Abstract
Guinea pigs infected by the peripheral route with the XJ pathogenic strain of Junin virus showed viscerotropism mainly in reticulo-phagocytic rich organs. By immunofluorescence, heavy infection of reticular-phagocytic cells was demonstrated, supporting the leading role of these cell types. Absence of neurotropism was demonstrated by the inability to recover infectious virus, as well as the absence of antigens, immunoglobulins, or 3rd component of complement deposits, in cells, vessels, or meninges. The correlation between infectivity and antigen expression observed in organs, and the absence of evidence of immunopathologic mechanisms, strongly suggest a direct viral effect in these experimental conditions. The results show that infection of guinea pigs by the peripheral route is an adequate model for human Argentine hemorrhagic fever with the exception of central nervous system involvement. Comparisons are made with infections produced in guinea pigs by attenuated strains, as well as with the disease in primates and humans.
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