The Common Cold Could Prevent Influenza Infection: Study
Thu, April 22, 2021

The Common Cold Could Prevent Influenza Infection: Study


A new study links the common cold to influenza. Instead of helping the latter, the former helps prime the immune system, crippling the infectivity of the influenza virus.

The role of the common cold in preventing influenza was unveiled by researchers at Yale University, a US private research university. They found that contracting the common cold could prime the immune system. This would prevent influenza from infecting the airways. The effect was due to an activated chemical called interferon, which signal cells of viral infections. They published their findings in the journal The Lancet Microbe.

The Disease Burden of Influenza

Every year, influenza infects hundreds of thousands of people worldwide. While there is a vaccine developed annually, it cannot provide 100% protection against the seasonal flu. This is because influenza viruses mutate quickly and can only be predicted by scientists. It is also a reason why some influenza viruses successfully caused epidemics and pandemics. Still, doctors recommend people to get their flu shots, if possible, to get some protection. The vaccine can lower the severity of the disease, speed up the recovery from symptoms, and reduce the risk of health complications.

According to Statista, a German portal for statistics, from 2010 to 2019, the 2017 to 2018 seasonal flu had the highest incidence of influenza in the US. An estimated 45 million cases were reported in that season. It followed by 35,520,883 cases in the 2018 to 2019 season, 34 million cases in the 2012 to 2013 season, 30 million cases in both the 2013 to 2014 and 2014 to 2015 seasons, 29 million in the 2016 to 2017 season, 24 million in the 2015 to 2016 season, 21 million in the 2010 to 2011 season, and 9.3 million in the 2011 to 2012 season.

Within the same period, the 2018 to 2019 season had the highest deaths due to influenza in the US at 61,000. It was followed by the 2014 to 2015 season at 51,000, the 2012 to 2013 season at 43,000, both the 2013 to 2014 and 2016 to 2017 season at 38,000 each, the 2010 to 2011 season at 37,000, the 2018 to 2019 season at 34,157, the 2015 to 2016 season at 23,000, and the 2011 to 2012 season at 12,000. The figures in both the confirmed cases and deaths were preliminary for the 2017 to 2018 and 2018 to 2019 influenza seasons.

The differences in cases and deaths each year are affected by various factors. The most influential of these factors are the characteristics of circulating influenza viruses, the timing of the season, the effectiveness of the vaccine, and the number of vaccinated individuals. If the majority of the population are vaccinated with an effective vaccine, the fewer the cases and deaths are expected.



The Common Cold Can Be an Ally against Influenza

The common cold is a viral infection of the upper respiratory tract. It can be caused by various types of viruses. But the dominant causative agent is the rhinovirus that can multiply in between the temperatures of 33 and 35 degrees Celsius. While rhinoviruses rarely induce severe symptoms, it can be a bothersome due to sneezing, stuffed nose, and the general feeling of unwell or malaise. Yet in a recent study, researchers show that rhinoviruses can be an ally against influenza viruses.



At Yale, researchers investigated how rhinoviruses and influenza viruses interact with each other. The interaction might explain if the annual season of the common cold would increase or decrease the cases of COVID-19. However, their investigation led them to two things: the influenza infectivity and the mystery around the 2009 H1N1 swine flu pandemic.

During that pandemic, no one could exactly explain what happened in Europe during the fall season. Experts predicted that the season would surge the cases in the continent. Yet the predicted surge did not happen. One particular event was observed: lots of people contracted the common cold. This garnered attention in the scientific community. Since both were respiratory infection agents, people would have been susceptible to two viruses.

Researchers analyzed the clinical data from more than 13,000 patients with symptoms of respiratory infection seen at Yale New Haven Hospital. That data was collected for three years. Their analysis showed that whenever the rhinovirus was present, the influenza virus was absent. Even during months when both viruses were active, the presence of rhinovirus would remove the other virus from the picture.

"When we looked at the data, it became clear that very few people had both viruses at the same time," said Dr. Ellen Foxman, the senior author of the study and assistant professor of laboratory medicine and immunobiology at Yale.

Next, they prepared lab experiments to determine how the two viruses would interact. Researchers created human airway tissue using stem cells, which yielded epithelial cells – cells that line the lungs' airways. These cells are often preferred by various respiratory viruses. Results revealed that cells exposed to the rhinovirus were less prone to the influenza virus. The cells could no longer be infected by the latter.

The cells were observed equipped with antiviral defenses. The defenses were primed by the common cold virus, which triggered the production of interferon. Because interferon was at excellent levels, the influenza virus failed to infect cells due to the lasting antiviral defenses. Researchers determined that the antiviral defenses could last for five days at least. This finding could explain why the cases of swine flu did not surge in Europe since most people had been exposed to the common cold. The rhinovirus prepped their immune systems and triggered interferon release before the deadly influenza virus invaded the continent. It might be a rare event when a common cold virus helped prevented lots of deaths from that influenza strain.

With those findings, researchers are now studying if the same thing can happen in COVID-19. They plan to use similar cells and infect them with the rhinovirus, and then, expose the cells to SARS-CoV-2.