scholarly journals Association of arthrogryposis in neonates with microcephaly due to Zika virus - a case serie

2016 ◽  
Vol 16 (suppl 1) ◽  
pp. S83-S88 ◽  
Author(s):  
Ana Catarina Matos Ishigami Alvino ◽  
Luísa Rocha Medeiros de Mello ◽  
Jucille do Amaral Meneses Meira de Oliveira
Keyword(s):  
Zika Virus ◽  
Joint Stiffness ◽  
The Body ◽  
Maternal Infection ◽  
Infection Period ◽  
Vaginal Deliveries ◽  
Congenital Zika Syndrome ◽  
Motor Nerves ◽  
Congenital Microcephaly ◽  
Peripheral Motor

Abstract Introduction: in 2015 an increasing number of congenital microcephaly cases were associated to maternal infection due to Zika virus. Some of these patients presented other alterations and arthrogryposis was the most frequently found. Arthrogryposis is defined as congenital joint contractures involving at least two different areas of the body. Description: arthrogryposis was found in 18 patients with congenital microcephaly due to Zika virus. 67% of the cases were vaginal deliveries. 50% of resuscitation performed in the delivery room was necessary. The mean birth weight was 2.371g, gestational age was 39 weeks and the head circumference was 28.3cm, 15 (83%) of these patients presented severe microcephaly. All the neonates resulted in concomitant hip joints and some also had knees, ankles and wrists affected. Nine neonates (50%) presented an early respiratory distress and four (22%) died due to respiratory failure. Discussion: the neurological result found in patients with Congenital Zika Syndrome seems to be associated to the maternal infection period. During the early stages of embryogenesis, in addition to microcephaly, could be related to the peripheral motor nerves leading to fetal akinesia, joint stiffness and arthrogryposis. These neonates tend to present greater morbimortality with the worst prognosis.

scholarly journals Zika Virus Pathogenesis: From Early Case Reports to Epidemics

Viruses ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 886 ◽  
Author(s):  
Ryan D. Pardy ◽  
Martin J. Richer
Keyword(s):  
Risk Factors ◽  
Zika Virus ◽  
Case Reports ◽  
Viral Persistence ◽  
The Body ◽  
Therapeutic Approaches ◽  
Zikv Infection ◽  
Congenital Zika Syndrome ◽  
Early Case ◽  
The Impact

For the first 60 years following its isolation, Zika virus (ZIKV) remained a relatively poorly described member of the Flaviviridae family. However, since 2007, it has caused a series of increasingly severe outbreaks and is now associated with neurological symptoms such as Guillain-Barré syndrome and congenital Zika syndrome (CZS). A number of reports have improved our understanding of rare complications that may be associated with ZIKV infection in adults, the areas of the body to which it spreads, and viral persistence in various tissues. Likewise, studies on the effect of ZIKV infection during pregnancy have identified risk factors for CZS and the impact this syndrome has on early childhood. Understanding these outcomes and the factors that drive ZIKV pathogenesis are key to developing vaccination and therapeutic approaches to avoid these severe and potentially debilitating symptoms.

scholarly journals Clinical Outcomes of a Zika Virus Mother–Child Pair Cohort in Spain

Pathogens ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 352 ◽  
Author(s):  
Antoni Soriano-Arandes ◽  
Marie Antoinette Frick ◽  
Milagros García López-Hortelano ◽  
Elena Sulleiro ◽  
Carlota Rodó ◽  
...  
Keyword(s):  
Zika Virus ◽  
Adverse Outcomes ◽  
Zikv Infection ◽  
Child Pair ◽  
Referral Hospitals ◽  
Congenital Zika Syndrome ◽  
Endemic Areas ◽  
Neurodevelopmental Abnormalities ◽  
Congenital Microcephaly

Background: Zika virus (ZIKV) infection has been associated with congenital microcephaly and other neurodevelopmental abnormalities. There is little published research on the effect of maternal ZIKV infection in a non-endemic European region. We aimed to describe the outcomes of pregnant travelers diagnosed as ZIKV-infected in Spain, and their exposed children. Methods: This prospective observational cohort study of nine referral hospitals enrolled pregnant women (PW) who travelled to endemic areas during their pregnancy or the two previous months, or those whose sexual partners visited endemic areas in the previous 6 months. Infants of ZIKV-infected mothers were followed for about two years. Results: ZIKV infection was diagnosed in 163 PW; 112 (70%) were asymptomatic and 24 (14.7%) were confirmed cases. Among 143 infants, 14 (9.8%) had adverse outcomes during follow-up; three had a congenital Zika syndrome (CZS), and 11 other potential Zika-related outcomes. The overall incidence of CZS was 2.1% (95%CI: 0.4–6.0%), but among infants born to ZIKV-confirmed mothers, this increased to 15.8% (95%CI: 3.4–39.6%). Conclusions: A nearly 10% overall risk of neurologic and hearing adverse outcomes was found in ZIKV-exposed children born to a ZIKV-infected traveler PW. Longer-term follow-up of these children is needed to assess whether there are any later-onset manifestations.

