Antivirals versus the common cold
– caution prescribed?
Curing the common cold has been regarded as almost the holy grail of healthcare. It is also considered to be extremely difficult; with ineffective treatments against human rhinoviruses (HRV) (the most common cause of viral respiratory tract infections) available and the development of a vaccine thus far has shown to be almost impossible.
At any one time, we have trillions of viral cells on our bodies (even when healthy) and we are only just beginning to explore and understand this potentially commensal relationship. Indeed, there is speculation amongst scientists that we actually rely on some viruses for our health. If we look at our commensal relationship with gut bacteria: occasionally we may need to take antibiotics to fight an invasive and harmful pathogen, which would otherwise cause us damage. The antibiotic does its job, but many do not differentiate friend from foe, which can lead to the wiping out of our commensal (friendly) gut bacteria. It can take weeks, months or even years for this microbial ecosystem to return to something like its former state – in the meantime, this allows for other (not so friendly) pathogens to sneak in and establish themselves. We also rely on commensal bacteria to help our immune system and many studies now indicate that children who take regular antibiotics are at greater risk of developing immune disorders like asthma and allergies.
How can we be certain that by targeting HRV with a broad antiviral treatment, as has been researched in recent years, we won’t inadvertently disrupt other – potentially beneficial – viruses we play host to?
However, current research published in Peptides (July 2017) highlights cathelicidins as a potential novel therapeutic strategy for the management of HRV infections. Cathelicidins (antimicrobial peptides) possess broad-spectrum antimicrobial activity against many bacterial and viral pathogens. In vitro research identified that the human cathelicidin LL-37, the porcine cathelicidin Protegrin-1 and the ovine cathelicidin SMAP-29 show efficient and direct antiviral activity towards HRV both before and after cell infection. Instead of inducing host cell death, they work directly against the viron. Crucially, the antiviral activity of LL-37 is found to be sequence specific – only acting on the specific viral target it is designed for (HRV1B replication in airway epithelial cells).
This finding could be a revolutionary new way of managing these types of infections – reducing morbidity and mortality worldwide – particularly in those most at risk (e.g., patients with asthma, COPD, etc.).
This leads us to ponder, and leave you with this thought: if this treatment were to come to fruition, should there be limitations on its availability or perhaps further research into cathelicidins’ effects on other viral cells to ensure no inadvertent damage to our commensal viral ecosystem?