#Genome Sequences of #Zika Virus Strains Recovered from #Amniotic Fluid, #Placenta, and Fetal #Brain of a #Microcephaly Patient in #Thailand, 2017 (Microbiol Resour Announc., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Microbiol Resour Announc. 2018 Sep 20;7(11). pii: e01020-18. doi: 10.1128/MRA.01020-18. eCollection 2018 Sep.

Genome Sequences of Zika Virus Strains Recovered from Amniotic Fluid, Placenta, and Fetal Brain of a Microcephaly Patient in Thailand, 2017.

Wongsurawat T1, Jenjaroenpun P1, Athipanyasilp N2, Kaewnapan B2, Leelahakorn N2, Angkasekwinai N3, Kantakamalakul W2, Sutthent R2, Ussery DW1,4, Horthongkham N2, Nookaew I1,4.

Author information: 1 Department of Biomedical Informatics, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA. 2 Department of Microbiology, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkoknoi, Bangkok, Thailand. 3 Department of Medicine, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkoknoi, Bangkok, Thailand. 4 Department of Physiology and Biophysics, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.

 

Abstract

We present here the complete genome sequences of Zika virus strains isolated from aborted fetal tissue (brain and placenta) and amniotic fluid of a microcephaly patient in Thailand in 2017. The virus genomes that were sequenced have an average length of 10,807 nucleotides.

PMID: 30533643 PMCID: PMC6256666 DOI: 10.1128/MRA.01020-18

Keywords: Zika Virus; Microcephaly; Thailand.

——

Advertisements

#Congenital #Zika Virus #Infection with Normal Neurodevelopmental Outcome, #Brazil (Emerg Infect Dis., abstract)

[Source: US Centers for Disease Control and Prevention (CDC), Emerging Infectious Diseases Journal, full page: (LINK). Abstract, edited.]

Volume 24, Number 11—November 2018 / Research Letter

Congenital Zika Virus Infection with Normal Neurodevelopmental Outcome, Brazil

Alessandra Lemos de Carvalho  , Carlos Brites, Tânia Barreto Taguchi, Suely Fernandes Pinho, Gúbio Campos, and Rita Lucena

Author affiliations: SARAH Network of Rehabilitation Hospitals, Salvador, Brazil (A.L. de Carvalho, T.B. Taguchi, S.F. Pinho); Federal University of Bahia, Salvador (C. Brites, G. Campos, R. Lucena)

 

Abstract

We describe a case of a 20-month-old girl with probable congenital Zika virus infection and normal neurodevelopment, despite microcephaly and abnormal neuroimaging. This case raises questions about early prognostic markers and draws attention to the need for investigation in suspected Zika cases, even if the child’s early neurodevelopment is normal.

Keywords: Zika Virus; Zika Congenital Syndrome; Microcephaly.

——

Can we better understand how #Zika leads to #microcephaly? A systematic review of the effects of the Zika virus on human #brain #organoids (J Infect Dis., abstract)

[Source: Journal of Infectious Diseases, full page: (LINK). Abstract, edited.]

Can we better understand how Zika leads to microcephaly? A systematic review of the effects of the Zika virus on human brain organoids

Bayu Sutarjono

The Journal of Infectious Diseases, jiy572, https://doi.org/10.1093/infdis/jiy572

Published: 26 September 2018

 

Abstract

Background

The emergence of human brain organoids represents a unique opportunity to better understand the genesis of congenital brain abnormalities, more strikingly microcephaly, caused by the Zika virus (ZIKV) infection during early pregnancy.

Methodology/Results

A systematic review was conducted to investigate how ZIKV leads to microcephaly in a novel experimental model that mimics early brain development. Studies were gathered by searching MEDLINE/Pubmed, LILACS, and LiSSa of the effects of ZIKV infection on human brain organoids. From 146 identified papers, 13 articles were selected for review. In summary, this review found that ZIKV of African, Latin American, and Asian lineages caused productive replication after 72 hours, preferentially infected neural progenitor cells over mature neurons, reduced both cell populations, and caused premature differentiation. Limited data involving only African and Latin American lineages showed a reduction in populations of proliferating cells and intermediate cells, and overall decreased viability. Furthermore, all three lineages caused heightened apoptosis and reduced organoid size.

Conclusion/Significance

This systematic review strengthened the hypothesis that ZIKV causes congenital microcephaly, as investigated in the human brain organoid model. It also demonstrated the coherence of outcomes by these studies to validate the utility of human brain organoids in future research of brain development.

Zika, organoid, microcephaly, neural progenitor cells

Issue Section: Major Article

© The Author(s) 2018. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.

This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)

Keywords: Zika Virus; Microcephaly; Organoids.

——

Association and #birth #prevalence of #microcephaly attributable to #Zika virus infection among #infants in Paraíba, #Brazil, in 2015-16: a case-control study (Lancet Child Adolesc Health, abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Lancet Child Adolesc Health. 2018 Mar;2(3):205-213. doi: 10.1016/S2352-4642(18)30020-8. Epub 2018 Jan 12.

