Abstract:
:Flavivirus encephalitis is believed to be the result of two main mechanisms: (i) direct damage to and dysfunction of neurons as a result of viral replication and (ii) destruction of the brain tissue by an inflammatory response. The differential impact of both mechanisms on the progression of flavivirus encephalitis has not been clearly determined. We have now studied the encephalitis caused by Modoc virus (MODV) infection in (i) severe combined immunodeficiency (SCID) mice, (ii) immunocompetent NMRI mice, and (iii) NMRI mice under varying immunosuppressive treatment regimens. In SCID mice, Modoc virus infection proved to be uniformly lethal (100%). The virus replicated extensively in neurons and no signs of inflammation of the brain were observed. In immunocompetent NMRI mice, intranasal (but not intraperitoneal) inoculation with MODV caused severe encephalitis accompanied by a fulminate inflammatory response. When NMRI mice, infected with MODV via the intraperitoneal route, were submitted to a brief immunosuppressive treatment, they also developed encephalitis with an obvious inflammatory component. These animals died significantly earlier than NMRI mice, which received immunosuppressive treatment for a longer period of time. In the latter group, no signs of inflammation of the brain were noted. These models thus allow us to distinguish between the impact of direct viral replication and that of immunological factors in the development of MODV encephalitis, and let us to conclude that (i) replication of the virus in neurons is sufficient to cause fatal encephalitis and (ii) immunological factors contribute significantly to disease progression.
journal_name
J Neuroviroljournal_title
Journal of neurovirologyauthors
Leyssen P,Paeshuyse J,Charlier N,Van Lommel A,Drosten C,De Clercq E,Neyts Jdoi
10.1080/13550280390173319subject
Has Abstractpub_date
2003-02-01 00:00:00pages
69-78issue
1eissn
1355-0284issn
1538-2443pii
D49FLAY42NKE11N3journal_volume
9pub_type
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