Spatiotemporal Analysis of the Population Risk of Congenital Microcephaly in Pernambuco State, Brazilby Alexander et al.
This study emphasizes the burden of microcephaly during the outbreak in Pernambuco, with estimates higher than in some previous studies, and with high risk in an inland region of the state for reasons which are yet to be clarified.
The discovery of the link between ZIKV infection and UPR activation has a broader relevance, since this pathway plays a crucial role in many distinct cellular processes and its induction by ZIKV may account for several reported ZIKV-associated defects.
The association between Zika virus infection and microcephaly in Brazil 2015–2017: An observational analysis of over 4 million birthsby Brady et al.
This study strengthens the evidence that congenital ZIKV infection, particularly in the first 2 trimesters of pregnancy, is associated with microcephaly and less frequently with other birth defects. The finding of no alternative causes for geographic differences in microcephaly rate lead the authors to hypothesize that the Northeast region of Brazil was disproportionately affected by this Zika outbreak, with 94% of an estimated 8.5 million total cases occurring in this region, suggesting a need for seroprevalence surveys to determine the underlying reason.
Exhaustive TORCH Pathogen Diagnostics Corroborate Zika Virus Etiology of Congenital Malformations in Northeastern Brazilby Moreira-Soto et al.
Data from this study support a link between maternal ZIKV infection and congenital malformations and suggest the occurrence of predominantly vector-borne ZIKV transmission in these cases. In addition, some highly prevalent TORCH pathogens may be misinterpreted as representative of ongoing ZIKV activity in the absence of exhaustive diagnostics in northeastern Brazil.
A clinical and histopathological study of malformations observed in fetuses infected by the Zika virusby Beaufrère et al.
The present study reports on the clinical and histopathological findings observed in three fetuses infected by the ZIKV. It emphasizes the severity of brain damages and the minimal visceral and placental changes observed upon ZIKV infection. This confirms the selective neurotropism of ZIKV. Finally, it allows us to describe the cascade of multifactorial developmental defects leading to microcephaly.
In order to understand the mechanism of Zika virus-associated microcephaly, the authors combined analysis of human fetuses infected with Zika virus, cultures of human neuronal stem cells and mice embryos. They showed that ZIKV infection of cortical progenitors controlling neurogenesis triggers a stress in the endoplasmic reticulum in the embryonic brain, inducing signals in response to incorrect protein con-formation.
High Zika Virus Seroprevalence in Salvador, Northeastern Brazil Limits the Potential for Further Outbreaksby Netto et al.
In this article, authors find that the high burden of Zika virus infection in a northeastern Brazilian metropolis questions the fate of the outbreak due to population protective immunity; that Zika virus infection predominantly affects geographic areas with low socioeconomic status, demonstrating a clear link between poverty and Zika virus infection; and, finally, additional evidence for the link between Zika virus infection and microcephaly.
High Zika Virus Seroprevalence in Salvador, Northeastern Brazil Limits the Potential for Further Outbreaks [Press Release]by ZIKAlliance
A study published this week in mBio demonstrates rapid spread of ZIKV in Salvador, a metropolis in northeastern Brazil representing one of the most affected areas during the American ZIKV outbreak, and infection rates exceeding 60%.
Evidence for congenital Zika virus infection from neutralizing antibody titers in maternal sera, north-eastern Brazilby Moreira-Soto et al.
Results from this study suggest that despite the inter-individual variability in immune responses, the magnitude of the maternal ZIKV-specific neutralizing antibody response may prove useful to corroborate congenital ZIKV infection, contributing to reliable estimates of the manifestation index of ZIKV-associated congenital disease. Further studies will be needed to evaluate the time-course of maternal neutralizing antibody responses to identify whether a high maternal PRNT titer can be used as an early marker of congenital infection aiding potential antiviral intervention strategies.
The key message from this study is that the large uncertainty around the risk estimate needs to be further investigated because of a) the possible existence of co-factors that are yet to be validated, b) the assumptions that the authors needed to make in the absence of good data for the proportion of women who were infected during pregnancy.
The results outlined in the article contribute to a better understanding of the ZIKVMTase, a central player in viral replication and host innate immune response, and lay the basis for the development of potential antiviral drugs.
The article concludes that infection with Flaviviridae can increase centrosome numbers and impair spindle positioning, thus potentially contributing to microcephaly in the case of Zika.