UC San Francisco scientists assembled an international research team that has figured out how SARS-CoV-2, the virus that causes COVID-19, hijacks proteins in host cells that serve as master regulators of key cellular processes. By doing so, the virus is able to rewire the cell’s internal circuitry to promote its own spread and survival. But the reliance of the virus on host-cell proteins may also prove to be its Achilles’ heel, as these same proteins can be easily targeted with existing drugs. In a study published June 28, 2020 in Cell, the researchers found that when SARS-CoV-2 infects cells, it assumes control over a family of enzymes known as kinases. Under normal circumstances, kinases serve as master regulators of metabolism, growth, movement, repair and other important cellular functions. Kinases work by attaching tiny chemical tags to proteins through a process known as phosphorylation. Once attached, these tags act as switches that turn proteins on or off, which keeps the complex machinery of the cell running smoothly. When a cell is commandeered by SARS-CoV-2, however, these same kinases behave in ways that disrupt normal cell function and transform the host cell into a virus factory. Cell division comes to a halt, inflammation pathways are activated, and the cell even begins to produce tentacle-like structures known as filopodia, which protrude from the cell's surface and may serve as molecular highways that help the virus spread rapidly to neighboring cells.