Association and birth prevalence of microcephaly attributable to Zika virus infection among infants in Paraíba, Brazil, in 2015-16: a case-control study.

Krow-Lucal ER1, de Andrade MR2, Cananéa JNA3, Moore CA4, Leite PL5, Biggerstaff BJ6, Cabral CM2, Itoh M7, Percio J8, Wada MY8, Powers AM6, Barbosa A9, Abath RB3, Staples JE6, Coelho GE5; Paraíba Microcephaly Work Group.

Collaborators (38): Araújo E, Medeiros ELA, Brant J, Cerroni M, de Barros Moreira Beltrão H, Fantinato FFST, Lise MLZ, Ohara PM, Resende E, Saad E, de St Maurice A, Dieke A, Harrist A, Kwit N, Marlow M, Soke G, de Arruda Pessoa R, da Silva RC, Diniz RC, de Araújo Ariette MC, Lira CF, Matos S, Wanderley TMM, Silva VOC, da Silva HS, Carmo EH, Carvalho M, Lentini N, Miranda R, Boland E, Burns P, Fischer M, Ledermann J, Coronado F, Dicent-Taillepierre J, Flannery B, Macedo de Oliveira A, Arena JF.

Author information: 1 Division of Vector-Borne Diseases, Centers for Disease Control and Prevention, Fort Collins, CO, USA; EIS Program Office, Centers for Disease Control and Prevention, Atlanta, GA, USA. 2 Epidemiologia Aplicada aos Serviços do Sistema Único de Saúde (Episus), Brasilia, Brazil. 3 Secretariat of Health, Paraíba, Brazil. 4 Division of Congenital and Developmental Disorders, Centers for Disease Control and Prevention, Atlanta, GA, USA. 5 National Dengue Control Program, Brazil Ministry of Health, Brasilia, Brazil. 6 Division of Vector-Borne Diseases, Centers for Disease Control and Prevention, Fort Collins, CO, USA. 7 EIS Program Office, Centers for Disease Control and Prevention, Atlanta, GA, USA. 8 Epidemiologia Aplicada aos Serviços do Sistema Único de Saúde (Episus), Brasilia, Brazil; National Dengue Control Program, Brazil Ministry of Health, Brasilia, Brazil. 9 Brazil Country Office, Centers for Disease Control and Prevention, Brasilia, Brazil.

 

Abstract

BACKGROUND:

In 2015, the number of infants born with microcephaly increased in Paraíba, Brazil, after a suspected Zika virus outbreak. We did a retrospective case-control investigation to assess the association of microcephaly and Zika virus.

METHODS:

We enrolled cases reported to the national database for microcephaly and born between Aug 1, 2015, and Feb 1, 2016, on the basis of their birth head circumference and total body length. We identified controls from the national birth registry and matched them to cases by location, aiming to enrol a minimum of two controls per case. Mothers of both cases and controls were asked about demographics, exposures, and illnesses and infants were measured at a follow-up visit 1-7 months after birth. We took blood samples from mothers and infants and classified those containing Zika virus IgM and neutralising antibodies as evidence of recent infection. We calculated prevalence of microcephaly and odds ratios (ORs) using a conditional logistic regression model with maximum penalised conditional likelihood, and combined these ORs with exposure probability estimates to determine the attributable risk.

FINDINGS:

We enrolled 164 of 706 infants with complete information reported with microcephaly at birth, of whom we classified 91 (55%) as having microcephaly on the basis of their birth measurements, 36 (22%) as small, 21 (13%) as disproportionate, and 16 (10%) as not having microcephaly. 43 (26%) of the 164 infants had microcephaly at follow-up for an estimated prevalence of 5·9 per 1000 livebirths. We enrolled 114 control infants matched to the 43 infants classified as having microcephaly at follow-up. Infants with microcephaly at follow-up were more likely than control infants to be younger (OR 0·5, 95% CI 0·4-0·7), have recent Zika virus infection (21·9, 7·0-109·3), or a mother with Zika-like symptoms in the first trimester (6·2, 2·8-15·4). Once Zika virus infection and infant age were controlled for, we found no significant association between microcephaly and maternal demographics, medications, toxins, or other infections. Based on the presence of Zika virus antibodies in infants, we concluded that 35-87% of microcephaly occurring during the time of our investigation in northeast Brazil was attributable to Zika virus. We estimate 2-5 infants per 1000 livebirths in Paraíba had microcephaly attributable to Zika virus.

INTERPRETATION:

Time of exposure to Zika virus and evidence of infection in the infants were the only risk factors associated with microcephaly. This investigation has improved understanding of the outbreak of microcephaly in northeast Brazil and highlights the need to obtain multiple measurements after birth to establish if an infant has microcephaly and the need for further research to optimise testing criteria for congenital Zika virus infection.

FUNDING:

Centers for Disease Control and Prevention.

Copyright © 2018 Elsevier Ltd. All rights reserved.

