Could the new coronavirus evolve to become more harmful?

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Viruses evolve over time, so researchers around the world are watching the new coronavirus for any changes that might affect how it is transmitted or the severity of the illness it causes, or changes that might influence the approach to drug and vaccine design.

Viruses change naturally by mutation. They may also evolve through “natural selection” to adapt to the challenges they face at different stages of their life cycle.[1] When in humans, they are attacked by the immune system as well as by drugs introduced to kill them. Outside the body, they may be destroyed by multiple environmental factors or by deliberate hygiene measures before they are able to infect someone else. Most genetic changes have no, or very little, effect on virus biology; these ‘neutral’ changes can fluctuate by chance over time.

Adaptation by natural selection is a two-stage process. First, slight changes to the genetic material – mutations – occur randomly when the virus replicates in the host. Most of these changes will have no effect on virus biology, but sometimes a mutation gives a virus a better chance of surviving and reproducing. A mutation might, for example, have allowed the new coronavirus, SARS-CoV-2, to jump from animals to humans. Or a random change in the make-up of the spikes, the projections covering the virus that help it enter cells, might improve its ability to enter a lung cell or to avoid antibodies produced by the immune system. A mutation might cause illness in people that is more or less severe.[2] Irrespective of the severity of illness, if an altered virus multiplies more quickly in the human body and so produces more infectious particles, or spreads more quickly through the human population, it will most likely come to replace the parental form through natural selection.

Mutation and vaccination

Mutation is a natural process that occurs more frequently in viruses – like coronaviruses – that have RNA rather than DNA as their genetic material. Multiple rounds of replication in the host, roughly every 30 minutes, also increase the chances of mutations occurring that might be favoured by natural selection or spread by chance through genetic drift. It is the rapid evolution of another group of RNA viruses, the influenza viruses, which means that a new flu vaccine is needed every year.

It is too soon to say whether the pattern of evolution in the new coronavirus will allow the development of a single vaccine that can provide long-lasting protection to all people, or whether new vaccines will need to be developed as the virus changes. Immunologists have begun to identify parts of the virus that stimulate an immune response and which seem to be consistent across different strains.[3] Monitoring changes in the genetic code for these proteins will help guide vaccine design.

Keeping a watch on viral change

Tracking changes in the genetic make-up of viruses is important for many reasons. First, the information can be used to build the virus equivalent of a family tree (also called a phylogenetic tree) which can, for example, provide information about the geographical spread of the virus and whether it has switched from an animal to a human host. Second, it provides a valuable resource for scientists researching vaccines. Third, if we are able to link changes in the genetic code to the way the virus causes disease then monitoring may provide information about changes in disease virulence.

There is an established, international network of virologists who study the influenza virus and share data on its changing genetic make-up through online databases, such as GISAID. Since the first SARS-CoV-2 virus was sequenced in January, GISAID has also become a platform to share and compare genetic information about the new coronavirus.[4]

Detailed studies of the course of infection within individuals show, as expected, mutations occurring and therefore the diversity of viruses increasing over time.[5] And analysis of the data collected from individuals around the world shows new variants of the virus arising in different geographic areas. This has allowed the origin of coronavirus infections in some countries to be traced back to the country from where they have originated, for example travellers returning from Iran to Australia and New Zealand.[6]

So far, there is no evidence that the mutations in SARS-CoV-2 affect the way the coronavirus is transmitted, its ability to cause infections, or the severity of the disease. Nor is there any evidence yet that mutations will hinder the development of vaccines. But the virus is being watched.

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  1. Grubaugh ND, Petrone ME, Holmes EC. We shouldn't worry when a virus mutates during disease outbreaks. Nature Microbiology. 2020 Apr;5(4):529-530. DOI: 10.1038/s41564-020-0690-4.

  2. Read AF, Kerr P. Do Pathogens Gain Virulence as Hosts Become More Resistant? The Scientist. 2017 Oct.

  3. Ahmed SF, Quadeer AA, McKay MR. Preliminary Identification of Potential Vaccine Targets for the COVID-19 Coronavirus (SARS-CoV-2) Based on SARS-CoV Immunological Studies. Viruses. 2020 Feb;12(3) DOI: 10.3390/v12030254.

  4. Genomic epidemiology of hCoV-19. GISAID. 2020 Mar.

  5. Shen Z, Xiao Y, Kang L, et al. Genomic diversity of SARS-CoV-2 in Coronavirus Disease 2019 patients. Clinical Infectious Diseases. 2020 Mar. DOI: 10.1093/cid/ciaa203.

  6. Eden JS, Rockett R, Carter I, et al. An emergent clade of SARS-CoV-2 linked to returned travellers from Iran. Virus Evolution. 2020 Jan;6(1):veaa027. DOI: 10.1093/ve/veaa027.

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