Abstract
Guinea pigs born from mothers infected before or during pregnancy with 10(3) PFU of the attenuated XJC13 or XJ0 strains of Junin virus (JV) by the intramuscular route showed 31.5% mortality that was not attributable to the mothers' clinical condition or to lack of care. There was a slight drop in mortality rate when the mothers were infected at the beginning or end of their gestation period. JV isolation from the 9 offspring killed from 1 to 125 days of age proved that virus transmitted transplacentally or soon after birth was able to persist, although titers were not higher than 10(2.7) PFU/g of tissue in various organs, including brain. Cell-associated viremia could thus account for viral spread after birth. Since an active humoral response was detected in the same animals, although Nt antibody titers were below 1:16, a state of tolerance did not exist in these congenitally infected animals. The carrier state appeared to modify guinea pig susceptibility to JV; after challenge with the pathogenic XJ strain of JV, 2 animals survived and developed normal humoral responses, while half of the remaining animals did not show typical signs of Argentine hemorrhagic fever. Although JV persistence appeared to cause no deleterious effects in surviving guinea pigs, its long-term risk remains to be determined.
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