You could be protected from coronavirus by the common cold

We often assume that viral infections are caused by individual types of virus. In reality, however, we are exposed to many viruses every day, and co-infection – where someone is infected with two or more types of virus at the same time – is widespread.

The cells that line our throat and lower airways are exposed to the environment around us, making them a primary target for respiratory virus co-infection. These range from common colds, which cause rhinoviruses, to more severe influenza viruses, which are often the cause of global pandemics.

One of the most common results of co-infection is virus interference, a phenomenon in which a virus outperforms and suppresses virus replication the other coinfecting viruses. Interestingly, there is growing evidence to suggest that rhinoviruses can interfere with the replication of other respiratory viruses, which tend to be more serious. You can even offer the host temporary protection from them.

The good news is that this apparently includes SARS-CoV-2 – the virus responsible for COVID-19. in the a new studyRhinoviruses have been shown to suppress the replication of this virus.


Most of the respiratory viruses that infect humans are rhinoviruses (from the Greek “rhinoceros” for “the nose”). Rhinoviruses, first identified in 1953, are extremely small respiratory viruses found around the world. As far as we know, they can only infect humans.

Rhinovirus infections can be serious in some cases. However, they usually infect us to cause the common cold, a relatively mild disease. In response to such an infection, our immune system produces virus-killing molecules called interferons.

Interferons are produced in response to infections with all types of viruses, but they are produced a lot faster and in larger quantities in response to rhinovirus versus other respiratory viruses. Even so, rhinoviruses have developed complex mechanisms that enable them to evade interferons and replicate efficiently. It is generally accepted that the rhinovirus-induced interferon response is the cause of the Symptoms of the common coldand not the virus itself.

While rhinoviruses are quite resistant to interferons, some other respiratory viruses are extremely sensitive to them. For example, influenza viruses cannot replicate properly in the presence of interferons.

Because rhinovirus infections cause such a large interferon response, the researchers came up with the idea that they could offer protection against infections from more deadly, interferon-sensitive viruses like influenza.

In recent years, several research groups have investigated this phenomenon in the laboratory. They found that cells infected with rhinovirus trigger an interferon response that prevents them from doing so infected with the influenza virus.

When rhinovirus infections block other respiratory viruses from replicating, this can affect their spread and distribution patterns. For example, Evidence of it This rhinovirus may have stopped the spread of the H1N1 influenza virus, or “swine flu”, during the 2009 global pandemic.

The cold and COVID-19

If rhinovirus infections can affect the replication and spread of pandemic influenza viruses, could this also be the case for interferon-sensitive coronaviruses such as SARS-CoV-2?

A team of scientists at the University of Glasgow recently set out to answer this question. They infected cell layers grown in the laboratory that replicate the conditions in the human airways simultaneously with rhinovirus, SARS-CoV-2 and both viruses.

Interestingly, SARS-CoV-2 replicated much more slowly in the co-infection scenario. However, rhinovirus replication did not change in the presence or absence of SARS-CoV-2.

To better replicate real-world conditions, the authors infected the cells with either rhinovirus or SARS-CoV-2 24 hours before co-infection with the other virus. Rhinovirus was able to suppress the replication of SARS-CoV-2 regardless of whether it was added before or after SARS-CoV-2, suggesting that rhinovirus infection caused cells to be active prior to SARS-CoV- 2 protects.

Next, the authors wanted to confirm that the inhibitory effect on SARS-CoV-2 replication was specifically caused by a rhinovirus-induced interferon response. They co-infected cells with both rhinovirus and SARS-CoV-2 in the presence of a drug that blocks the virus-killing properties of interferons called BX795.

In this part of the experiment, BX795 allowed SARS-CoV-2 to replicate at a level comparable to that of a single SARS-CoV-2 infection. This confirmed that a rhinovirus-induced interferon response is actually responsible for the blockade of SARS-CoV-2 replication that was observed in the co-infection experiments without BX795.

Using mathematical simulations, the authors also found that more frequent rhinovirus infections in the population would lead to a reduced SARS-CoV-2 infection rate. Taken together, these results confirm that rhinovirus infections suppress the replication of SARS-CoV-2, which in turn can reduce the number of new cases in the population.

So can rhinoviruses protect us from SARS-CoV-2 infection? The short answer is yes. However, it is important to note that the rhinovirus-induced interferon response is an example of innate immunity, which means that its effects only last as long as the invading rhinovirus is in your body.

If you are recovering from a cold and come in contact with SARS-CoV-2 a week later, it is unlikely that you have enough interferons to successfully block the SARS-CoV-2 infection. Long-term immunity, in which highly specific antibodies are produced, is only achieved through direct contact with the virus in question – either in the wild or through vaccination.

So if you are someone who has not yet had COVID-19 or has not been vaccinated, you are only protected if you are lucky enough to catch a cold at the same time. Rhinoviruses can play a critical role in controlling the spread of SARS-CoV-2 in the human population. However, vaccination is likely to remain the most effective route.

Matthew James, Research Associate, Wellcome Wolfson Institute for Experimental Medicine, Queen’s University Belfast

This article is republished by The conversation under a Creative Commons license. read this original article.


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