Yale study shows COVID-19 infection can be hampered by the common cold
A compelling new study has demonstrated how acute exposure to the common cold can slow the onset of a SARS-CoV-2 infection by stimulating the immune system to jump into action early. The research shows in impressive detail how the immune system can be primed for action by a rhinovirus infection allowing it to more effectively stifle the early replication of coronavirus.
SARS-CoV-2, the coronavirus that causes COVID-19, is known to enter the body through the nose or mouth and begin its first wave of replication in the upper respiratory tract. In these first first days of infection, before any symptoms of COVID-19 disease appear, the virus has demonstrated a clever ability to evade detection from the body’s primary defense mechanisms.
Antigens, T-cells, and other more comprehensive immune responses can take days to get going, so our bodies have a more immediate cellular mechanism to act as an alarm for viral infection. These frontline signaling proteins are called interferons.
When a cell is infected by a virus it produces interferons, which serve as a kind of emergency beacon letting nearby cells know a viral invader is close. Interferons play a number of roles, primarily helping orchestrate immune cell activities. However, some viruses have evolved clever strategies to avoid interferon signaling allowing several days of unimpeded replication before other immune defenses catch up.
This new study, led by a team of scientists from Yale University School of Medicine, first set out to better understand what happens in those first few days of SARS-COV-2 infection. To do this the researchers looked at patients undergoing routine pre-operative COVID-19 screening, allowing them to catch pre-symptomatic subjects at the very earliest stages of infection.
Ellen Foxman, senior author on the new study, says following these patients through the earliest stages of viral infection revealed SARS-CoV-2 can rapidly replicate in the first two to three days of infection before the immune system catches on. The data indicates the viral load can double every six hours over this period.
"There appears to be a viral sweet spot at the beginning of COVID-19, during which the virus replicates exponentially before it triggers a strong defense response," Foxman explains.
Prior research has shown the presence of the common cold in a community can disrupt the spread of influenza outbreaks. So Foxman and the team then moved into the lab and began experimenting with human airway tissue models to find out if, and how, a rhinovirus infection can hamper the replication of SARS-CoV-2 in these early pre-symptomatic stages.
And the team’s hypothesis proved correct. When airway cells were infected with rhinovirus prior to SARS-CoV-2 exposure, interferons were primed and quickly stifled the coronavirus’s ability to replicate.
“One virus blocks the replication of an unrelated virus,” Foxman recently said in an interview with Inverse. “At first glance, it’s counterintuitive. But if the timing is right and the [SARS-CoV-2] viral load is low enough, it can happen.”
Unfortunately this doesn’t immediately offer clues to new COVID-19 treatments. While there are trials currently investigating whether infusions of interferons can help SARS-CoV-2 infected patients the treatment could be dangerous if administered too late. One feature of severe COVID-19 leading to death is an overactive immune response.
Nevertheless, these results do shed light on previously unknown ways viruses interact and interfere with one another. And this new study helps us understand why some people may ultimately present with mild or asymptomatic COVID-19 infections while others display high viral loads and end up with severe disease.
"There are hidden interactions between viruses that we don't quite understand, and these findings are a piece of the puzzle we are just now looking at," adds Foxman.
The new study was published in the Journal of Experimental Medicine.
Source: Yale University