Human metapneumovirus (HMPV), which belongs to the a family, has shown the emergence of the A2b2 clade as the dominant global genotype. Whether this represents true evolutionary selection or surveillance artefacts remains unclear. We analysed 315 complete HMPV genome sequences (1994–2024) from the Nextstrain database using sampling-corrected statistical approaches, including temporal homogeneity testing, rarefaction analysis, and entropy-based dynamics to examine non-random patterns in A2b2 emergence. Temporal homogeneity testing revealed strong directional evolution towards A2b2 dominance (Z = −46.62, p < 0.001), confirming non-random patterns rather than surveillance artefacts. The clade showed strong persistence (206 self-transitions) with limited backward transitions. After controlling for sampling bias, A2b2 represented 68.3% (95% CI: 58.2–78.4) of isolates in 2023–2024. A2b2 demonstrated significantly higher temporal entropy (2.1) than other clades (A1: 1.2, A2a: 1.5, A2b1: 2.0), indicating more complex dynamics. Geographic rarefaction revealed significant regional structuring, with Africa showing the highest diversity (3.00, 95% CI: 1.00–3.05) despite lower sampling. HMPV A2b2’s global expansion represents genuine directional evolution with potential selective advantages, similar to patterns in respiratory syncytial virus. These findings underscore the need for enhanced genomic surveillance and integration of HMPV monitoring into respiratory virus surveillance frameworks to track emerging variants and assess public health implications.

Several recent studies conclude that an increase in the pathogenicity of SARS-CoV-2 cannot be ruled out. However, it should be noted that SARS-CoV-2 is a ‘direct’ respiratory virus – meaning it is usually spread by the respiratory route but does not routinely pass through the lymphatics like measles and smallpox. Providing its tropism does not change, it will be unique if its pathogenicity does not decrease until it becomes similar to common cold viruses. Ewald noted in the 1980s that respiratory viruses may evolve mildness because their spread benefits from the mobility of their hosts. This review examines factors that usually lower respiratory viruses’ severity, including heat sensitivity (which limits replication in the warmer lungs) and changes to the virus’s surface proteins. Other factors may, however, increase pathogenicity, such as replication in the lymphatic system and spreading via solid surfaces or faecal matter. Furthermore, human activities and political events could increase the harmfulness of SARS-CoV-2, including the following: large-scale testing, especially when the results are delayed; transmission in settings where people are close together and not free to move around; poor hygiene facilities; and social, political, or cultural influences that encourage sick individuals to remain active, including crises such as wars. If we can avoid these eventualities, SARS-CoV-2 is likely to evolve to be milder, although the timescale is uncertain. Observations of influenza-like pandemics suggest it may take around two decades for COVID-19 to become as mild as seasonal colds.