Opinion

With the arrival of fall come colds, a stuffy nose, a dry cough, sneezing, headaches, a sore throat, a slight fever, loss of appetite, and fatigue… In some cases, it can lead to complications and become a serious health problem.

Most of these symptoms are caused by viruses. We tend to think that there are only the flu, coronavirus, or respiratory syncytial virus (RSV), but the list also includes parainfluenza, rhinovirus, enterovirus, adenovirus, metapneumovirus, bocavirus… Many of these viruses also have different strains.

Respiratory viruses have their seasonal peaks, although not all follow the same pattern. Right now,COVID-19 cases are on the risethroughout Spain. If you have a cold right now, it might be COVID-19. The virus continues to evolve; there are new variants; natural immunity from past infections may wane; and vaccination rates may also be declining. This would partly explain this resurgence of the SARS-CoV-2 coronavirus.

 Source: SiVIRA Report (Week 39/2026)

How Respiratory Viruses Spread
A recent studyanalyzed the behavior of 18 respiratory viruses from October 2022 to September 2025. Specifically, the researchers collected data on four influenza viruses (three type A and one type B), two RSV viruses, two seasonal coronaviruses (NL63 and OC43), four types of parainfluenza, rhinovirus, enterovirus, adenovirus, metapneumovirus, bocavirus, and, of course, SARS-CoV-2. In total, they analyzed 32,782 samples.

Although the study has some limitations (the data are limited to Catalonia and come from symptomatic individuals who visited participating centers, and thus do not represent the entire infected population), the results show the patterns of each virus’s waves and the periods during which they overlap.

RSV and influenza exhibited the most pronounced seasonality. While RSV activity began in October, influenza activity began in early November. The peak of RSV occurred approximately one month before that of influenza. Furthermore, its decline was more prolonged, so the two epidemics overlapped for part of their course. It is also worth noting that influenza A exhibited a more distinct annual pattern than influenza B.

Rhinoviruses and enteroviruses, meanwhile, circulated throughout the year, but their activity peaked in the fall and spring. Rather than a single season, they exhibited a pattern with two peaks. It was also observed that rhinovirus positivity decreased during SARS-CoV-2 epidemic periods.

Other viruses were active at different times of the year. The seasonal coronavirus OC43 and bocavirus began to rise between October and November and reached prolonged peaks between February and April. Their activity coincided with that of metapneumovirus, which peaked somewhat later. Coronavirus 229E reached its highest levels around April. Later on, the second peak of rhinovirus and parainfluenza 3 activity appeared.

In the case of adenoviruses, the NL63 coronavirus, and parainfluenza viruses 1 and 4, the detection rates and stability of these viruses did not allow for the identification of outbreaks using the procedure employed. Their circulation was described as low and consistent throughout the year.

The study suggests that, following the disruptions caused by the pandemic, many respiratory viruses have returned to their regular epidemic cycles.

The COVID virus is not yet a winter virus
SARS-CoV-2 exhibited the most striking behavior. Since 2023, its circulation has been predominantly summertime: outbreaks began in the spring, peaked between August and September, and declined by early winter. In the winter of 2022, a minor wave was still observed; in 2023, another, less pronounced wave appeared; and that winter spike was no longer evident in 2024. Furthermore, the onset of the last two summer waves occurred on virtually the same dates.

Ultimately, the summer pattern of SARS-CoV-2 calls into question the expectation that it would eventually behave like a predominantly winter virus.

Viruses Interfere with One Another
This study demonstrates that outbreaks of respiratory viruses do not coincide with one another and that a long-known phenomenon ofviral interference exists. Edward Jenner had already noticed that his smallpox vaccine was not as effective if the patient had herpes. It was as if having two active infections at the same time disrupted the immune response.

Viral interference was observed again in the 1960s when the first live-attenuated vaccines were developed against certain enteroviruses,such as the polio virus. It was soon found that these vaccines also provided protection against severe respiratory infections. Their administration to children reduced the number of cases caused by other, unrelated respiratory viruses.

This viral interference was due to the vaccine inducing a nonspecific immune response. It was clear that the presence of one virus could inhibit or affect the growth of another.

Studying these types of interactions or multiple infections is not easy, since our immune system is constantly fighting viruses and bacteria. Viruses can interfere with one another because the arrival of the first one triggers defenses that hinder the replication of the next one.

When cells detect an infection, they produceinterferons, proteins that act as alarm signals. These alert neighboring cells and activate mechanisms that inhibit viral replication. This establishes a transient antiviral state capable of acting against viruses other than the one that triggered the response. For example, in cell cultures, it has been observed that rhinoviruses—which cause many colds—can reduce the replication of SARS-CoV-2. This interference could contribute to the alternating waves of certain respiratory viruses.

However, the explanation is not that simple. Interference depends not only on viruses, but also on human behavior, environmental conditions, the weather, asymptomatic infections, and even school schedules. Furthermore, the outcome may depend on which virus arrives first, how much time elapses between the two infections, and how the body responds.

For example, two infections can also occur simultaneously and worsen the disease. This is the case withcoinfection with SARS-CoV-2 and the flu, which is more severe than either infection alone. Therefore, while this interaction helps us understand the behavior of epidemics, it does not mean that having a cold guarantees protection against another infection.

However, interactions between viruses can also be negative, with an antagonistic effect, depending on whether or not the second virus belongs to the same family or type as the first virus. This is, for example, what happens in the case of infections with subtypes of the influenza virus:the first prevents the disease caused by the second.

Understanding how some viruses interfere with others may allow us in the future to use one to combat another. We could, for example, develop a nasal spray containing a modified or defective virus that would only stimulate the innate immune system, thereby protecting us against infection by other viruses. Perhaps to prevent a deadly viral infection, we need to induce an infection with a different, protective virus. After all, that’s what vaccines are all about. But for now, don’t forget to get your vaccines this fall.

This article was originally published in The Conversation. Read the original.