| First Author | Maruzuru Y | Year | 2018 |
| Journal | Cell Host Microbe | Volume | 23 |
| Issue | 2 | Pages | 254-265.e7 |
| PubMed ID | 29447697 | Mgi Jnum | J:272685 |
| Mgi Id | MGI:6284966 | Doi | 10.1016/j.chom.2017.12.014 |
| Citation | Maruzuru Y, et al. (2018) Herpes Simplex Virus 1 VP22 Inhibits AIM2-Dependent Inflammasome Activation to Enable Efficient Viral Replication. Cell Host Microbe 23(2):254-265.e7 |
| abstractText | The AIM2 inflammasome is activated by DNA, leading to caspase-1 activation and release of pro-inflammatory cytokines interleukin 1beta (IL-1beta) and IL-18, which are critical mediators in host innate immune responses against various pathogens. Some viruses employ strategies to counteract inflammasome-mediated induction of pro-inflammatory cytokines, but their in vivo relevance is less well understood. Here we show that the herpes simplex virus 1 (HSV-1) tegument protein VP22 inhibits AIM2-dependent inflammasome activation. VP22 interacts with AIM2 and prevents its oligomerization, an initial step in AIM2 inflammasome activation. A mutant virus lacking VP22 (HSV-1DeltaVP22) activates AIM2 and induces IL-1beta and IL-18 secretion, but these responses are lost in the absence of AIM2. Additionally, HSV-1DeltaVP22 infection results in diminished viral yields in vivo, but HSV-1DeltaVP22 replication is largely restored in AIM2-deficient mice. Collectively, these findings reveal a mechanism of HSV-1 evasion of the host immune response that enables efficient viral replication in vivo. |
