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The longer high levels of viral multiplication occur \u2013 permitted by high levels of transmission \u2013, the more the virus can adapt to the human host and find ways to success. The third wave of the COVID\u201019 pandemic is starting in different parts of the world, emphasizing that transmission containment measures that are being imposed are not adequate. Part of the consideration in determining containment measures is the rationale that vaccination will soon stop transmission and allow a return to normality. However, vaccines themselves represent a selection pressure for evolution of vaccine\u2010resistant variants, so the coupling of a policy of permitting high levels of transmission\/virus multiplication during vaccine roll\u2010out with the expectation that vaccines will deal with the pandemic, is unrealistic. In the absence of effective antivirals, it is not improbable that SARS\u2010CoV\u20102 infection prophylaxis will involve an annual vaccination campaign against \u2018dominant\u2019 viral variants, similar to influenza prophylaxis. Living with COVID\u201019 will be an issue of SARS\u2010CoV\u20102 variants and evolution. It is therefore crucial to understand how SARS\u2010CoV\u20102 evolves and what constrains its evolution, in order to anticipate the variants that will emerge. Thus far, the focus has been on the receptor\u2010binding spike protein, but the virus is complex, encoding 26 proteins which interact with a large number of host factors, so the possibilities for evolution are manifold and not predictable a priori. However, if we are to mount the best defence against COVID\u201019, we must mount it against the variants, and to do this, we must have knowledge about the evolutionary possibilities of the virus. In addition to the generic cellular interactions of the virus, there are extensive polymorphisms in humans (e.g. Lewis, HLA, etc.), some distributed within most or all populations, some restricted to specific ethnic populations and these variations pose additional opportunities for\/constraints on viral evolution. We now have the wherewithal \u2013 viral genome sequencing, protein structure determination\/modelling, protein interaction analysis \u2013 to functionally characterize viral variants, but access to comprehensive genome data is extremely uneven. Yet, to develop an understanding of the impacts of such evolution on transmission and disease, we must link it to transmission (viral epidemiology) and disease data (patient clinical data), and the population granularities of these. In this editorial, we explore key facets of viral biology and the influence of relevant aspects of human polymorphisms, human behaviour, geography and climate and, based on this, derive a series of recommendations to monitor viral evolution and predict the types of variants that are likely to arise.<\/jats:p>","DOI":"10.1111\/1462-2920.15487","type":"journal-article","created":{"date-parts":[[2021,3,26]],"date-time":"2021-03-26T08:24:14Z","timestamp":1616747054000},"page":"2339-2363","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":35,"title":["<scp>SARS\u2010CoV<\/scp>\n                    \u20102 biology and variants: anticipation of viral evolution and what needs to be done"],"prefix":"10.1111","volume":"23","author":[{"given":"Ruibang","family":"Luo","sequence":"first","affiliation":[{"name":"Department of Computer Science The University of Hong Kong  Bonham Road Pokfulam Hong 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