Background

ALS, MS and other neurologic diseases may arise from pathogenic activation of endogenous retrovirus hERVK. These viruses were long assumed to be permanently inactive.

The ERVK class of endogenous retroviruses have become embedded in the human genome over millions of years. These were previously thought to be vestigial inactive DNA. However researchers at the University of Manitoba are pioneering research showing that they play a role in neurologic diseases.

Technology Overview

Researchers have discovered a novel neurotoxic protein which is derived from hERVK. The protein is expressed in certain neurologic diseases.

Invention: A novel mode of neuron toxicity.

• A peptide derived from an alternatively-expressed endogenous retrovirus-K (ERVK) envelope protein is analogous to the neurotoxic peptides called conotoxins (Pfam: PF08087, Toxin_18), which are known to inhibit voltage-gated calcium channels.
• Termed conotoxin-like protein (CTXLP), this viral toxin depletes select calcium channels and calcium channel-associated transcriptional regulators.
• Transcripts and protein for this virus-derived toxin is implicated with ALS, MS, schizophrenia, HIV infection, rheumatoid arthritis and cancers. Endogenous retrovirus-K (ERVK) is the most biologically active genome-fixed ERV in humans, with 91 full-length provirus loci

Benefits

Conotoxin-like protein (CTXLP) is uniquely similar to a neurotoxic cone snail venom protein. It is not well known within the human genome because retroviral genomic components are typically excluded from genomic sequence analysis.

Applications

Neurological disease diagnosis and therapy.

Opportunity

• Available for licensing
• Seeking development partner