Congenital guinea pig infection with attenuated Junin virus strains.

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.

Congenital and perinatal infection with Junin virus in guinea pigs.

Junin virus infection in guinea pigs is known to be similar to human Argentine hemorrhagic fever (AHF). The guinea pig was chosen as a model for transplacental transmission of Junin virus, as both guinea pig and man have a similar placental structure. Pregnant guinea pigs were infected with the pathogenic XJ strain of Junin virus intramuscularly route at different stages of pregnancy. The group infected during the last third of pregnancy produced 16 newborn, but mortality reached 100%: 18% were born with typical AHF hemorrhagic signs, 54% without signs, and the remainder were stillborn. Virus was recovered from organs of newborns, as well as placental tissues. A second group, infected in the second third of pregnancy, died with intrauterine fetuses, all of which showed hemorrhagic signs and virus present. In a last group, infected in the first third of pregnancy, fetuses were free from macroscopic lesions. In order to determine whether lactation may be an alternative infection route in guinea pigs, mother guinea pigs were infected with Junin virus at different times postparturition. The 84% noninfected newborn housed together with their infected mothers died during the suckling period, half with typical AHF signs. Junin virus transmission from mother to fetus was thus proved, and lactation may be considered as an alternative perinatal infection route.