Abstract
Confirming ZIKV congenital infection is challenging because viral RNA is infrequently detected. We compared the presence of anti-ZIKV-IgM and the persistence of anti-ZIKV-IgG antibodies over 18 months in two cohorts of infants born to ZIKV-infected mothers: Cohort one: 30 infants with typical microcephaly or major brain abnormalities (Congenital Zika Syndrome-CZS); Cohort two: 123 asymptomatic infants. Serum samples obtained within 6 months of age were tested for anti-ZIKV-IgM. Anti-ZIKV-IgG was quantified in sequential samples collected at birth, 3–6 weeks, 3, 6, 12, and 18 months. ZIKV-RNA was never detected postnatally. Anti-ZIKV-IgM antibodies were detected at least once in 15/25 (60.0%; 95%CI: 38.7–78.9) infants with CZS and in 2/115 (1.7%; 95%CI: 0.2–6.1) asymptomatic infants. Although anti-ZIKV-IgG was always positive within 3–6 weeks of age, IgG levels decreased similarly over time in both cohorts. IgG levels decreased similarly in ZIKV-IgM-positive and ZIKV-IgM-negative CZS infants. Differently from other congenital infections, IgM would fail to diagnose 40% of severely symptomatic infants, and the persistence of IgG is not a useful marker for discriminating congenital infection among infants exposed to maternal ZIKV infection.
Highlights
This study was embedded in the Natural History of Zika Virus Infection in Gestation (NATZIG) project, which is a prospective population-based cohort study undertaken in the Ribeirão Preto region, Northeastern São Paulo State, Brazil [2]
Birth weight (2694 g versus 3101 g) and head circumference (28.3 cm versus 33.4 cm) were consistently lower in Congenital Zika Syndrome (CZS) infants compared to asymptomatic ones
All infants classified as CZS had major detectable neurologic abnormalities
Summary
The most well-known consequences of the intrauterine transmission of Zika virus (ZIKV) infection from mother to fetus are microcephaly and related severe brain abnormalities with neurological effects, defined as Congenital Zika Syndrome (CZS) [1]. As with other congenital infections, the ZIKV might have a broad clinical spectrum [2,3,4]. Overall, considering estimates of a 20–30% vertical transmission rate [4] and the reported estimates of pregnancy losses (4–7%) and congenital disabilities characterized by CZS (5–14%) [5], one could suppose that up to 10% of infants born to ZIKV-infected mothers would be infected but clinically inapparent, limiting the identification of the virus [2]. Since the primary targets of ZIKV infection are mainly the central nervous system and eyes, infected infants without severe end-organ disease are most likely to benefit from long-term follow-up and the prevention of developmental delays by stimulation and rehabilitation
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