Recent Human Metapneumovirus Outbreak in East Asia: The Time to Shift Immunological Gears is Now
Authors: Carp Theodor-Nicolae 
Published: February 2025

Recently, there has been a significant outbreak of clinical pneumonia caused by the Human Metapneumovirus, particularly in Northern regions of the People’s Republic of China, causing thousands of hospitalisation cases. Such an outbreak has grown fresh concerns with regards to a potential spread of the novel infectious disease to several other world countries and causation of public health-related difficulties that may be similar in nature with the effects of the SARS-CoV-2-induced COVID-19 pandemic, which occurred from March 2020 to March 2022 before the disease finally became endemic in nature. Throughout the COVID-19 pandemic, a novel immunological research narrative was developed, in which a wider inclusion of natural immunity-based elements was recommended as part of an update in general approaches contained by immunotherapeutic and vaccine-related clinical research. Particularly, it has been suggested that a fairly decreased concentration of Type I and Type III elements from the host interferon system be placed in the central area of the natural immunity-based immunisation and immunisation adjuvance. Several clinical trials have confirmed the important position of such interferon system elements in the natural immunity department responsible for immunising functions. Given the fact that major components of the natural immune system have recently shown to display considerable adaptive immunity-like traits, such as specificity and long-term “memory”, natural immunity-based vaccination may now be deemed as scientifically plausible, contrary to initial scientific projections that they can only constitute vaccine adjuvants. Approaches as such may include a low dose of Type I and Type III Interferon-, and perhaps protollin-based treatment of nasopharyngeal tissues, as well as of natural and adaptive lymphocytes, and of plasmacytoid dendritic cells also, which represent both factories for Type I and Type III Interferons, as well as valid immune system-based vaccine candidates against infectious and oncological diseases, alongside natural and adaptive lymphocytes. Such components of the immune system may be utilised in combination to confer the most effective version of such an overall candidate of a clinical response. Other vaccine candidates may involve live-attenuated viral genomes either lacking the interferon-suppressive genes or containing them as the only slightly active genetic regions, with the overall purpose of stimulating an evolutionary push of the interferon-encoding genes to outcompete the already advanced stages of microbial evolution, whose stronghold seems to be largely upon the host interferon system. Other approaches may also involve the development of live-attenuated pathogen-derived vaccines that have Interferon I and III-encoding genes inserted into the viral genome as its sole active genetic components. There may be a novel, experimental process involving the isolation of common cold-inducing viruses, such as Rhinoviral agents, during the beginning of local, seasonal outbreaks and perhaps inducing their weakening as well, in clinical laboratories that are located in multiple distinct geographical areas of the hemisphere where the fall season has begun, prior to the performance of a small-scale gene editing through the insertion of active Type I and Type III Interferon-encoding genes into the genome of such viruses, prior to their release back into the local environment, via the performance of CRISPR-Cas9. Specifically, microbial genes involved in the causation of pathogenesis and maintenance of pathophysiology would be substantially attenuated, and genes involved in microbial reproduction and transmission perhaps not as much. Such a process may turn such viruses and possibly also other microbes into spreadable vaccines, as the immune system would automatically be activated once viruses as such undergo receptor-mediated endocytosis and start expressing their genes. At least some of the genes encoding proteins that antagonise the host interferon system could be removed prior to the insertion of human genes encoding various elements of it, particularly in situations where microbial agents are known to antagonise it in a problematic manner, whether directly or indirectly. If an overall procedure as such is performed accurately and matches all bioethical guidelines, then at least only common cold diseases in the upper respiratory tract, including the Rhinovirus-induced disease, may be prevented in many cases and probably even gradually become eradicated in the end, given the fact that an automatic synthesis of Type I and Type III Interferons by pathogenic microbes could lead to a robust and proportional rate of immune sensitisation that would lead to their lysis and disposal, making it probable that even microbes that are normally causative of major clinical disease would be destroyed before they would be able to induce the first symptoms. Active genes encoding Pattern Recognition Receptor (PRR) Activators matching to the microbe could also be inserted into its genome, perhaps to restore normative levels of microbial sensing by the host, natural immune system. Perhaps, inhalers and injectable sera containing a fairly decreased dosage of such potential transmissible factories for Type I and Type III Interferons, and possibly also for specific Pattern Recognition Receptor Activator and/or Agonist proteins, as such may be prepared to fill in any remote gap to the production of a full, herd-immunity effect throughout human populations. Such a potential overall update in vaccine innovation and development could even impact the evolutionary trajectory of various single drug and multidrug antibiotic resistant pathogenic bacteria, which can represent additional, unnecessary burdens for patients with various viral infections.