Chemokine receptor Ccr7 restricts fatal west nile virus encephalitis

Susana V. Bardina, Julia A. Brown, Daniela Michlmayr, Kevin W. Hoffman, Janet Sum, Alexander G. Pletnev, Sergio A. Lira, Jean K. Lim

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


West Nile virus (WNV) is a mosquito-transmitted flavivirus that can cause debilitating encephalitis. To delineate the mechanisms behind this pathology, we studied Ccr7-deficient mice, which afforded us the capacity to study infection in mice with disrupted peripheral cellular trafficking events. The loss of Ccr7 resulted in an immediate pan-leukocytosis that remained elevated throughout the infection. This leukocytosis resulted in a significant enhancement of leukocyte accumulation within the central nervous system (CNS). Despite an excess of virus-specific T cells in the CNS, Ccr7-deficient mice had significantly higher CNS viral loads and mortality rates than wild-type animals. Mechanistically, the elevated trafficking of infected myeloid cells into the brain in Ccr7-deficient mice resulted in increased levels of WNV in the CNS, thereby effectively contributing to neuroinflammation and lowering viral clearance. Combined, our experiments suggest that during WNV infection, Ccr7 is a gatekeeper for nonspecific viral transference to the brain.

Original languageEnglish
Article numbere02409-16
JournalJournal of Virology
Issue number10
StatePublished - 1 May 2017


  • Arbovirus
  • Cell trafficking
  • Chemokine receptors
  • Chemokines
  • Hostpathogen interactions
  • Leukocytes
  • Neuroimmunology
  • Viral pathogenesis


Dive into the research topics of 'Chemokine receptor Ccr7 restricts fatal west nile virus encephalitis'. Together they form a unique fingerprint.

Cite this