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Published: 05 December 2016

In:

Science 

Author:

Gretchen Vogel

It may have sounded like good news. Two weeks ago, the World Health Organization (WHO) announced that the Zika epidemic was no longer a Public Health Emergency of International Concern, a designation reserved for acute threats that Zika received in February. WHO’s downgrade came after several months of dropping case numbers.

But as the agency was keen to point out, the change just means that Zika has evolved from a cross-border emergency to another long-term public health challenge that needs the world’s attention. The virus is now firmly entrenched in Latin America, which is already battling several other mosquito-borne diseases.

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Published: 17 November 2016

In:

The Journal of Experimental Medicine

Authors:

Shahzada Khan, Erik M. Woodruff, Martin Trapecar, Krystal A. Fontaine, Ashley Ezaki, Timothy C. Borbet, Melanie Ott, Shomyseh Sanjabi

Abstract

Understanding the host immune response to vaginal exposure to RNA viruses is required to combat sexual transmission of this class of pathogens. In this study, using lymphocytic choriomeningitis virus (LCMV) and Zika virus (ZIKV) in wild-type mice, we show that these viruses replicate in the vaginal mucosa with minimal induction of antiviral interferon and inflammatory response, causing dampened innate-mediated control of viral replication and a failure to mature local antigen-presenting cells (APCs). Enhancement of innate-mediated inflammation in the vaginal mucosa rescues this phenotype and completely inhibits ZIKV replication. To gain a better understanding of how this dampened innate immune activation in the lower female reproductive tract may also affect adaptive immunity, we modeled CD8 T cell responses using vaginal LCMV infection. We show that the lack of APC maturation in the vaginal mucosa leads to a delay in CD8 T cell activation in the draining lymph node and hinders the timely appearance of effector CD8 T cells in vaginal mucosa, thus further delaying viral control in this tissue. Our study demonstrates that vaginal tissue is exceptionally vulnerable to infection by RNA viruses and provides a conceptual framework for the male to female sexual transmission observed during ZIKV infection.

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Published: 23 November 2016

In:

Morbidity and Mortality Weekly Report (MMWR)

Authors:

Vanessa van der Linden, MD; André Pessoa, MD; William Dobyns, MD; A. James Barkovich, MD; Hélio van der Linden Júnior, MD; Epitacio Leite Rolim Filho, MD, PhD; Erlane Marques Ribeiro, MD, PhD; Mariana de Carvalho Leal, MD, PhD; Pablo Picasso de Araújo Coimbra, MD; Maria de Fátima Viana Vasco Aragão, MD, PhD; Islane Verçosa, MD; Camila Ventura, MD, PhD; Regina Coeli Ramos, MD; Danielle Di Cavalcanti Sousa Cruz, MD; Marli Tenório Cordeiro, PhD; Vivian Maria Ribeiro Mota; Mary Dott, MD; Christina Hillard, MA; Cynthia A. Moore, MD, PhD

Congenital Zika virus infection can cause microcephaly and severe brain abnormalities (1). Congenital Zika syndrome comprises a spectrum of clinical features (2); however, as is the case with most newly recognized teratogens, the earliest documented clinical presentation is expected to be the most severe. Initial descriptions of the effects of in utero Zika virus infection centered prominently on the finding of congenital microcephaly (3). To assess the possibility of clinical presentations that do not include congenital microcephaly, a retrospective assessment of 13 infants from the Brazilian states of Pernambuco and Ceará with normal head size at birth and laboratory evidence of congenital Zika virus infection was conducted. All infants had brain abnormalities on neuroimaging consistent with congenital Zika syndrome, including decreased brain volume, ventriculomegaly, subcortical calcifications, and cortical malformations. The earliest evaluation occurred on the second day of life. Among all infants, head growth was documented to have decelerated as early as 5 months of age, and 11 infants had microcephaly. These findings provide evidence that among infants with prenatal exposure to Zika virus, the absence of microcephaly at birth does not exclude congenital Zika virus infection or the presence of Zika-related brain and other abnormalities. These findings support the recommendation for comprehensive medical and developmental follow-up of infants exposed to Zika virus prenatally. Early neuroimaging might identify brain abnormalities related to congenital Zika infection even among infants with a normal head circumference (4).

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Published: 16 November 2016

In: 

Rapid Risk Assessment - European Centre for Disease Prevention and Control

Conclusions and options for response

European Union/European Economic Area (EU/EEA) Member States should consider a range of mitigation
measures regarding the Zika virus epidemic due to:

- the current circulation of Zika virus on several continents
- the evidence of an association between Zika virus infection during pregnancy and congenital
malformations of the central nervous system (CNS)
- the association between Zika virus infection and Guillain–Barré syndrome (GBS)
- the risk of local vector-borne transmission in Europe in areas where potential vectors are still active (e.g. Madeira) during the 2016 autumn season; in the continental EU, the risk of local vector-borne transmission will decrease in the coming months because the season for Zika virus transmission by vectors will become unfavourable
- the possibility of sexual transmission from returning travellers
- the risk of Zika virus transmission via substances of human origin (SoHO).
The options for risk reduction and the definitions below are based on the current evidence, which take into
account current uncertainties. These are subject to change as new evidence emerges.

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