|
by Sarah Wornow Edited by Alyscia Batista You probably don’t have to think back too far to remember the last time you caught a cold. With adults averaging around two to four colds per year, coming down with a cold seems inevitable. [1] But what if there was a vaccine that could prevent you from getting infected in the first place?  Available from: https://www.vejthani.com/2019/03/the-common-cold/ Current vaccines for most diseases are comprised of weak strains of a virus that are injected into the host’s body, allowing for the body to react and generate an immune response against that specific virus. Unfortunately, this straightforward method doesn’t work for a cold vaccine for two reasons. First, the viruses that cause the cold, enteroviruses and rhinoviruses, have the ability to rapidly mutate and gain drug resistance, making a single vaccine ineffective at adapting to the virus; second, there are over 160 different known strains of the virus that can cause the cold, making a general vaccine impossible due to the enormous range of viral diversity. [2]
Scientists are now turning to a new approach for creating a common cold vaccine. Using a method known as host-mediated therapy, researchers are looking to create a vaccine that would attack the physical connection made between the virus and the host’s cells. After a virus enters a host, it travels throughout the body until it attaches itself to a cell by linking to proteins found on the cell’s surface. Through this connection, the virus can then hijack the cell’s functions and rapidly replicate. By potentially blocking that connection, the virus wouldn’t be able to connect to the cell and there would be no pathogenesis, or spread of the disease. With this innovative way of thinking, a single vaccine can be created against a wide range of viral strains. There’s just one major problem that arises with this new approach. Scientists, up until now, had no knowledge of any protein that linked enteroviruses to a host’s cells. With findings published in late September, researchers at UCSF and the Stanford School of Medicine have discovered the protein responsible for linking an enterovirus with a host. The protein SETD3 has been found to physically attach to the invading virus, allowing for that virus to take over the functions of the host cell. As a result, more viruses are created and pathogenesis ensues. The discovery of SETD3’s role in pathogenesis came as a surprise to many scientists. SETD3 is a well-known protein that aids in muscle contractions, which largely has nothing to do with viruses. [3] How important, then, is SETD3 in aiding pathogenesis, if it also serves a major role in muscle contractions? To answer that question, the researchers used the gene editing tool CRISPR to genetically modify mice to lack the SETD3 gene. When these mice were infected by a variety of enteroviruses, they remained healthy and showed no symptoms of an infection. Human lung cells also showed immunity to the virus after SETD3 was edited out of their genome. These findings show SETD3 plays a critical role in viral pathogenesis. [4] Without any protein to link the virus to the cell, the virus couldn’t replicate. Even though these findings appear to push forward the creation of a cold vaccine, there are a few limitations to the application of this discovery. For one, completely editing out the SETD3 gene in mice had unintended consequences. While they developed normally and were immune to the common cold, due to SETD3’s role in muscle contractions, female mice were unable to reproduce because they couldn’t contract the muscles in their wombs. Additionally, the implications of silencing SETD3 haven’t been studied before in humans. Studying human lung cells in culture is vastly different from studying human cells in the body, so even though lung cells in culture showed no signs of infection, the results could be different if tested clinically. Despite these setbacks, the potential for a common cold vaccine has moved closer to becoming a reality thanks to this finding. SETD3 could be a common feature found to link most, if not all, enteroviruses to a host cell. Considering the possible limitations of this research, a cold vaccine may not appear in the near future, but certainly there will be a greater understanding of host-mediated therapy and the impacts this type of treatment could have on a vast array of diseases. Citations [1] DerSarkissian, Carol. Common Cold. [Internet] [Cited 2019 Nov 8] Available from: https://www.webmd.com/cold-and-flu/common_cold_overview [2] Chen, Angus. Why Haven't We Cured the Common Cold Yet? [Internet] [Cited 2019 Nov 2] Available from: https://www.scientificamerican.com/article/why-havent-we-cured-the-common-cold-yet/ [3] Bates, Sofie. Disabling one protein might one day lead to a cure for the common cold. [Internet] [Cited 2019 Nov 3] Available from: https://www.sciencenews.org/article/common-cold-virus-disable-protein [4] Diep J, Ooi Y, Wilkinson A, Peters C, Foy E, Johnson J, et. al. Enterovirus pathogenesis requires the host methyltransferase SETD3. Nature Microbiology [Internet] [Cited 2019 Nov 2] Available from: https://www.nature.com/articles/s41564-019-0551-1#Sec2
0 Comments
Leave a Reply. |