scholarly journals Multimerization of Zika Virus-NS5 causes a ciliopathy and forces premature neurogenesis

2019 ◽  
Author(s):  
Murielle Saade ◽  
Diego S Ferrero ◽  
José Blanco-Ameijeiras ◽  
Elena Gonzalez-Gobartt ◽  
Victor M Ruiz-Arroyo ◽  
...  
Keyword(s):  
Zika Virus ◽  
Primary Cilia ◽  
Neural Progenitor Cells ◽  
Fetal Brain ◽  
Ependymal Cells ◽  
Host Proteins ◽  
Cellular Events ◽  
Neural Tissues ◽  
Congenital Zika Syndrome ◽  
Congenital Microcephaly

AbstractZika virus (ZikV) is a flavivirus that infects neural tissues, causing congenital microcephaly. ZikV has evolved multiple mechanisms to restrict proliferation and enhance cell death, although the underlying cellular events involved remain unclear. Here we show that the ZikV-NS5 protein interacts with host proteins at the base of the primary cilia in neural progenitor cells, causing an atypical non-genetic ciliopathy and premature neuron delamination. Furthermore, in human microcephalic fetal brain tissue, ZikV-NS5 persists at the base of the motile cilia in ependymal cells, which also exhibit a severe ciliopathy. While the enzymatic activity of ZikV-NS5 appears to be dispensable, the Y25, K28 and K29 residues in the protein, that are involved in NS5-oligomerization, are essential for the localization and interaction with components of the cilium base, promoting ciliopathy and premature neurogenesis. These findings lay the foundation to develop therapies that target ZikV-NS5-multimerization, preventing the developmental malformations associated with congenital Zika syndrome

Zika Virus Infection in Pregnancy, Microcephaly, and Maternal and Fetal Health: What We Think, What We Know, and What We Think We Know

2016 ◽  
Vol 141 (1) ◽  
pp. 26-32 ◽  
Author(s):  
Maria Gabriela Alvarado ◽  
David A. Schwartz
Keyword(s):  
Brain Damage ◽  
Zika Virus ◽  
Experimental Studies ◽  
Fetal Brain ◽  
Zikv Infection ◽  
Host Genetics ◽  
Fetal Infection ◽  
Congenital Zika Syndrome ◽  
Experimental Laboratory ◽  
Congenital Microcephaly

Context.—The global epidemic of Zika virus (ZIKV) infection has emerged as an important public health problem affecting pregnant women and their infants. Objectives.—To review the causal association between ZIKV infection during pregnancy and intrauterine fetal infection, microcephaly, brain damage, congenital malformation syndrome, and experimental laboratory models of fetal infection. Many questions remain regarding the risk factors, pathophysiology, epidemiology, and timing of maternal-fetal transmission and disease. These include mechanisms of fetal brain damage and microcephaly; the role of covariables, such as viral burden, duration of viremia, and host genetics, on vertical transmission; and the clinical and pathologic spectrum of congenital Zika syndrome. Additional questions include defining the potential long-term physical and neurobehavioral outcomes for infected infants, whether maternal or fetal host genetics influence the clinical outcome, and whether ZIKV infection can cause maternal morbidity. Finally, are experimental laboratory and animal models of ZIKV infection helpful in addressing maternal-fetal viral transmission and the development of congenital microcephaly? This communication provides current information and attempts to address some of these important questions. Data Sources.—Comprehensive review of published scientific literature. Conclusions.—Recent advances in epidemiology, clinical medicine, pathology, and experimental studies have provided a great amount of new information regarding vertical ZIKV transmission and the mechanisms of congenital microcephaly, brain damage, and congenital Zika syndrome in a relatively short time. However, much work still needs to be performed to more completely understand the maternal and fetal aspects of this new and emerging viral disease.

scholarly journals Placental Morphologic Similarities Between ZIKV-Positive and HIV-Positive Pregnant Women

2021 ◽  
Vol 12 ◽  
Author(s):  
Daiane Cristine Martins Ronchi ◽  
Mineia Alessandra Scaranello Malaquias ◽  
Patrícia Zadorosnei Rebutini ◽  
Letícia Arianne Panini do Carmo ◽  
Plínio Cézar Neto ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Zika Virus ◽  
Hiv Positive ◽  
Control Group ◽  
Hofbauer Cells ◽  
Congenital Zika Syndrome ◽  
Global Concern ◽  
Conventional Microscopy ◽  
Congenital Microcephaly ◽  
The Relationship

