| First Author | Wu B | Year | 2015 |
| Journal | Clin Vaccine Immunol | Volume | 22 |
| Issue | 8 | Pages | 883-95 |
| PubMed ID | 26018534 | Mgi Jnum | J:315397 |
| Mgi Id | MGI:6830335 | Doi | 10.1128/CVI.00170-15 |
| Citation | Wu B, et al. (2015) Herpes Simplex Virus 1 Suppresses the Function of Lung Dendritic Cells via Caveolin-1. Clin Vaccine Immunol 22(8):883-95 |
| abstractText | Caveolin-1 (Cav-1), the principal structural protein of caveolae, has been implicated as a regulator of virus-host interactions. Several viruses exploit caveolae to facilitate viral infections. However, the roles of Cav-1 in herpes simplex virus 1 (HSV-1) infection have not fully been elucidated. Here, we report that Cav-1 downregulates the expression of inducible nitric oxide synthase (iNOS) and the production of nitric oxide (NO) in dendritic cells (DCs) during HSV-1 infection. As a result, Cav-1 deficiency led to an accelerated elimination of virus and less lung pathological change following HSV-1 infection. This protection was dependent on iNOS and NO production in DCs. Adoptive transfer of DCs with Cav-1 knockdown was sufficient to confer the protection to wild-type (WT) mice. In addition, Cav-1 knockout (KO) (Cav-1(-/-)) mice treated with an iNOS inhibitor exhibited significantly reduced survival compared to that of the nontreated controls. We found that Cav-1 colocalized with iNOS and HSV-1 in caveolae in HSV-1-infected DCs, suggesting their interaction. Taken together, our results identified Cav-1 as a novel regulator utilized by HSV-1 to evade the host antiviral response mediated by NO production. Therefore, Cav-1 might be a valuable target for therapeutic approaches against herpesvirus infections. |
