Abstract:
:Infection of mice with the flaviviruses West Nile virus (WNV) and Murray Valley encephalitis (MVE) induces cytolytic T-cell responses which are highly cross-reactive on target cells infected with heterologous flaviviruses. Of C57BL/6 mice infected with low doses (10(2)-10(6) PFU) of either virus, 30-40% develop encephalitis and die within 10-12 days. Mice with defects in the Fas or granule exocytosis (perforin and granzymes A and B) pathway of cellular cytotoxicity display reduced mortality and increased survival time when infected with MVE and are protected from encephalitis when deficient in both pathways. This contrasts with infection with WNV where defects in these cytolytic mechanisms increase the percentage of mice that succumb to encephalitis. Thus, no generalizations as to protective or detrimental effects of cytolytic effector functions in recovery from closely related flavivirus infections can be made. Virus-host immune interactions have to be assessed individually and cannot be generalized.
journal_name
Immunol Cell Bioljournal_title
Immunology and cell biologyauthors
Wang Y,Lobigs M,Lee E,Müllbacher Adoi
10.1046/j.0818-9641.2004.01227.xsubject
Has Abstractpub_date
2004-04-01 00:00:00pages
170-3issue
2eissn
0818-9641issn
1440-1711pii
ICB1227journal_volume
82pub_type
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