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      State by state implementation of Zika virus testing guidance in the United States in 2017 and 2018

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          Abstract

          In 2015 and 2016, outbreaks of the Zika virus began occurring in the Americas and the Caribbean. Following the introduction of this new threat, the United States’ Centers for Disease Control and Prevention (CDC) issued testing guidance for the nation’s state public health laboratories. We collected and analyzed testing guidance for all fifty states and the District of Columbia for both 2017 and 2018. In both years, state testing guidance was consistent for men and non-pregnant women, but there was notable variation in guidance for pregnant women. In addition, there were changes between the two years as testing algorithms shifted toward guidance that recommended testing in more limited circumstances. States adopted large, or complete, portions of CDC testing guidance, but were not required to conform completely, 33% of states had identical guidance in 2017 and 49% in 2018. Some of these trends, such as specifying that testing be contingent on travel, or sexual contact with an individual who has recently traveled, to an area where the Zika virus was circulating, presents a potential deficiency in the United States surveillance capacity. Understanding variations in state testing guidance enables public health professionals to better understand ongoing surveillance. This analysis provides insight into the testing practices for the various states across the country. Better understanding of how states approach Zika testing, and how that testing changes over time, will increase the public health community’s ability to interpret future Zika case counts.

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          First report of autochthonous transmission of Zika virus in Brazil

          In the early 2015, several cases of patients presenting symptoms of mild fever, rash, conjunctivitis and arthralgia were reported in the northeastern Brazil. Although all patients lived in a dengue endemic area, molecular and serological diagnosis for dengue resulted negative. Chikungunya virus infection was also discarded. Subsequently, Zika virus (ZIKV) was detected by reverse transcription-polymerase chain reaction from the sera of eight patients and the result was confirmed by DNA sequencing. Phylogenetic analysis suggests that the ZIKV identified belongs to the Asian clade. This is the first report of ZIKV infection in Brazil.
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            Genomic epidemiology reveals multiple introductions of Zika virus into the United States

            Zika virus (ZIKV) is causing an unprecedented epidemic linked to severe congenital syndromes 1,2 . In July 2016, mosquito-borne ZIKV transmission was reported in the continental United States and since then, hundreds of locally-acquired infections have been reported in Florida 3,4 . To gain insights into the timing, source, and likely route(s) of ZIKV introduction, we tracked the virus from its first detection in Florida by sequencing ZIKV genomes from infected patients and Aedes aegypti mosquitoes. We show that at least four introductions, but potentially as many as 40, contributed to the outbreak in Florida and that local transmission likely started in the spring of 2016 - several months before initial detection. By analyzing surveillance and genetic data, we discovered that ZIKV moved among transmission zones in Miami. Our analyses show that most introductions are linked to the Caribbean, a finding corroborated by the high incidence rates and traffic volumes from the region into the Miami area. Our study provides an understanding of how ZIKV initiates transmission in new regions.
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              Teratogenic effects of the Zika virus and the role of the placenta.

              The mechanism by which the Zika virus can cause fetal microcephaly is not known. Reports indicate that Zika is able to evade the normal immunoprotective responses of the placenta. Microcephaly has genetic causes, some associated with maternal exposures including radiation, tobacco smoke, alcohol, and viruses. Two hypotheses regarding the role of the placenta are possible: one is that the placenta directly conveys the Zika virus to the early embryo or fetus. Alternatively, the placenta itself might be mounting a response to the exposure; this response might be contributing to or causing the brain defect. This distinction is crucial to the diagnosis of fetuses at risk and the design of therapeutic strategies to prevent Zika-induced teratogenesis.
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                Author and article information

                Contributors
                Journal
                Prev Med Rep
                Preventive Medicine Reports
                2211-3355
                24 April 2020
                June 2020
                24 April 2020
                : 18
                : 101097
                Affiliations
                The Johns Hopkins Center for Health Security, 621 East Pratt Street Suite 210, Baltimore, MD 21202, United States
                Author notes
                [* ]Corresponding author. mtrotoc1@ 123456jh.edu
                Article
                S2211-3355(20)30057-7 101097
                10.1016/j.pmedr.2020.101097
                7199004
                3dbcf292-29a3-477f-be0b-afa4c729b7cf
                © 2020 The Authors. Published by Elsevier Inc.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 27 September 2019
                : 4 February 2020
                : 19 April 2020
                Categories
                Short Communication

                cdc, centers for disease control and prevention,us, united states,dc, washington district of columbia,zika virus,united states,testing guidance

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