It’s the leading infectious cause of birth defects: every year in the U.S., infection with human cytomegalovirus (HCMV) leaves more than 5,000 children with permanent problems like hearing loss or developmental disabilities, according to the CDC (http://www.cdc.gov/cmv/trends-stats.html). Researchers working to understand the ins and outs of how the virus assembles itself inside our cells and moves on to infect other cells and other individuals hope to one day find a way to stop the virus before it does its damage. A paper published in mBio this week reveals the ways one protein contributes to the reorganization of human cell membranes that helps viruses assemble and leave the cell.
The protein pUL71 is a component of the tegument – proteins that line the inside of the viral envelope and play roles in replicating the virus’ DNA and other processes. In the study, researchers used a mutant virus that doesn’t express pUL71 to examine what this specific part of the tegument does. It turns out pUL71 is kind of like a microscopic UPS Store: it creates a place for viruses to be packed up and shipped away. The pUL71 mutant was able to accumulate viral genomes and proteins, but it couldn’t produce and release infectious virions, pointing to a key role for pUL71 in the establishment and/or maintenance of a working viral assembly compartment that is required for normal virus trafficking and departure from infected cells.