Abstract
Absent in melanoma 2 (AIM2) inflammasome is a multiprotein complex which plays a pivotal role in the host immune response to multiple pathogens. The role of AIM2 in human cytomegalovirus (HCMV) infection is poorly studied. Thus, using a small inference RNA (siRNA) approach and THP-1 derived macrophage cells infected with HCMV AD169 strain, we investigated the impact of HCMV infection on AIM2-mediated molecular events. Compared to wild-type cells, AIM2-defiecient macrophages showed a limited ability to activate caspase-1, process IL-1β, and induce cell death. In addition, AIM2-defiecient cells were unable to efficiently control HCMV infection, as the transcription of virus DNA polymerase gene UL54 and major tegument protein gene UL83 were higher compared to wild-type cells. In conclusion, HCMV infection induces an AIM2 inflammasome response, which negatively influences viral life cycle.
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