| First Author | Zhong C | Year | 2012 |
| Journal | Cell Death Differ | Volume | 19 |
| Issue | 5 | Pages | 882-90 |
| PubMed ID | 22139131 | Mgi Jnum | J:203610 |
| Mgi Id | MGI:5527523 | Doi | 10.1038/cdd.2011.178 |
| Citation | Zhong C, et al. (2012) Granzyme K inhibits replication of influenza virus through cleaving the nuclear transport complex importin alpha1/beta dimer of infected host cells. Cell Death Differ 19(5):882-90 |
| abstractText | The influenza A virus is a causative agent of influenza, which infects human cells and uses host factors to accomplish viral genome replication as part of its life cycle. The nucleoprotein (NP) and PB2 of the influenza virus associate with importin alpha1 to gain access to the host nucleus through a ternary import complex. Killer cell-mediated cytotoxicity is the primary mechanism of eliminating the influenza virus. Here, we showed that lymphokine-activated killer cells participated in the elimination of the influenza virus. Granzyme (Gzm) K inhibition elevated viral replication in vitro and aggravated viral infection in vivo. We identified that importin alpha1 and its transport partner protein importin beta are physiological substrates of GzmK. Proteolysis of these two substrates wrecked their association to generate the importin alpha1/beta dimer and disrupted transportation of viral NP to the nucleus, leading to inhibition of influenza virus replication. |