Zika virus (ZIKV) caused global concern due to Brazil's unexpected epidemic, and it was associated with congenital microcephaly and other gestational intercurrences. The study aimed to analyze the placenta morphometric changes of ZIKV-infected pregnant women (ZIKV group; n = 23) compared to placentas of HIV-infected (HIV group; n = 24) and healthy pregnant women (N-control group; n = 22). It also analyzed the relationship between the morphometric results and pathological alterations on conventional microscopy, gestational trimester of infection, and presence of the congenital Zika syndrome (CZS). There was a significant increase in area (p = 0.0172), as well as a higher number of knots (p = 0.0027), sprouts (p < 0.0001), and CD163 +Hofbauer cells (HCs) (p < 0.0001) in the ZIKV group compared to the N-control group, suggesting that villous dysmaturity and HCs hyperplasia could be associated with ZIKV infections. The HIV group had a higher area (p < 0.0001), perimeter (p = 0.0001), sprouts (p < 0.0001), and CD163 + HCs (p < 0.0001) compared to the N-control group, demonstrating that the morphometric abnormalities found in the ZIKV and HIV group are probably similar. However, when ZIKV and HIV groups are compared, it was observed a higher number of sprouts (p = 0.0066) and CD163+ HCs (p < 0.0001) in the first one, suggesting that placental ZIKV congenital changes could be more pronounced.

scholarly journals Is Zika Virus an Emerging TORCH Agent? An Invited Commentary

2017 ◽  
Vol 8 ◽  
pp. 1178122X1770899 ◽  
Author(s):  
Mohammad Zare Mehrjardi
Keyword(s):  
Public Health ◽  
Zika Virus ◽  
Imaging Modality ◽  
Fold Increase ◽  
Northeastern Brazil ◽  
Caribbean Region ◽  
Fetal Ultrasound ◽  
Zikv Infection ◽  
Congenital Zika Syndrome ◽  
Congenital Microcephaly

Zika virus (ZIKV) is a mosquito-borne arbovirus from the family Flaviviridae, which had caused some epidemics since its discovery in 1947 without any significant impacts on public health. In 2015, however, a 20-fold increase in congenital microcephaly cases in northeastern Brazil was attributed to prenatally acquired ZIKV infection. Traditionally, TORCH agents have 4 common characteristics including causing a mild illness in infected mother, vertical transmission to fetus, developing several anomalies in the affected fetus, and in some instances, maternal therapy may not ameliorate fetal prognosis. Prenatal ZIKV infection has shown the aforementioned characteristics during the recent epidemics in South America and the Caribbean region; therefore, it should be considered as an emerging TORCH agent that may seriously threaten public health. Fetal ultrasound can be used as a safe, inexpensive, and easy-to-access imaging modality for detecting suspicious cases of congenital Zika syndrome in utero and suggesting confirmatory diagnostic examinations to these patients.

scholarly journals Association between Genetic Variants in NOS2 and TNF Genes with Congenital Zika Syndrome and Severe Microcephaly

Viruses ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 325
Author(s):  
Julia A. Gomes ◽  
Eduarda Sgarioni ◽  
Juliano A. Boquett ◽  
Ana Cláudia P. Terças-Trettel ◽  
Juliana H. da Silva ◽  
...  
Keyword(s):  
Risk Factors ◽  
Zika Virus ◽  
Genetic Variants ◽  
Educational Level ◽  
Congenital Anomalies ◽  
Family Income ◽  
First Trimester ◽  
In Utero ◽  
Zikv Infection ◽  
Congenital Zika Syndrome

Zika virus (ZIKV) causes Congenital Zika Syndrome (CZS) in individuals exposed prenatally. Here, we investigated polymorphisms in VEGFA, PTGS2, NOS3, TNF, and NOS2 genes as risk factors to CZS. Forty children with CZS and forty-eight children who were in utero exposed to ZIKV infection, but born without congenital anomalies, were evaluated. Children with CZS were predominantly infected by ZIKV in the first trimester (p < 0.001) and had mothers with lower educational level (p < 0.001) and family income (p < 0.001). We found higher risk of CZS due the allele rs2297518[A] of NOS2 (OR = 2.28, CI 95% 1.17–4.50, p = 0.015). T allele and TT/CT genotypes of the TNF rs1799724 and haplotypes associated with higher expression of TNF were more prevalent in children with CZS and severe microcephaly (p = 0.029, p = 0.041 and p = 0.030, respectively). Our findings showed higher risk of CZS due ZIKV infection in the first trimester and suggested that polymorphisms in NOS2 and TNF genes affect the risk of CZS and severe microcephaly.

