Four deadly outbreaks of coronaviruses have occurred in the past 20 years: SARS (severe acute respiratory syndrome) in 2002 and 2003, MERS (Middle East respiratory syndrome) in 2012, and the ongoing COVID-19 emerging in 2019. Scientific evidence and environmental reality suggest that new and possibly more dangerous coronaviruses should be expected in the future.

At this point, understanding of the universe of endemic and potentially new coronaviruses is very limited. Although coronaviruses are distributed throughout the world, the most important hotspots of betacoronaviruses (the coronaviruses that led to these epidemics) are in Southeast Asia and adjacent areas of South and Southwest China. Numerous bat species transmit sarbecoviruses (SARS-like viruses, including SARS-CoV-2) to each other and to other mammals, including humans, doing so at a high rate. The relentless and rapid generation of new genomes through mixed infection and homologous genetic recombination results in substantial genetic diversity of coronaviruses – similar to that observed in the evolution of influenza A virus in wild birds, other animals and humans.

To gain insight into the natural history and pathogenesis, it is important to study coronaviruses that were probably once pandemic but have now become endemic. We are talking about four viruses, the betacoronaviruses OC43 and HKU1 and the alphacoronaviruses 229E and NL63. They, causing mainly mild upper respiratory tract infections (common cold), continue to survive and evolve in the face of high population immunity.

The COVID-19 pandemic has called to life a number of restrictive measures to control the spread of SARS-CoV-2 coronavirus, including mass vaccination. However, no matter how effective the existing vaccines are, their protective power wanes over time, leading to the need for repeat vaccinations. Vaccinations that prevent severe or fatal disease have failed to curb “breakthrough” infections when the pathogen is transmitted to others. The protective power of vaccines dropped dramatically after new variants of coronavirus, such as Beta (B.1.351) and Delta (B.1.617.2), emerged. The current wave of the Omicron variant (B.1.1.529) has weakened vaccine protection even more.

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People who previously recovered from COVID-19 are still reinfected with it. Moreover, immunity after natural infection with SARS-CoV-2 combined with immunity acquired after vaccination failed to prevent the emergence and rapid spread of viral variants.

The SARS-CoV-2 coronavirus is unlikely to ever be eliminated, let alone completely eradicated. It will probably continue to circulate around the planet indefinitely in the form of periodic outbreaks and endemics. Other animal coronaviruses with unknown transmissibility and lethality, which can be transmitted to humans and then mutate uncontrollably, may well emerge in the foreseeable future.

With this in mind, leading experts from the National Institute of Allergy and Infectious Diseases (NIAID), part of the U.S. National Institutes of Health (NIH), David Morens, Jeffery Taubenberger, and Anthony Fauci, have urged the global biotechnology industry to develop universal vaccines against coronaviruses.

Science must prioritize the development of vaccines that offer significantly broader protection and sustained immunity, not only against SARS-CoV-2, but also against other animal-origin coronaviruses that could cause future zoonotic outbreaks and pandemics.

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A universal coronavirus vaccine should prevent infection by all sarbecoviruses and merbecoviruses, including their mutant and recombinant variants. The vaccine should trigger a rapid and robust immune response, have no immunogenicity limitations, and not cause antibody-dependent disease enhancement upon subsequent exposure to the wild-type virus.

A universal coronavirus vaccine should prevent virus transmission to healthy individuals and shorten the viral shedding period, form strong herd immunity, and not lead to mutant strains escaping neutralization.

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The development of universal coronavirus vaccines will require solving fundamental questions related to the nature of protective immunity. Thus, unlike respiratory viruses that cause systemic infections (measles, rubella, varicella), non-systemic respiratory viruses such as endemic coronaviruses, influenza viruses, respiratory syncytial virus, parainfluenza viruses and SARS-CoV-2 mainly infect epithelial cells on mucosal surfaces and have limited contact with the systemic immune system. In other words, they trigger incomplete and transient protective immunity, allow reinfection, and generate a suboptimal response to systemically administered vaccines.

It is necessary to start now to study the correlates of human immunity generated both after natural SARS-CoV-2 infection and vaccination, including by assessing the persistence of the response and its localization (mucosal and systemic). Challenge clinical trials with cold coronaviruses will be important here. Such studies can significantly improve the efficacy of universal coronavirus vaccines, helping to determine immunogen design and optimal vaccination routes and methods.

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Alex Avisoni

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