Bovine viral diarrhea virus actively replicate in bovine monocyte-derived dendritic cells and use them as viral reservoirs

CAPOZZO AV, FRANCO-MAHECHA OL, CZEPLUCH W, CARODOSO N AND GRIGERA PR

Milan

Conferencia; Front. Immunol. Conference Abstract: 15th International Congress of Immunology (ICI).; 2013

15th International Congress of Immunology (ICI)

Bovine viral diarrhea virus (BVDB) causes immune-suppression and persists in the host for long periods of time. The mechanisms underlying these behaviors have not been completely elucidated. The aim of this work was to study the interaction between BVDV (Type 1, cp) and bovine DC. Bovine DC-CD11b+ were differentiated in culture from purified CD14+ peripheral-blood monocytes and treated with infectious or inactivated virus for one hour, in the presence or absence of specific antibodies. Pre-incubation with anti E2 antibodies complete block DC infection. In the absence of anti E2 antibodies, the virus infected and rapidly replicated in DC. Negative strand RNA and viral non-structural protein NS3 were detected as soon as 3 hours post-infection. Extracellular virus increased 2 logs/IDTC50 titers in 6 hours. Infection down-regulated the expression of MHC-I, II and co-stimulatory molecules, that were not recovered by treating with mitogens. Synthesis of pro-inflammatory cytokines was not impaired. Infected DC were also unable to present FMDV antigens to T-cells. Infected DC remained inactivated and did not undergo apoptosis. The ability of BVDV to actively replicate in DC, keeping them alive and arrested in an immature state could be an evidence of a mechanism of the virus to evade the immune system while mantaining persistent infections. It may also explain the complete lack of adaptive responses observed in cattle up to three weeks post infection.