In exogenous retroviruses, LTRs act as promoters. Genome has all
the genes (gag, pol, env), LTRs make sure they, and genomic RNA,
is made. But just as a side-effect of the reverse transcription
process, every integrated retrovirus (provirus) has two
identical LTRs, U3-R-U5. A viral genome just has an R-U5 on the
5′ end, and a U3-R on the 3′ end. This is one of the ways that
retroviruses can cause cancer. Just due to chance, the
retrovirus inserts just upstream of an oncogene. Throw an active
promoter upstream, you get cancer. Ek. Well, when dealing with
ERVs, obviously ERV LTRs 5′ of an oncogene would be detrimental,
thus not passed on. But that doesnt mean that ERV LTRs arent
contributing at all to gene expression. Assuming an ERV plops
down upstream of a random gene, the LTR could: - Be silenced
epigenetically, or through mutations– nothing happens - Provide
an alternative promoter for, up/down regulating gene expression,
tissue specificity - Provide an alternative start site, creating
an isoform of coded p