Preconceptual Zika virus asymptomatic infection protects against secondary prenatal infection.

Lucien H Turner,Rahul J D'Mello,Giang Pham,Tony T Jiang,Makayla R Braunlin,Tony T Jiang,Adrienne Wilburn,Sing Sing Way,Jeremy M Kinder,Adrienne Wilburn,Ted C Pierson

doi:10.1371/journal.ppat.1006684

Lucien H Turner, Rahul J D'Mello + Show 9 more

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https://doi.org/10.1371/journal.ppat.1006684

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Pregnant women, and their fetal offspring, are uniquely susceptible to Zika virus and other microbial pathogens capable of congenital fetal infection. Unavoidable exposure to Zika virus in endemic areas underscores the need for identifying at-risk individuals, and protecting expecting mothers and their fetal offspring against prenatal infection. Here we show that primary Zika virus asymptomatic infection in mice confers protection against re-infection, and that these protective benefits are maintained during pregnancy. Zika virus recovery was sharply reduced in maternal tissues and amongst fetal concepti after prenatal challenge in mothers with resolved subclinical infection prior to pregnancy compared with mice undergoing primary prenatal infection. These benefits coincide with expanded accumulation of viral-specific antibodies in maternal serum and fetal tissues that protect against infection by the identical or heterologous Zika virus genotype strains. Thus, preconceptual infection primes Zika virus-specific antibodies that confer cross-genotype protection against re-infection during pregnancy.

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The ongoing Zika virus (ZIKV) epidemic has triggered an explosion in cases of fetal death, microcephaly and other birth defects in surviving infants with congenital infection [1,2,3,4]
We show that primary Zika virus asymptomatic infection in mice confers protection against re-infection, and that these protective benefits are maintained during pregnancy
Expecting mothers are uniquely susceptible to Zika virus infection that often spreads to vital tissues of the developing fetus

Summary

Introduction

The ongoing Zika virus (ZIKV) epidemic has triggered an explosion in cases of fetal death, microcephaly and other birth defects in surviving infants with congenital infection [1,2,3,4]. These sequelae usually occur in parallel with higher and more prolonged maternal viremia for up to 15 weeks following prenatal infection [5,6,7,8,9]. Considering ZIKV-associated morbidity is largely confined to infection during pregnancy, there is an urgent need for improved strategies for protecting against congenital fetal invasion and prenatal infection susceptibility. This urgency persists even though several ZIKV candidate vaccines have recently been shown to confer very promising protection in animal infection models [13,14,15,16,17,18,19,20,21], since clinical validation of efficacy and safety, especially with increasingly recognized immunological shifts that physiologically occur during human allogeneic pregnancies, have not been demonstrated

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