs accumulate mutations that render them replication-incompetent, but some can still influence host biology through regulatory or coding elements.

In vertebrates, ERVs can constitute a substantial portion of the genome. In humans, roughly 8 to 10 percent of the genome is derived from retroviral sequences, including long terminal repeats (LTRs) that can act as promoters or enhancers, and various internal genes such as gag, pol, and env that are typically inactivated by mutations. The distribution of ERVs varies among species, reflecting different infection histories and genomic repair processes. Some ERVs exist as solo LTRs following recombination events that delete internal regions.

ERVs have played both detrimental and beneficial roles in host evolution. Beneficially, several ERV-derived genes have been co-opted for normal biology, most notably certain envelope proteins that are essential for placental development in mammals. LTRs and other ERV motifs can regulate nearby gene expression, contributing to developmental programs and immune responses. Conversely, ERVs can contribute to disease through insertional mutagenesis, abnormal expression, or immune dysregulation, with associations reported in certain cancers and autoimmune or neurological disorders, though causal links are under investigation.

Research on ERVs informs understanding of genome evolution, host–virus interactions, and gene regulation, and holds potential for therapeutic applications targeting ERV activity or exploiting ERV-derived proteins.