Location: Virus and Prion ResearchTitle: Effect of porcine reproductive and respiratory syndrome virus infection of porcine alveolar macrophages on Toll-like receptors elicitation of type I interferon responses) Author
Submitted to: Clinical and Vaccine Immunology
Publication Type: Peer reviewed journal
Publication Acceptance Date: 1/6/2009
Publication Date: 3/1/2009
Citation: Miller, L.C., Lager, K.M., Kehrli, Jr., M.E. 2009. Role of Toll-Like Receptors in Activation of Porcine Alveolar Macrophages by Porcine Reproductive and Respiratory Syndrome Virus. Clinical and Vaccine Immunology. 16(3):360-365. Interpretive Summary: The pig respiratory virus, porcine reproductive and respiratory syndrome virus (PRRSV), causes highly significant losses to the swine industry worldwide. The ability of the virus to persist in its host shows that it has mechanisms to evade host immune response. The type I interferon system is an essential component of the host antiviral response. In this study, we investigated whether PRRSV suppressed the ability of a certain type of the pig’s immune cells to activate important aspects of the host immune response. We found that PRRSV infection appears to suppress important aspects of host immunity which suggests that may contribute to the ability of PRRSV to establish persistent infections in pigs.
Technical Abstract: Control of virus replication initially depends on rapid activation of the innate immune responses. Toll-like receptor (TLR) ligands are potent inducers of innate immunity against viral infections. Porcine reproductive and respiratory syndrome virus (PRRSV) initiates infection in pulmonary alveolar macrophages (PAMs), elicits weak immune responses, and establishes a persistent infection. To understand the role of ssRNA and dsRNA intermediates in eliciting host immunity, we sought to determine if Toll-like receptors (TLRs), particularly those that respond to viral molecular patterns, are involved in PRRSV infection. Activation of TLR-3 in PAMs with dsRNA, increased gene expression for interferon-a and suppressed PRRSV infectivity. In contrast, treating PAMs with LPS for TLR-4 did not influence PRRSV infectivity.