LAUSR

With their limited size and coding capacity, all viruses must exploit their host cells for the machinery and raw material they require for replication. At the same time, infected cells deploy an armada of antiviral effector proteins the virus must evade or counteract. This backand-forth assault, commonly referred to as an “arms race,” impacts viral replication, tropism, and disease severity [1]. How viruses engage with their intracellular environments at the molecular level forms an overlapping research landscape for both virology and cell biology. Host factors are proteins encoded by cellular genes that affect an intruding virus. Those that ablate viral replication or spread are antiviral factors, while those that enable or enhance the infection perform pro-viral roles and are host dependency factors (HDFs). All of these participate in the battle between pathogen and host and are often under strong evolutionary selection. The identities and functions of these proteins can be as unique and diverse as viruses themselves. It is unsurprising that despite development of powerful systems-level methodologies, we still possess an incomplete knowledge of the virus–host interface for even the beststudied pathogens.