The heterogeneity in the immune response and efficiency of viral dissemination in brain infected with herpes simplex virus type 1 through peripheral or central route

Abstract

Using immunohistochemistry on adjacent brain sections, we studied the correlation between the dissemination of the virus, the inflammatory responses and the expression of major histocompatibility complex (MHC) proteins in rat brain infected with herpes simplex virus (HSV-1) F strain by either corneal scarification or intracerebral injection. Our results showed that the mortality of the corneally infected rats was much higher than that of the intracerebrally infected rats, due to a more extensive dissemination of the virus in the brain, particularly in the brain stem. The inflammatory responses were similar in brains infected through either route, as demonstrated by the expression of MHC I/II antigens on infiltrating lymphocytes, leukocytes and macrophage/microglia cells. While there was strong immunoreactivity for HSV-1 antigens in the cerebral cortex, the infiltrates were only located in subcortical areas, especially the hippocampus. Therefore, the distribution of these immune cells did not always overlap with the regions of viral infection. These results suggest that HSV-1 disseminate more efficiently from the peripheral to the central nervous system (CNS) than from CNS to CNS, which is independent of the immune responses, and that the cerebral cortex may immunologically respond to HSV-1 infection differently from other brain regions.

Injection of the sciatic nerve with TMEV: A new model for peripheral nerve demyelination

“…Studies utilizing poliovirus (Solomon & Willison, 2003;Sabin & Ward, 1941;Sabin, 1956), herpes simplex virus (Hemachudha, Wacharapluesadee et al, 2005;Faber, Pulmanausahakul et al, 2004;Song & Jia, 1999;Fujiki & Tashiro, 1997), and rabies virus (Hemachudha, Wacharapluesadee et al, 2005;Faber, Pulmanausahakul, Nagao et al, 2004) have shown that virus can be transported to the CNS during viral replication following infection of the PNS. We therefore asked whether TMEV was also capable of spreading from the PNS to the CNS following direct injection of the sciatic nerve.…”

Inflammation and viral infection as disease modifiers in schizophrenia

“…In non-replicating neurons, this stalled pro-and anti-inflammatory action can be advantageous since lytic infection and latency is forestalled. In replicating cells, the virus can be transmitted after division to both daughter cells by peripheral and central routes ( 97 ) and may remain indefinitely due to ineffective clearance by surrounding T-cells and the ambiguity of the immunological response ( 98 ). Neurogenesis occurs in ependymal cells ( 99 ) and this process is impaired in schizophrenia ( 11 ) in association with elevated PVM cell CD163 expression ( 8 ).…”