Molecular Characterization of Transcriptome-wide Interactions between Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus and Porcine Alveolar Macrophages in vivo

Zhou, Ping; Zhai, Shanli; Zhou, Xiang; Lin, Ping; Jiang, Tengfei; Hu, Xueying; Jiang, Yunbo; Wu, Bin; Zhang, Qingde; Xu, Xuewen; Li, Jin-ping; Liu, Bang

The results of this study showed that Tongcheng piglets exhibited typical clinical signs following infection with HP-PRRSV WUH3 strain. The lung damage caused by the infection was regional and mild at 5 and 7 dpi ( Figure 1C and D), but further observation for a longer period of time was not performed in this study. The slow reproduction rate of the virus (viremia) at 3 to 7 dpi ( Figure 1B ) suggested a near balance between the viral replication and the defense mechanisms in the PAMs. Transcriptomic analysis of the PAMs at 5 dpi identified 321 DE genes under the filter of 1.5-fold change, and the number of upregulated genes (219) was greater than that of downregulated genes (102). In comparison, an in vitro transcriptomic analysis of PAMs revealed that only small numbers (no more than 100) of DE genes (threshold of 1.5-fold change) were identified at 1 to 12 hours post PRRSV infection, and the overall effect of PRRSV on the host transcription machinery was downegulation [8] . It is not sure whether there is a conversion of the overall effect of PRRSV on host transcription machinery from downregulation to upregulaton as time goes on, or the change is only the effect of the difference between in vitro and in vivo assays. As compared with the number of DE genes in this study, some thousands of DE genes (threshold of almost 1.5-fold change) were identified in lung tissues at 4 and 7 dpi following both PRRSV and HP-PRRSV infection, by high-throughput deep sequencing assays [6, 7] . This great number of DE genes might result from the huge amount of data obtained by the deep-sequencing method and from the many cell types in lung tissues.