Why the study?
Does macrophage maturity and modulation affect viral replication and mortality in Junín virus-infected rats?
Does macrophage maturity and modulation affect viral replication and mortality in Junín virus-infected rats?
Macrophage maturity is essential to inhibit Junín virus replication and confer protection on the adult host.
Does not yet inform Junín virus management; extends preclinical evidence for macrophage maturity limiting replication in rats.
Replication of Junín virus in peritoneal macrophages from newborn rats was greater for prototype strain XJ than for strain XJC13, whereas in cells from adult animals viral multiplication proved minimal. Transfer of peritoneal adherent cells from normal adult to strain XJ-infected newborn rats lowered mortality significantly. Silica blockade of macrophages protected two-day-old strain XJ-infected animals and depressed brain titers of virus significantly, whereas treatment had no effect on strain XJC13-infected rats. Macrophages from infected two-day-old rats caused illness and death in recipient animals. Silica blockade rendered macrophage-mature 11-day-old rats partially susceptible to infection with Junín virus. Thus pathogenicity of strain XJ in the two-day-old rat by the intraperitoneal route depends on the ability to replicate in peritoneal macrophages, whereas strain XJC13 is nonlethal because it fails to multiply efficiently in these cells. Macrophage maturity seems essential to inhibit viral replication and thus confer protection on the adult host.
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Blejer et al. (1986) studied this question.
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