Influenza Transformation: The Future of the Novel Coronavirus?

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Influenza Transformation: The Future of the Novel Coronavirus?

At the end of 2019, a new coronavirus swept across the country, ushering in a three-year battle against the epidemic.

The symptoms of this disease appeared as early as the 1880s, when half of the residents of St. Petersburg, Russia, were attacked by this respiratory disease. The elderly were significantly higher than the young, with a dry cough as the main symptom, some people experiencing “taste and smell disorders,” and an increase in the number of deaths.

This sounds remarkably similar to “COVID-19.”

As early as 2002, a different kind of flu occurred in Guangzhou, Guangdong Province, China, with more severe symptoms, leading to cases of mysterious pneumonia. Soon, this disease spread to Hong Kong, Singapore, Canada, the United States, and other places, causing global panic. This was the SARS virus.

It wasn’t until 2005 that scientists pointed out that whether it was in Russia more than 100 years ago, or the SARS and COVID-19 that occurred in China, the pandemic was not caused by the influenza virus, but by coronaviruses.

Recently, an article on the front page of Science speculated on the future outcome of COVID-19 based on the development of its four Relatives. Currently, these four viruses appear every autumn and winter, accounting for 30% of colds.

However, these four viruses may have caused more severe diseases earlier, giving some virologists hope for the future of COVID-19. “Virologist Lia van der Hoek from the Amsterdam University Medical Center predicts: “These four viruses foreshadow the future development of COVID-19.” SARS-CoV-2 (the pathogen of COVID-19) may become a common cold.

Influenza Transformation: The Future of the Novel Coronavirus?

The Overlooked Relatives of SARS-CoV-2

More than a century ago, the epidemic that swept through Russia was caused by a coronavirus called OC43. Initially thought to have spread from cattle to humans in 1889, causing a pandemic that killed nearly a million people. The Russian “influenza” coronavirus is still circulating today, causing symptoms no more severe than a cold, responsible for 30% of colds each year.

NL63’s ancestors are the tricolored bats of Maryland. According to a 2012 estimate in the Journal of Virology, gene comparisons with bat viruses suggest that NL63 was transmitted to humans 563 to 822 years ago. NL63 was first discovered in a nasal sample from a 7-month-old infant in the Netherlands, with symptoms mainly fever, red eyes, and runny nose. Ron Fouchier’s laboratory at the nearby Erasmus Medical Center also found a seemingly identical virus, and the results of the two teams’ research were published online within weeks in early spring 2004.

Today, NL63 coronavirus still exists in humans, but with a low infection rate. Due to its low pathogenicity, it generally only causes respiratory symptoms similar to the common cold, so its current threat to humans is relatively small.

Almost 100% of people may have been infected with the coronavirus HCoV-229E. As an important pathogen causing human upper respiratory tract infections, 229E often causes common colds in humans and is currently one of the most common strains of common coronaviruses. 229E infection shows seasonal fluctuations, with peaks in spring and winter, an incubation period of 2-5 days, and a general susceptibility in the population. Multiple serological studies have shown that almost 100% of children have been infected with the 229E coronavirus in early childhood.

HKU1’s evolutionary history is the most obscure, as its gene sequence is close to that of mouse hepatitis virus, suggesting it originated from rodents. It was first discovered in a 71-year-old man with unexplained pneumonia in 2005 by a research team led by clinical microbiologist Patrick Woo at the University of Hong Kong.

Studies have shown that the HKU1 coronavirus has a seasonal pattern, peaking in late autumn and winter, with a significantly lower infection rate in the population than other respiratory coronaviruses. Its symptoms are also relatively mild, but for patients with underlying diseases and immunosuppression, it can exacerbate symptoms and cause serious respiratory diseases.

Can SARS-CoV-2 “Influenza-ize”?

When SARS-CoV-2 began to ravage the world, researchers began to consider whether immunity to its four milder relatives could weaken the impact of this new virus. Because all coronaviruses have the same basic protein pool, repeated exposure to the common cold may accumulate an immune response that could alleviate COVID-19. But why is it that even though only four coronaviruses are quietly circulating among humans, the immunity built up by repeated infections is cracked by the new coronavirus?

The problem lies in the spike protein of the new coronavirus, which is significantly different from its four cousins, so antibodies against the common cold coronaviruses cannot prevent SARS-CoV-2 infection or alleviate the symptoms it causes. An article published in 2023 in Science Translational Medicine even suggests that antibodies against OC43 may interfere with the body’s production of antibodies against the spike protein of the new coronavirus, further increasing the risk of persistent debilitating symptoms known as “Long Covid.”

However, there is also the opposite view that immunity to “colds” caused by coronaviruses is beneficial. T cells isolated from patients who have never been infected with the new coronavirus can recognize and destroy cells infected with SARS-CoV-2. In the early stages of the epidemic, pre-existing immunity to common cold coronaviruses did significantly reduce infection, and at least in some cases, this may be related to the similarity between the sequences of common colds and SARS-CoV-2. But now it’s basically meaningless, as people on Earth are either vaccinated or infected and already have specific immunity.

All four common cold coronaviruses were highly lethal at first but became weak later on. However, whether this outcome will be repeated in the new coronavirus is still unknown. Scientists who hold the opposite view believe that there has never been a tendency for weakening in HIV, so there is no evolutionary pressure to weaken the new coronavirus. This remains a key unresolved issue.