Prolonged Shedding of Zika Virus Associated with Congenital Infection

Oliveira, Danielle Bruna Leal; Almeida, Flávia Jacqueline; Durigon, Edison Luiz; Mendes, Érica Araújo; Braconi, Carla Torres; Marchetti, Ivan; Andreata-Santos, Robert; Cunha, Marielton dos Passos; Alves, Rúbens Prince dos Santos; Pereira, Lennon Ramos; Melo, Stella Rezende; Neto, Daniel Ferreira Lima; Mesquita, Fernando Silveira; Araújo, Danielle Bastos; Favoretto, Silvana Regina; Sáfadi, Marco Aurélio Palazzi; Ferreira, Luís Carlos S.; Zanotto, Paolo M. A.; Botosso, Viviane Fongaro; Berezin, Eitan N.

doi:10.1056/nejmc1607583

Cited by 83 publications

(65 citation statements)

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“…In addition, because many reports focus on a single component of the syndrome, some infants may be included in more than one report. Although the numbers are small, recent reports provide evidence that the distinctive brain and eye anomalies of congenital ZIKV infection can occur without microcephaly; 10,17,22,36,39,70 however, for some infants hydrocephaly was the underlying cause of the normal head circumference measurement. 17,37 Expansion of the CZS phenotype to include infants with microcephaly but without brain anomalies has been suggested in a recent case-control study, however, it is unclear if these infants represented the effects of intrauterine growth restriction because information on other growth parameters at birth was not provided.…”

Section: Discussionmentioning

confidence: 99%

Characterizing the Pattern of Anomalies in Congenital Zika Syndrome for Pediatric Clinicians

et al. 2017

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ontracted through the bite of an infected mosquito or through sexual or other modes of transmission, Zika virus (ZIKV) infection can be prenatally passed from mother to fetus. 1 The virus was first identified in the region of the Americas in early 2015, when local transmission was reported in Brazil. 2 Six months later, a notable increase in the number of infants with congenital microcephaly was observed in northeast Brazil. 3,4 Clinical, epidemiologic, and laboratory evidence led investigators to conclude that intrauterine ZIKV infection was a cause of microcephaly and serious brain anomalies. [5][6][7] However, as with other newly recognized teratogens, these features likely represent a portion of a broader spectrum.A comprehensive review of the English literature, identified by searching Medline and EMBASE for Zika from inception through Sep-tember 30, 2016, was done to better characterize the spectrum of anomalies in fetuses and infants with presumed or laboratoryconfirmed ZIKV infection. A constellation of anomalies that is both consistent and unique, called congenital Zika syndrome (CZS), has emerged but specific components and presumed pathogenetic mechanisms previously have not been well-delineated. [8][9][10] Zika virus infection has spread to more than 45 countries in the Americas and 3 US territories, and, most recently, local transmission was confirmed in the continental United States in the state of Florida. 11 Mosquito-borne transmission of ZIKV in other areas of the United States is possible based on the estimated range of its vectors (Aedes aegypti and Aedes albopictus). 12 Recognition of the CZS phenotype by pediatric clinicians will help ensure appropriate and timely evaluation and follow-up of affected infants.IMPORTANCE Zika virus infection can be prenatally passed from a pregnant woman to her fetus. There is sufficient evidence to conclude that intrauterine Zika virus infection is a cause of microcephaly and serious brain anomalies, but the full spectrum of anomalies has not been delineated. To inform pediatric clinicians who may be called on to evaluate and treat affected infants and children, we review the most recent evidence to better characterize congenital Zika syndrome.OBSERVATIONS We reviewed published reports of congenital anomalies occurring in fetuses or infants with presumed or laboratory-confirmed intrauterine Zika virus infection. We conducted a comprehensive search of the English literature using Medline and EMBASE for Zika from inception through September 30, 2016. Congenital anomalies were considered in the context of the presumed pathogenetic mechanism related to the neurotropic properties of the virus. We conclude that congenital Zika syndrome is a recognizable pattern of structural anomalies and functional disabilities secondary to central and, perhaps, peripheral nervous system damage. Although many of the components of this syndrome, such as cognitive, sensory, and motor disabilities, are shared by other congenital infections, there are 5 features that are rarely seen w...

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Section: Discussionmentioning

confidence: 99%

Characterizing the Pattern of Anomalies in Congenital Zika Syndrome for Pediatric Clinicians

et al. 2017

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“…Periodic monitoring of these infants may be helpful for early recognition of potential late sequelae of congenital infections. Two recent studies observed neurologic abnormalities in infants whose mothers acquired Zika virus infection in the third trimester of pregnancy; for 1 of these infants, neurologic abnormalities were first identified at 6 months of age ( 7 , 40 ) . …”

Section: Discussionmentioning

confidence: 99%

Zika Virus RNA Replication and Persistence in Brain and Placental Tissue

Bhatnagar¹,

Rabeneck²,

Martines³

et al. 2017

Emerg. Infect. Dis.

189

188

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Zika virus is causally linked with congenital microcephaly and may be associated with pregnancy loss. However, the mechanisms of Zika virus intrauterine transmission and replication and its tropism and persistence in tissues are poorly understood. We tested tissues from 52 case-patients: 8 infants with microcephaly who died and 44 women suspected of being infected with Zika virus during pregnancy. By reverse transcription PCR, tissues from 32 (62%) case-patients (brains from 8 infants with microcephaly and placental/fetal tissues from 24 women) were positive for Zika virus. In situ hybridization localized replicative Zika virus RNA in brains of 7 infants and in placentas of 9 women who had pregnancy losses during the first or second trimester. These findings demonstrate that Zika virus replicates and persists in fetal brains and placentas, providing direct evidence of its association with microcephaly. Tissue-based reverse transcription PCR extends the time frame of Zika virus detection in congenital and pregnancy-associated infections.

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“…We found that ZIKV-related microcephaly in the newborns may be a factor significantly associated with high levels of anxiety and low scores in psychological well-being domain of their mothers during the first 24 h after birth (dos Santos Oliveira et al 2016). We found that ZIKV-related microcephaly in the newborns may be a factor significantly associated with high levels of anxiety and low scores in psychological well-being domain of their mothers during the first 24 h after birth (dos Santos Oliveira et al 2016).…”

Section: Dear Editormentioning

confidence: 93%