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Elucidating Zika virus immune responses in macaque infants
Infants exposed to Zika virus in utero can develop severe neurological abnormalities after birth. However, little is known about the ability of infants to produce immune responses against Zika virus. Vannella and colleagues followed four asymptomatic nonhuman primate infants that were born to mothers infected with Zika virus during pregnancy. All four produced antiviral immune responses, but these responses did not protect the animals against another Zika virus infection 1 year after birth. Given the similarity of nonhuman primates to humans, these results provide new insights that may apply to the postnatal susceptibility of asymptomatic human offspring born to Zika virus–infected mothers.
Abstract
There is limited information about the impact of Zika virus (ZIKV) exposure in utero on the anti-ZIKV immune responses of offspring. We infected six rhesus macaque dams with ZIKV early or late in pregnancy and studied four of their offspring over the course of a year postpartum. Despite evidence of ZIKV exposure in utero, we observed no structural brain abnormalities in the offspring. We detected infant-derived ZIKV-specific immunoglobulin A antibody responses and T cell memory responses during the first year postpartum in the two offspring born to dams infected with ZIKV early in pregnancy. Critically, although the infants had acquired some immunological memory of ZIKV, it was not sufficient to protect them against reinfection with ZIKV at 1 year postpartum. The four offspring reexposed to ZIKV at 1 year postpartum all survived but exhibited acute viremia and viral tropism to lymphoid tissues; three of four reexposed offspring exhibited spinal cord pathology. These data suggest that macaque infants born to dams infected with ZIKV during pregnancy remain susceptible to postnatal infection and consequent neuropathology.
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