Scientists in Brazil recently reported that two people were simultaneously infected with two different variants of SARS-CoV-2, the virus that causes COVID-19.
This co-infection did not appear to have an effect on the severity of the patients’ disease and both recovered without the need for hospitalization.
Although this is one of the few such cases reported with SARS-CoV-2 – and the study is yet to be published in a scientific journal – scientists have observed infections with multiple strains of other respiratory viruses, such as influenza.
This has raised questions about how these viruses can interact in an infected person and what it could mean to generate new variants.
Viruses are masters of evolution, constantly mutating and creating new variants with each cycle of replication. Selective host pressure, such as our immune response, also stimulates these adaptations.
Most of these mutations will not have a significant effect on the virus. But those who favor the virus ̵
The appearance of these mutations comes down to the error-prone replication mechanism used by viruses. RNA viruses, such as influenza and hepatitis C, generate a relatively large number of errors each time they replicate. This creates “quasi-species” of the virus population, more like a swarm of viruses, each with related but non-identical sequences.
Interactions with host cells and the immune system determine the relative frequencies of the individual variants, and these coexisting variants may affect the development of the disease or how well the treatment works.
Compared to other RNA viruses, coronaviruses have a lower mutation rate. This is because they are equipped with a correction mechanism that can correct some of the errors that occur during replication.
However, there is evidence of viral genetic diversity in patients infected with SARS-CoV-2.
The detection of multiple variants in a human may be the result of coinfection of the different variants or the generation of mutations in the patient after the initial infection.
One way to distinguish these two scenarios is by comparing the sequences of variants circulating in the population with those of the patient.
In the Brazilian study mentioned above, the identified variants correspond to different lines that were previously found in the population, suggesting co-infection of the two variants.
This coinfection raised concerns about SARS-CoV-2, acquiring new mutations even faster.
This is because coronaviruses can also undergo major changes in their genetic sequence through a process called recombination. When two viruses infect the same cell, they can exchange large parts of their genomes with each other and create completely new sequences.
This is a known phenomenon in RNA viruses. New variants of influenza are generated by a similar mechanism called “reassortment”. The genome of influenza virus, unlike coronavirus, consists of eight segments or strands of RNA.
When two viruses infect the same cell, these segments mix and match to produce viruses with a new combination of genes. Interestingly, pigs can be infected with different strains of influenza viruses and are called “mixing vessels” that mix them into new strains. The 2009 H1N1 pandemic virus arose from the re-assortment of human, avian and two swine flu viruses.
In coronaviruses that contain only one RNA strand in each viral particle, recombination can only occur between RNA strands derived from one or more viruses in the same cell.
Evidence of recombination has been found in both the laboratory and in a patient infected with SARS-CoV-2, suggesting that this may stimulate the generation of new variants. In fact, the ability of SARS-CoV-2 to infect human cells has been suggested to have evolved through recombination of the protein jump between closely related animal coronaviruses.
It is important to note that this requires both viruses to infect the same cell. Even if a person is infected with several variants, if he replicates in different parts of the body, he will not interact with each other.
In fact, this is observed in patients where different quasi-types of coronaviruses have been found in the upper and lower airways, suggesting that the viruses in these areas do not mix directly with each other.
Evidence to date does not indicate that infection with more than one variant results in more severe disease. And although it is possible, very few cases of coinfection have been reported.
More than 90 percent of infections in the UK are currently from B117, the so-called Kent variant. With such a high prevalence of one variant in the population, coinfections are unlikely to occur.
Still, observing this landscape allows scientists to track the emergence of these new variants of anxiety and to understand and respond to any changes in their transmission or vaccine efficacy.
Maitreya Shivkumar, Senior Lecturer in Molecular Biology, University of De Montfort.
This article is republished by The Conversation under a Creative Commons license. Read the original article.