Complications and Sequelae in Patients With Congenital Microcephaly Associated With Zika Virus Infection: Two-Year Follow-Up

2021 ◽  
pp. 088307382098316
Author(s):  
Luane A. Gouvea ◽  
Marlos Martins ◽  
Daniela Vivacqua ◽  
Julia Rosseto ◽  
Giulia Lima ◽  
...  
Keyword(s):  
Developmental Delay ◽  
Zika Virus ◽  
Median Number ◽  
Global Developmental Delay ◽  
Spastic Diplegia ◽  
Long Term Follow Up ◽  
Congenital Microcephaly ◽  
Auditory Impairment ◽  
Worse Prognosis

Background: We aim to describe the long term follow-up of a cohort of children exposed in utero to the Zika virus. Methods: Descriptive study of a cohort of microcephalic children due to Zika virus. Logistic regression was used to evaluate variables associated with worse prognosis epilepsy. Results: We followed 28 children (15 females), with a median follow-up of 24 months (IQR = 12-28). During the follow-up, 1 infant died. The median head circumference at birth was 29 cm (IQR = 27-31). All presented a global developmental delay. The most frequent central nervous system abnormalities were on cortical development in 22 participants; dysgenesis of corpus callosum in 13; ventriculomegaly in 25; and calcifications in 24. A total of 9 presented ocular abnormalities, 4 auditory impairment. During follow-up, 12 presented with sleep disorders, 10 with irritability, and 23 with epilepsy (2 with generalized tonic-clonic, 3 with generalized tonic-clonic and spasms, 12 with spasms, 3 tonic and spasms, and 3 motor focal and spasms). The median age at the begin of the epilepsy was 4 months (IQR = 2-10), the median number of drugs used to control the epilepsy was 2 (IQR = 2-3). Maternal illicit drug use during pregnancy was associated with worse prognosis epilepsy (Lennox-Gastaut syndrome, West syndrome, or status epilepticus). A total of 19 presented with dysphagia, 10 children required gastrostomy. Conclusion: Children with microcephaly due to Zika virus presented with several complications during follow-up, as epilepsy, spastic diplegia, and global developmental delay.

Associations of DNA Methylation Mortality Risk Markers with Congenital Microcephaly from Zika Virus: A Study of Brazilian Children Less than 4 Years of Age

2021 ◽  
Vol 67 (1) ◽  
Author(s):  
Jamaji C Nwanaji-Enwerem ◽  
Lars Van Der Laan ◽  
Elorm F Avakame ◽  
Kristan A Scott ◽  
Heather H Burris ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Mortality Risk ◽  
Zika Virus ◽  
Clinical Decision Making ◽  
Linear Models ◽  
Adult Mortality ◽  
Plasminogen Activator Inhibitor 1 ◽  
Congenital Microcephaly ◽  
Pai 1 ◽  
Brazilian Children

ABSTRACT Background Zika virus (ZIKV)-associated congenital microcephaly is an important contributor to pediatric death, and more robust pediatric mortality risk metrics are needed to help guide life plans and clinical decision making for these patients. Although common etiologies of pediatric and adult mortality differ, early life health can impact adult outcomes—potentially through DNA methylation. Hence, in this pilot study, we take an early step in identifying pediatric mortality risk metrics by examining associations of ZIKV infection and associated congenital microcephaly with existing adult DNA methylation-based mortality biomarkers: GrimAge and Zhang’s mortality score (ZMS). Methods Mortality measures were calculated from previously published HumanMethylationEPIC BeadChip data from 44 Brazilian children aged 5–40 months (18 with ZIKV-associated microcephaly; 7 normocephalic, exposed to ZIKV in utero; and 19 unexposed controls). We used linear models adjusted for chronological age, sex, methylation batch and white blood cell proportions to evaluate ZIKV and mortality marker relationships. Results We observed significant decreases in GrimAge-component plasminogen activator inhibitor-1 [PAI-1; β = −2453.06 pg/ml, 95% confidence interval (CI) −3652.96, −1253.16, p = 0.0002], and ZMS-site cg14975410 methylation (β = −0.06, 95% CI −0.09, −0.03, p = 0.0003) among children with microcephaly compared to controls. PAI-1 (β = −2448.70 pg/ml, 95% CI −4384.45, −512.95, p = 0.01) and cg14975410 (β = 0.01, 95% CI −0.04, 0.06, p = 0.64) results in comparisons of normocephalic, ZIKV-exposed children to controls were not statistically significant. Conclusion Our results suggest that elements of previously-identified adult epigenetic markers of mortality risk are associated with ZIKV-associated microcephaly, a known contributor to pediatric mortality risk. These findings may provide insights for efforts aimed at developing pediatric mortality markers.

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