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Significance Malaria is a deadly disease affecting hundreds of millions of people. Cerebral malaria is a type of severe disease with a high mortality rate. However, the causes leading to cerebral malaria, likely including parasite and host factors, are still elusive. Here we discover and investigate a host gene (receptor transporter protein 4 [RTP4]) that can regulate host type I interferon responses and symptoms of experimental cerebral malaria. RTP4 also significantly affects West Nile virus load in the brains of infected mice, but not in the heart and the spleen. This study reveals important roles of RTP4 in antimalarial and antiviral immunity, particularly in brain infection and pathology. RTP4 is a potential target for therapy in some neurological diseases.

RTP4 inhibits IFN-I response and enhances experimental cerebral malaria and neuropathology