2023-05-23 15:59:52
Have you ever wondered why some people can get sicker than others, even when they catch the same virus? We don’t yet know why that is. Viral factors (such as differences in the strain of a virus) play a role in this variability, but they cannot explain the wide range of responses in different individuals infected with the same virus. A number of reception factors were also considered, including pre-existing immunity, age, gender, weight, and microbiome.
Another important factor is the molecular biology within your cells. DNA is in the form of a long double helix strand. So you might expect the cell to always read genetic information in order, starting at one end and going to the other. But this is not the case. DNA contains transposable elements sometimes called “junk DNA”, which can alter regions of the genome that are being read at any given time.
The work published in Cell genomics by an international team led by Dr Guillaume Bourque, who studied the role of these transposable elements on the severity of the disease following infection with the influenza A virus.
By examining data from 39 individuals before and following infection with the influenza A virus, the researchers were able to identify changes in the accessibility (ie “readability”) of transposable elements. To do this, the researchers used an approach combining different multiomics datasets, which characterize and quantify collections of biomolecules in cells or organisms. One was the transcriptome, which consists of all copies of RNA transcribed from DNA in the cell. The other was the epigenome, which is the set of chemical modifications of DNA that alter gene expression. An advantage of this multiomics approach is that they were able to identify families of transposable elements with accessibility changes, which would likely have been missed by previous approaches.
By considering these changes in transposable elements following viral infection, they might identify several transcription factors (proteins that turn specific genes on or off) that likely contribute to a person’s response to infection. Using these results, the researchers were able to create a model capable of predicting an individual’s viral load following infection with influenza A.
“A number of questions remain, such as whether the link between transposable elements and viral load is really causal and whether these changes would be consistent over time,” says lead author Xun Chen. “But these findings are an important step towards understanding the role these factors play in the variability of disease severity in individuals.”
The authors include researchers from Kyoto University in Japan, McGill University and the University of Montreal in Canada, and the University of Chicago in the United States.
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#multiomics #approach #insight #severity #influenza
