Abstract
Silica injections of mice have been reported to kill macrophages, thus allowing herpes simplex virus (HSV) to spread rapidly and leading to an increased severity of HSV infection. Thus, silica presumably could be used to eliminate lactic dehydrogenase virus (LDV) (a model for slow viruses), which is known to multiply exclusively in macrophages. Contrary to expectation, it was found that the LDV titers were increased in silica-injected mice as compared to the titers in control mice. Counts of peritoneal cells at different periods after silica injection showed that silica-induced macrophage damage in vivo resulted in proliferation and migration of macrophages, thus providing additional target cells for LDV replication and leading to high LDV titers. In vitro, silica ingestion also damaged the macrophages, but since no replacement of cells could occur by infiltration, decreased LDV titers were found. Similar findings were obtained with HSV. It is suggested that all persistent viruses multiplying in macrophages will show a similar recrudescence under comparable conditions.
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