Like a scene out of a sci-fi movie, cells invaded by the coronavirus can sprout probing appendages bedecked with viral bits.
Human cells infected with SARS-CoV-2, the coronavirus that causes COVID-19, formed more numerous and longer extremities, called filopodia, than uninfected cells, researchers report online June 28 in Cell. High-resolution electron microscopy confirmed the presence of these filopodia in infected monkey cells and captured SARS-CoV-2 viral particles budding from the projections. These protrusions may have unexplored roles in spreading the virus, and could serve as targets for future antiviral therapies.
Similar spindly projections are found on some healthy cells, where the structures serve different roles. Repair cells, for example, send out filopodia to detect chemical cues to navigate to wound sites.
Other viruses, including the coronavirus behind the SARS epidemic, also can cause cells to sprout filopodia. Some viruses, such as Marburg and Ebola, travel along filopodia of infected cells and may use the structures to move directly from one cell to another.
The extensions “are highways for transport,” says Robert Grosse, a cell biologist at the University of Freiburg in Germany.
More work is needed to confirm what role filopodia play in a COVID-19 infection. Microscopy of infected cells over time would provide insight into whether these cell-to-cell connections affect viral spread, says Mark Denison, a virologist at Vanderbilt University Medical Center in Nashville not involved in the study.
The filopodia observed in the new study contained a protein called CK2. Cells dosed with silmitasertib, a CK2-inhibiting molecule in clinical trials for various cancers, were more resistant to a SARS-CoV-2 infection than untreated counterparts. That suggests that CK2 could be a target for future coronavirus drug treatments, Grosse says (SN: 3/10/20).