Researchers have discovered the first “pressure-driven infection mechanism” in a human virus, which blasts infectious DNA into cells with pressure eight times higher than that of a typical car tire.
The study, published in the Journal of the American Chemical Society, suggests that this discovery could open the door to new treatments for viral infections.
It was found that the HSV-1 virus enters human cells, settles on the nucleus and then blasts its way into DNA using high pressure built up from a “nanometer-scale protein shell” called the capsid, researchers explain. The capsid is the shell that contains the viral genome.
The researchers say that the viruses responsible for infections such as influenza and HIV are quickly becoming resistant to drugs that target viral proteins. The proteins can quickly disguise themselves and become resistant to ant-viral drugs as a result of genetic mutation.
For example, previous research published in PLoS Computational Biology has suggested that drug resistance to HIV, the virus that causes AIDS, can be caused by pre-existing mutations, which can actually progress even more once treatment is initiated.
Findings such as this one have led to a search for weaknesses in viruses that do not involve viral proteins, the researchers add, a reason why this study was conducted.
Previous research has also shown many viruses that infect bacteria, called bacteriophages, use the same pressure-driven mechanism in order to blast their DNA into bacteria nuclei.
They add that the same mechanism also exists in eight related viruses, including chickenpox in children, shingles in adults, and the virus responsible for mononucleosis.
The researchers believe that evolution has meant that this technique is now apparent in viral infection, paving the way for the development of treatments that can defeat particular viruses, such as HSV-1, in the same way.
“Despite billions of years of evolution separating eukaryotic viruses and bacteriophages, pressure-driven DNA ejection has been conserved. This suggests it is a key mechanism for viral infection and thus presents a new target for antiviral therapies.”