H PRRSV induced up regulation of anti apoptotic genes in infected lungs including the BCL2 related mye loid cell leukemia ref 3 sequence 1, Bcl 2 related protein A1, putative inhibitor of apopto sis, adrenomedullin and IL10, and the down reg ulation of pro apoptotic genes including p53 protein, apoptosis inducing TAF9 like domain 1, apoptosis related protein 1, secreted apoptosis related protein 3 and nucleoside diphosphate kinase homolog 5. These actions of H PRRSV serve to inhibit apoptosis, possibly prolonging the life span of the cell and thereby increasing the yield of pro geny virions. Discussion The results from the present study are in agreement with previous research that demonstrated that H PRRSV infected pigs exhibit severe clinical symptoms including persistent high fever, reddening of the skin, conjunctivi tis, dyspnoea and severe diffuse pulmonary consolidation lesions.

Histopathological examination demon strated robust interstitial pneumonia in the lungs with thickening of alveolar septa accompanied by extensive infiltration of immune cells. The H PRRSV virus replicates prolifically in the lungs, spleen and lym phoid organs. During infection an invading virus is recognized by PRRs that engage PAMPs and trigger sig naling pathways within infected cells that are involved in innate immune and adaptive immune responses. Host immune responses are normally protective but if numerous cells are infected before immune induction, immune mediated destruction can result in severe or fatal pathological consequences.

Glo bal profiling of transcriptional changes occurring in host lungs during H PRRSV viral infection, analyzed using high throughput Solexa sequencing, has provided important information regarding how H PRRSV viruses trigger and regulate host immune responses and cause disease. QPCR assays demonstrated that the H GSK-3 PRRSV virus replicated rapidly and persisted in infected cells. Substantial viral antigen was detected in alveolar cells and bronchiolar epithelial cells. The ability of a virus to induce and sustain an infection depends partly on its ability to block host innate immune responses or to modulate the activity of antiviral effector proteins. Production of type I IFN is an innate antiviral immune reac tion in virus infected cells that prevents viral replication and restricts the spread of the virus to neighboring cells. However, the present study demonstrated that H PRRSV infection suppressed production of SPI IFN and down regulated expression of IFN a. Pre vious in vitro and in vivo studies have demon strated that PRRSV infection results in minimal IFN a production or suppresses its production, and IFN a has been shown to inhibit PRRSV replication.