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Effect of silica on virus infections in mice and mouse tissue culture
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.
Insights
Silica injections unexpectedly increased lactic dehydrogenase virus (LDV) and herpes simplex virus (HSV) in mice by causing macrophage proliferation, contrary to expectations of virus elimination. This highlights how silica affects macrophage populations and viral replication dynamics.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Macrophages are key host cells for persistent viruses like lactic dehydrogenase virus (LDV) and herpes simplex virus (HSV).
- Silica is known to induce macrophage death, suggesting a potential method for controlling macrophage-dependent viral infections.
Purpose of the Study:
- To investigate the effect of silica injections on lactic dehydrogenase virus (LDV) titers in mice.
- To understand the underlying mechanisms of silica's impact on macrophage populations and viral replication.
Main Methods:
- Mice were injected with silica, and peritoneal cell counts were analyzed over time.
- LDV and herpes simplex virus (HSV) titers were measured in silica-injected and control mice.
- In vitro experiments assessed silica's effect on macrophages and viral replication.
Main Results:
- Silica injection paradoxically increased LDV titers in vivo due to macrophage proliferation and migration, creating more target cells.
- In vitro, silica damaged macrophages, leading to decreased LDV titers in the absence of cell replenishment.
- Similar recrudescence patterns were observed for HSV, suggesting a broader phenomenon.
Conclusions:
- Silica-induced macrophage damage in vivo can lead to increased viral loads for viruses replicating in these cells.
- The outcome of silica treatment on viral titers depends on the in vivo environment's capacity for macrophage replacement.
- Persistent viruses that multiply in macrophages may experience recrudescence under conditions that promote macrophage proliferation.