Immune system proteins called chemokines mobilize at infection sites and attract pathogen-fighting immune cells to the sites. But HIV-1, the virus that causes AIDS, exploits the release of a particular chemokine—CCL2—to exit host cells so it can infect new cells and replicate further. A study by Vinayaka Prasad, Ph.D., and coworkers David O. Ajasin and Vasudev Rao, M.B.B.S., published online on June 7 in eLife, describes the novel mechanism involved. CCL2 mobilizes a protein from the host cell’s actin cytoskeleton to the cellular locations of virus budding and release.  The newly discovered mechanism is broadly applicable to the replication of numerous DNA and RNA viruses and suggests a target for drugs that could stop HIV-1 from multiplying. The many CCL2 antagonists that are currently in clinical trials for treating other diseases could be directed towards blocking the spread of HIV-1. Dr. Prasad is professor of microbiology & immunology at Einstein. Other key contributors include Einstein investigators Ganjam Kalpana, Ph.D., Anne Bresnick, Ph.D., and Andras Fiser, Ph.D.