Background:
Zika virus infection during pregnancy has been recently
associated with congenital microcephaly and other severe neural tube
defects. However, the magnitude of confirmed cases and the scope of
these anomalies have not been extensively documented. This review
focuses on the magnitude of laboratory-confirmed congenital Zika virus
cases among probable cases and describing the patterns of congenital
anomalies allegedly caused by the Zika virus, information which will
inform further research in this area. Methods: We conducted a
literature search for English-language articles about congenital Zika
virus infection using online electronic databases (PubMed/MEDLINE,
POPLINE, Embase, Google Scholar, and Web of Knowledge). The search terms
used were, “zika”, “pregnancy”, [year], “microcephaly”, “infants”,
“children”, “neonates”, “foetuses”, “neural tube defect”, and “CNS
manifestations” in different combinations. All articles reporting cases
or case series between January 2015 and December 2016 were included.
Data were entered into a Microsoft Excel database and analysed to obtain
proportions of the confirmed cases and patterns of anomalies.
Results: A total of 24
articles (11 case series, 9 case reports, and 4 others) were found to be
eligible and included in this review. These articles reported 919 cases,
with or without microcephaly, presumed to have congenital Zika virus
infection. Of these cases, 884 (96.2%) had microcephaly. Of the 884
cases of microcephaly, 783 (88.6%) were tested for Zika virus infection,
and 216 (27.6%; 95% confidence interval, 24.5% to 30.8%) were confirmed
to be Zika virus-positive. In addition to microcephaly, other common
abnormalities reported – out of 442 cases investigated – were
calcifications of brain tissue (n=240, 54.3%), ventriculomegaly (n=93,
20.8%), cerebellar hypoplasia (n=52, 11.7%), and ocular manifestations
(n=46, 10.4%). Conclusion:
Based on the available literature, Zika virus infection
during pregnancy might lead to a wide array of outcomes other than
microcephaly. There is a need for more epidemiological studies in
Zika-endemic areas, particularly in Africa, to ascertain the role of
Zika virus in causing congenital neurological
defects.
IL-27 signaling activates skin cells to induce innate antiviral proteins and protects against Zika virus infection