Activation and cell death in human dendritic cells infected with Nipah virus

• NiV replicates at low levels in DCs.
• NiV infection induces the expression proinflammatory cytokines.
• NiV infection partially activates and induces apoptosis in DCs.
• DCs infected by NiV unable to prime CD4 and CD8 T cells and undergo cell death.
• Interestingly, DCs treated with inactivated NiV also show signs of apoptosis.

Nipah virus (NiV) is a highly pathogenic paramyxovirus that causes pulmonary disease and encephalitis in humans with 40–70% fatality. Interactions between NiV and the human immune system remain poorly understood. Here, we demonstrate the effects of NiV infection on DC and T cell function. Using an in vitro system, we found that NiV infects and replicates at low levels in DCs and induces the expression of TNF-α, IL-1α, IL-1β, IL-8, and IP-10. NiV infection activates DCs, and upregulates the expression of CD40, CD80, and CD86. Also have reduced levels of bcl2 and high levels of active caspase 3, suggesting the induction of apoptosis. DCs infected by NiV are unable to efficiently prime CD4 and CD8 T cells, but instead induce apoptosis in T cells. Interestingly, DCs treated with inactivated NiV also show signs of apoptosis. These findings indicate that NiV infected DCs could play an important role in NiV pathogenesis.