vital for the invasion, replication, escape, and spreading of its viral genome. These three genes are gag (encodes for structural proteins for the viral core), pol (encodes for reverse transcriptase, integrase, and protease), and env (encodes for coat proteins for the virus's exterior). These viral proteins are encoded as polyproteins. In order to carry out their life cycle, the retrovirus relies heavily on the host cell's machinery. Protease degrades peptide bonds of the viral polyproteins, making the separate proteins functional. Reverse transcriptase functions to synthesize viral DNA from the viral RNA in the host cell's cytoplasm before it enters the nucleus. Integrase guides the integration of viral DNA into the host genome. Over time, the genome of ERVs not only acquire point mutations, but also shuffle and recombine with other ERVs. ERVs with a decayed sequence for the env become more likely to propagate. Role in genomic evolution Endogenous retroviruses can play an active role in shaping genomes. Most studies in this area have focused on the genomes of humans and higher primates, but other vertebrates, such as mice and sheep, have also been studied in depth. The long terminal repeat (LTR) sequences that flank ERV genomes frequently act as alternate promoters and enhancers, often contributing to the transcriptome by producing tissue-specific variants. In addition, the retroviral proteins themselves have been co-opted to serve novel host functions, particularly in reproduction and development. Recombination between homologous retroviral sequences has also contributed to gene shuffling and the generation of genetic variation. Furthermore, in the instance of potentially antagonistic effects of retroviral sequences, repressor genes have co-evolved to combat them. About 90% of endogenous retroviruses are solo LTRs, lacking all open reading frames (ORFs). Solo LTRs and LTRs associated with complete retroviral sequences have been shown to act as transcriptional elements on host genes. Their range of action is mainly by insertion into the 5' UTRs of protein coding genes; however, they have been known to act upon genes up to 70–100 kb away. The majority of these elements are inserted in the sense direction to their corresponding genes, but there has been evidence of LTRs acting in the antisense direction and as a bidirectional promoter for neighboring genes. In a few cases, the LTR functions as the major promoter for the gene. For example, in humans AMY1C has a complete ERV sequence in its promoter region; the associated LTR confers salivary specific