Impact of PRRSV on activation and viability of antigen presenting cells

Abstract

Porcine reproductive and respiratory syndrome (PRRS) is one of the most important diseases of swine industry. The causal agent, PRRS-virus (PRRSV), is able to evade the host immune response and survive in the organism causing transient infections. Despite all scientific efforts, there are still some gaps in the knowledge of the pathogenesis of this disease. Antigen presenting cells (APCs), as initiators of the immune response, are located in the first line of defense against microorganisms, and are responsible for antigen recognition, processing and presentation. Dendritic cells (DCs) are the main type of APC involved in antigen presentation and they are susceptible to PRRSV infection. Thus, PRRSV replication in DCs may trigger off different mechanisms to impair the onset of a host effective immune response against the virus. On the one side, PRRSV may impair the basic functions of DCs by regulating the expression of major histocompatibility complex class II and CD80/86. Other strategy followed by the virus is the induction of cell death of APCs by apoptosis, necrosis or both of them. The impairment and/or cell death of APCs could lead to a failure in the onset of an efficient immune response, as long as cells could not properly activate T cells. Future aspects to take into account are also discussed in this review.

Keywords: Porcine reproductive and respiratory syndrome, Antigen presenting cells, Dendritic cells, Immune response, Major histocompatibility complex class II, CD80/86, Cell death, Apoptosis

Core tip: Porcine reproductive and respiratory syndrome virus (PRRSV) is able to evade the host immune response and survive in the organism causing transient infections. PRRSV interacts with antigen presenting cells, specifically with dendritic cells, causing a regulation of major histocompatibility complex class II and/or CD80/86 and cell death by apoptosis and/or necrosis.