| First Author | Licon Luna RM | Year | 2002 |
| Journal | J Virol | Volume | 76 |
| Issue | 7 | Pages | 3202-11 |
| PubMed ID | 11884544 | Mgi Jnum | J:126472 |
| Mgi Id | MGI:3761407 | Doi | 10.1128/JVI.76.7.3202-3211.2002 |
| Citation | Licon Luna RM, et al. (2002) Lack of both Fas ligand and perforin protects from flavivirus-mediated encephalitis in mice. J Virol 76(7):3202-11 |
| abstractText | The mechanism by which encephalitic flaviviruses enter the brain to inflict a life-threatening encephalomyelitis in a small percentage of infected individuals is obscure. We investigated this issue in a mouse model for flavivirus encephalitis in which the virus was administered to 6-week-old animals by the intravenous route, analogous to the portal of entry in natural infections, using a virus dose in the range experienced following the bite of an infectious mosquito. In this model, infection with 0.1 to 10(5) PFU of virus gave mortality in approximately 50% of animals despite low or undetectable virus growth in extraneural tissues. We show that the cytolytic effector functions play a crucial role in invasion of the encephalitic flavivirus into the brain. Mice deficient in either the granule exocytosis- or Fas-mediated pathway of cytotoxicity showed delayed and reduced mortality. Mice deficient in both cytotoxic effector functions were resistant to a low-dose peripheral infection with the neurotropic virus. |
