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Have you ever wondered why some people can get sicker than others, even when they get the same virus? It is still not clear why this is. viral factors (like differences in the strain of a virus) play a role in this variability, but cannot explain the wide range of responses in different individuals infected with the same virus. A number of host factors age, gender, weight, and microbiome have also been considered, including pre-existing immunity.
Another important factor is the molecular biology within your cells. DNA is shown as a long double helix strand. Thus, one would expect the cell to always read the 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 change the 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 in disease severity after influenza A virus infection.
By examining data from 39 people before and after infection with the influenza A virus, the researchers were able to identify changes in the accessibility (ie, “readability”) of the transposable elements. To do this, the researchers used an approach that combines several multi-omics data sets, which characterize and quantify collections of biomolecules in cells or organisms. One was the transcriptome, which consists of all the transcribed RNA copies of the DNA in the cell. The other was the epigenome, which is the set of chemical changes in DNA that modify gene expression. An advantage of this multiomics approach is that they were able to identify families of transposable elements with changes in accessibility, which would probably not have been detected in previous approaches.
By considering these changes in transposable elements after viral infection, they could identify several transcription factors (proteins that turn specific genes on or off) that are likely to contribute to someone’s response to infection. Using these findings, the researchers were able to create a model that could predict an individual’s viral load after influenza A infection.
“Several questions remain, such as whether the link between transposable elements and viral load is truly causal and whether these changes would be consistent over time,” says lead author Xun Chen. “But these findings are an important step toward understanding the role these factors play in the variability of disease severity among 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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