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Significance Viruses are important causes of human disease and provide tools for understanding host immune defense mechanisms. Poxviruses are good models for probing the immune system because many replicate well in human cells, some cause severe disease, and nearly half of the 200 viral genes are devoted to host interactions. The virus/host equilibrium can be perturbed by mutating a viral gene and restored by suppressing the opposing host genes. To find relevant host genes for one such poxvirus mutation, we used a high-throughput human genome-wide RNAi screen and monitored virus spread. Three proteins were identified: Two participate in processive DNA replication and another activates transcription of one of the DNA replication proteins to form a putative antiviral network.

Triad of human cellular proteins, IRF2, FAM111A, and RFC3, restrict replication of orthopoxvirus SPI-1 host-range mutants