[1][2] Most HERVs in the genome today are not able to replicate, because of genetic changes such as frame shifts, premature stop codons, and recombination in their long terminal repeats (LTRs).

[4] A complete HERV includes specific genes – gag, pro, pol and env – flanked on either side by the long terminal repeats, which act like bookends.

[citation needed] Performing southern blots with primate blood samples, and gag, pol, and pro probes, suggested that HERV-W entered the genome of catarrhine monkeys over 23 million years ago.

This data implies that the HERV-W genome integrated into its host's germ-line around 63 million years ago, expanded in the era of Old and New World monkeys, and then evolved independently.

[citation needed] HERV-W is named for the fact that many in the group use a tryptophan tRNA at the primer binding site (PBS).

In macrophage cell cultures of patients with MS, several retroviral-like particles with reverse transcriptase (RT) activity were detected and given the name multiple sclerosis retroviruses (MSRVs).

[11] The primer binding site (PBS) of this HERV was discovered to be similar to avian retroviral PBSs, which use tRNATRP.

[10] Overlapping cDNAs spanned a 7.6 kb complete HERV with RU5- gag- pol- env- U3R sequences, a polypurine tract, and a primer binding site (PBS).

[10] Performing a BLASTn query search with the expressed sequence tags (ESTs) database for the cDNA clones derived from the probes, revealed that 53% of related transcripts were found in placental cells.

[15] One-to-two days after transfection, numerous multinucleated giant cells, or syncytia, had formed, indicating the HERV-W env gene can cause homotypic and heterotypic cell-cell fusion.

HERV-W's main gene expression is ERVWE-1 which is a highly fusogenic env glycoprotein, which is also called syncytin-1 because it induces the formation of syncytia (multinucleated cells).

[20] Using monoclonal, fluorescently-labeled antibodies, the Frendo Lab was able to visualize the Env-W expression at the apical membrane of the synctiotrophoblast in first-trimester placentas.

[23] Analyzing 40 full-term placental tissues with immunohistochemical staining and RT in-situ PCR shows strong expression of syncytin-1 in syncytiotrophoblasts compared to cytotrophoblasts.

In contrast to this data, placental micro-vesicles, which also have high expression of syncytin-1, have been shown through peripheral blood mononuclear cell assays to activate the immune system through the production of cytokines and chemokines.

The 780 bp LTR's that flank the env, pro, pol, and gag genes provide a range of regulatory sequences such as promoters, enhancers, and transcription-factor binding sites.

[citation needed] However, using a luciferase reporter gene assay, HERV-Ws that have incomplete LTR's were still found to have promoter activity.

[26] This experiment was performed with human astrocytic cells and showed that TNFa has the ability to activate the ERVWE-1 promoter through an NF-κB element.

Influenza produces glial cells missing 1 (GCM1) that can act as enhancers to reduce the repression of histone modification of HERV-Ws.

[32] Specifically, cytokine production is elevated in the MS PBMC cultures as compared to the healthy controls and as mediated by the surface unit of the MSRV-Env protein.

[33] Finally, it was discovered—through TLR-4 signaling assays, cytokine ELISAs, OPC cell cultures, and statistical analysis—that MSRV-Env is a highly potent TLR-4 activator.

[34] MSRV-Env in vitro and in vivo induces TLR4 dependent pro-inflammatory stimulus and weakens the precursor cells of oligodendrocytes, which produce myelin thorougout the central nervous system (CNS).

[37] To date, not much hard evidence has been found to support a strong correlation between HERV-W transcripts and schizophrenia (SZ).

[36] They found a weak correlation between HERV's –K, -E, -F; and that env-W expression was constant in patients with schizophrenia and bipolar disorder (BD) compared to controls.

[citation needed] As knowledge about the mechanism of production for HERV-W transcripts is growing, scientists are beginning to synthesize drugs that can interrupt the MSRV pathway.

A humanized monoclonal antibody called GNbAc1, of the IgG4 class, binds with high specificity and affinity to the extracellular domain of the MSRV-Env protein.

[citation needed] On Jan 2019, the drug GNbAC1 was granted the name Temelimab by the World Health Organization (WHO)[39] The Insanity Virus