Research paperMacrophages and microglia in HSV-1 infected mouse brain
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Cited by (34)
Herpes simplex virus infection causes cellular β-amyloid accumulation and secretase upregulation
2007, Neuroscience LettersModulation of microglia and CD8<sup>+</sup> T cell activation during the development of stress-induced herpes simplex virus type-1 encephalitis
2007, Brain, Behavior, and ImmunityCitation Excerpt :In addition to CD8+ T cells, microglia also have been suggested to play a role in the immune response to HSV-1 within the CNS. For example, following intranasal inoculation with HSV-1, the brains of BALB/c mice demonstrated widespread microglia proliferation (Esiri et al., 1995). In addition, microglia increase their expression of MHC class I and class II molecules following a corneal HSV-1 infection in rats (Song and Jia, 1999; Weinstein et al., 1990).
Herpes-simplex virus encephalitis is characterized by an early MMP-9 increase and collagen type IV degradation
2006, Brain ResearchCitation Excerpt :Other MMPs are also capable of degrading gelatin but recent reports indicate MMP-9 as the main protease involved in disruption of the basement membrane during acute CNS inflammation (Asahi et al., 2001; Lo et al., 2002). In acute HSE, encephalitic lesions are in close vicinity to perivascular infiltrates (Chan et al., 1989) and are characterized by edema, necrosis and petechiae (Esiri et al., 1995). Disruption of the BBB is associated with vasogenic edema, which is caused by the shift of intravascular fluid into the extravascular compartment and accompanied by disturbance of the cerebral microcirculation and metabolic disturbances.
Murine gammaherpesvirus-68 infects microglia and induces high levels of pro-inflammatory cytokine production
2003, Journal of Neuroimmunology