Fig. 3.

Summary of pathogens and their interactions with the choroid plexus. (Hydrocephalus) Inflammation can cause obstruction of CSF flow from the lateral ventricles leading to increased intraventricular pressure. Ventricular hemorrhage and infection can induce inflammation dependent hypersecretion of CSF, promoting hydrocephalus. The hypersecretion occurs via TLR4-NF-κB and the NKCC1 transporter. (ZIKA) The ZIKA virus is shown to preferentially infect pericytes within the CP. This infection precedes CSF and brain invasion—the mechanism of transmigration unknown. Depending on the developmental stage, neural progenitor cells may be exposed to the CSF and thus susceptible to infection. (JC Virus) During the lytic phase, JC virus may disseminate hematogenously to the CP or possibly by B cells. The CP epithelial cells express viral receptors and are susceptible to infection. Extracellular vesicles secreted by the CP into the CSF can contain JC virion and transport these to glia in the brain. (HIV) HIV can be found within the CP, which may act as a reservoir for viral replication. Phylogenetic analysis indicates distinct clustering of HIV in the brain and spleen, whereas the CP contains virus from both clusters. This suggests there is unique selective pressure within the CP towards CNS tropism of HIV. FIV is capable of transmigrating across the BCSFB. (Borrelia burgdorferi) CSF findings indicate increased inflammatory cytokines, lymphocytic pleocytosis, and Bb. Infection of CP epithelial cells with Bb induce an increase in secretion of inflammatory and chemotactic cytokines, as well as the downregulation of junctional proteins. (SARS-CoV-2) Early findings suggest that viral presence in CNS is rare but neurological complications more common, characterized by increased cytokines and lymphocytes in the CSF. The CP expresses binding receptors for viral fusion. The CP may provide a route of entry for SARS-CoV-2 in rare circumstances, or more likely, relay inflammatory signaling to the CNS. Created with BioRender.com