A cure for the common cold
Posted on 2020-01-23
Researchers have recently become one step closer to finding the cure for the common cold, an infectious disease familiar to us all. It has long been notoriously difficult to cure, costing the US economy roughly $40 billion a year. However, efforts to make human cells (the site of viral reproduction) an undesirable host, offers a new hope to render the cold virus ineffective.
Viruses temporarily infect other cells in order to reproduce and, upon rupturing their host cell, release huge quantities of new infectious viruses. Scientists have identified a key protein required by numerous viruses to multiply inside human cells. By disabling this protein, infections may not spread.
This has been recognised by Microbiologist Jan Carette at the Stanford University School of Medicine. He was able to demonstrate that in mice and human cells engineered to lack this protein, viruses were unable to reproduce.
Carette and his team used the gene-editing tool CRISPR to randomly disable a single gene in each of the cells. By infecting these altered cells with a virus known to cause the common cold, they hoped to locate which protein-encoding gene was necessary for the virus to thrive.
The team then used the different viral proteins like hooks, observing which proteins latched onto human cells. The viruses repeatedly fished out one protein in particular, SETD3. The importance of this protein was further investigated by injecting several types of enterovirus into mice that had been engineered to lack a functioning SETD3 gene – none of these mice got sick. Human lung cells lacking in the gene also remained healthy.
Notably, EV-C68, implicated in Acute Flaccid Myelitis (a much deadlier virus) was injected into human cells lacking SETD3 and could not replicate, suggesting this has the exciting potential to cure more than just the common cold.
However, disabling the gene could present new problems. Though the engineered mice appeared healthy and were fertile, they were unable to push their children out of the womb during birth. This could be due to the protein's presumed role in muscle contractions. Researchers, therefore, hypothesise that synthesising a drug that inhibits protein-viral interactions, without disturbing ‘normal’ SETD3 cellular function, may be a more viable solution.
Adults may catch on average two to three colds a year. There are a few hundred viruses that can be responsible for this, and these viruses rapidly mutate (undergoing spontaneous genetic changes), making it difficult to manufacture a cure. While it’s far from a catch-all cure, the study presents interesting new finds that could lead to new breakthroughs in the future.
abx031188 - SET Domain Containing 3 (SETD3) Antibody
abx335986 - SET Domain Containing 3 (SETD3) Antibody (FITC)
abx933053 - SETD3 siRNA
abx974275 - Mouse SETD3 shRNA Plasmid