Volume 23, Issue 2
  • ISSN: 0002-9637
  • E-ISSN: 1476-1645



A suitably timed pre-existing infection greatly enhanced the intracerebral replication and mortality of peripherally inoculated Japanese B encephalitis (JBE) virus in mice. This increased mortality was associated with a decreased survival time and the effect was maximal when virus challenge occurred 7 days following infection with , and was absent by 21 days following helminthic infection. Titration of mouse sera and brains indicated that the increased virulence was paralleled by great increases in the ability of JBE virus to replicate in central nervous system (CNS) tissues. No evidence of increased duration or magnitude of JBE viremia was observed in -infected mice at any time. JBE virus killed normal and -infected mice equally upon intracerebral inoculation. It is suggested that infection may provide new routes of access for JBE virus into CNS tissues, or that the parasitic infection abrogates the host defense mechanism which normally aborts JBE virus replication in the brain. The applicability of these results to man is discussed.


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