Strong persistence of viral infection

Infections caused by viruses, such as respiratory syncytial virus, measles, parainfluenza and Ebola, are acute. These viruses cause disease quickly and live within a host for a limited time. But in some cases the effects of the infection, and presence of the virus can lead to chronic problems.

Viral infection leads to defective viral genomes, DVG which involved in triggering an immune response, can also kick off a molecular pathway that keeps infected cells alive. The study used a novel technique to examine the presence of DVGs on a cell-by-cell basis to show that DVG-enriched cells had strategies to survive during an immune-system attack.

Partial viral genomes are produced in infected cells when a virus begins to replicate rapidly, leading to defective versions that contain large deletions. DVGs are increasingly believed to be important components of viral infections.

DVGs are critical in stimulating an immune response to respiratory viruses, they are also critical for stimulating an immune response to the human virus RSV, the presence of DVGs in human respiratory samples from infected patients correlates with enhanced antiviral immune responses.

Researchers used a sophisticated technique that allowed them to differentiate full-length genomes from the partial genomes of DVGs at the single-cell level. They studied cells in culture infected with the Sendai virus, or with RSV, a virus that often affects infants and can lead to chronic respiratory problems.

To dig deeper into how the DVGs were influencing the course of infection, the researchers infected cells either with a version of the Sendai virus that lacked DVGs or one enriched in DVGs. The cells infected with the virus high in DVGs survived more than twice as long as those infected with virus lacking DVGs.

 Adding purified DVGs boosted the cells' survival time, indicating a direct role for the DVGs in promoting cell survival.
The results were similar in parallel experiments with RSV, suggesting that the pro-survival role of DVGs held across viral types.

The researchers next were curious to know what molecular pathways might enable the DVG-rich cells to avoid apoptosis. An analysis of highly-expressed genes in DVG-enriched cells compared to the cells with full-length viral genomes revealed that a host of pro-survival genes were activated in the DVG-rich cells.
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