Sept. 4 (UPI) — Sometimes a virus lies dormant inside a host cell. Other times, the virus destroys everything.
According to a new study, whether a virus lies idle or goes on the attack depends on how the virus’ DNA is packaged.
The research, published this week in the journal eLife, could also explain the behavior human-infecting viruses.
“I found for the first time that the mechanics of how DNA is packaged inside a virus determine the course of infection,” Alex Evilevitch, professor of pathobiology at the University of Illinois, said in a news release.
When viruses invade bacteria, they follow one of two pathways, “lytic” and “latent.”
Lytic viral infections seize the host cell’s resources and use them to quickly replicate. The multiplying virus eats the cell and invades the next host, repeating the process.
When a virus is latent, its DNA incorporates itself into the host cell’s genome. When the cell divides, the virus’ DNA is copied along with the cell’s genome.
“The many viral infections that we carry can remain latent for a very long time. Sometimes they go lytic, and that’s when we develop symptoms,” Evilevitch said.
Evilevitch and his colleagues set out to identify what causes a virus to switch from latent to lytic.
Many studies have focused on the shape and behavior of protein capsids, which protect viral DNA and smuggle it into host cells.
For the latest study, Evilevitch used isothermal titration calorimetry to measure the stresses and strains exerted on viral DNA molecules prior to being injected into a host cell.
Isothermal titration calorimetry, ITC, measures small thermal energy changes in a system. To better understand differences between viral infection pathways, Evilevitch and his research partners tracked thermal energy changes as thousands of viral particles as they interacted with bacteria cells.
ITC measurements revealed two distinct patterns. A large spike in thermal energy revealed the hundreds of viruses simultaneously injecting their DNA in the bacteria cells. The second pattern featured slow, sporadic infections.
The data showed latent infections are synchronous, while lytic infects invade in an uncoordinated fashion. Irregular infections quickly killed their host cells. Synchronized infections preserved their host cells.
In followup experiments, scientists found an increase in temperature triggered an increase in synchronous infections. Researchers determined heat made virus DNA molecules more flexible and fluid. An increase extracellular magnesium ion concentrations had a similar impact.
“The DNA becomes more flexible; it has more of a fluid character,” Evilevitch said. “As a result, it’s more likely to be ejected — like toothpaste out of a tube. But if it’s solid, it’s going to get stuck inside the tube.”
The research shows environmental conditions can alter the mechanics of virus DNA, which influence the infection pathway. In the future, researchers could manipulate virus DNA to prevent an infection from becoming lytic.