PMID: 30169255 DOI: 10.1016/S2352-4642(18)30020-8

Keywords: Zika Virus; Zika Congenital Infection; Microcephaly; Brazil.

——

Correlation between #apoptosis and in situ immune response in #fatal cases of #microcephaly caused by #Zika virus (Am J Pathol., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Am J Pathol. 2018 Aug 16. pii: S0002-9440(18)30153-6. doi: 10.1016/j.ajpath.2018.07.009. [Epub ahead of print]

Correlation between apoptosis and in situ immune response in fatal cases of microcephaly caused by Zika virus.

de Sousa JR1, Azevedo RSS1, Martins Filho AJ2, Araujo MTF2, Moutinho ERC2, Baldez Vasconcelos BC3, Cruz ACR4, Oliveira CS1, Martins LC1, Baldez Vasconcelos BH5, Casseb LMN1, Chiang JO1, Quaresma JAS6, Vasconcelos PFC7.

Author information: 1 Department of Arbovirology and Hemorrhagic Fevers, Evandro Chagas Institute, Ministry of Health, Ananindeua, Brazil. 2 Department of Pathology, Evandro Chagas Institute, Ministry of Health, Ananindeua, Brazil. 3 Center of Biological and Health Sciences, State University of Pará, Belém, Brazil. 4 Department of Arbovirology and Hemorrhagic Fevers, Evandro Chagas Institute, Ministry of Health, Ananindeua, Brazil; Center of Biological and Health Sciences, State University of Pará, Belém, Brazil. 5 Tropical Medicine Center, Federal University of Pará, Belém, Brazil. 6 Department of Pathology, Evandro Chagas Institute, Ministry of Health, Ananindeua, Brazil; Center of Biological and Health Sciences, State University of Pará, Belém, Brazil; Tropical Medicine Center, Federal University of Pará, Belém, Brazil. Electronic address: pedrovasconcelos@iec.pa.gov.br. 7 Department of Arbovirology and Hemorrhagic Fevers, Evandro Chagas Institute, Ministry of Health, Ananindeua, Brazil; Center of Biological and Health Sciences, State University of Pará, Belém, Brazil. Electronic address: pedrovasconcelos@iec.pa.gov.br.

 

Abstract

Zika virus (ZIKV) is a single-stranded positive-sense RNA flavivirus that possesses a genome approximately 10.7 Kb in length. Although pro- and anti-inflammatory cytokines, and apoptotic markers belonging to the extrinsic and intrinsic pathways are suggested to be involved in fatal cases of ZIKV-induced microcephaly, their exact roles and associations are unclear. To address this, brain tissue samples were collected from 10 individuals, five of whom were diagnosed as ZIKV-positive with microcephaly and a further five were flavivirus-negative controls that died because of other causes. Examination of material from the fatal cases of microcephaly revealed lesions in the cerebral cortex, edema, vascular proliferation, neuronal necrosis, gliosis, neuronophagy, calcifications, apoptosis, and neuron loss. The expression of various apoptosis markers in the neural parenchyma, including FASL, FAS, BAX, BCL2, and Caspase 3 differed between ZIKV-positive cases and controls. Further investigation of Th1 and Th2 cytokines confirmed a greater anti-inflammatory response in fatal ZIKV-associated microcephaly cases. Finally, an analysis of the linear correlation between tumor necrosis facor-α, interleukin (IL)-1β, IL-4, IL-10, transforming growth factor-β, and IL-33 expression, and various apoptotic markers, suggested that the immune response may be associated with the apoptotic phenomenon observed in ZIKV-induced microcephaly.

PMID: 30121258 DOI: 10.1016/j.ajpath.2018.07.009

Keywords: Zika Virus; Microcephaly; Viral Pathogenesis.

——

#Correlation between #apoptosis and in situ immune response in #fatal cases of #microcephaly caused by #Zika virus (Am J Pathol., abstract)

[Source: American Journal of Pathology, full page: (LINK). Abstract, edited.]

Correlation between apoptosis and in situ immune response in fatal cases of microcephaly caused by Zika virus

Jorge R. de Sousa, Raimunda S.S. Azevedo, Arnaldo J. Martins Filho, Marialva T.F. Araujo, Ermelinda R.C. Moutinho, Barbara C. Baldez Vasconcelos, Ana C.R. Cruz, Consuelo S. Oliveira, Lívia C. Martins, Beatriz H. Baldez Vasconcelos, Livia M.N. Casseb, Jannifer O. Chiang, Juarez A.S. Quaresma, Pedro F.C. Vasconcelos

DOI: https://doi.org/10.1016/j.ajpath.2018.07.009

Published online: August 16, 2018 – Accepted: July 16, 2018 – Received in revised form: July 12, 2018 – Received: February 20, 2018

 

Abstract

Zika virus (ZIKV) is a single-stranded positive-sense RNA flavivirus that possesses a genome approximately 10.7 Kb in length. Although pro- and anti-inflammatory cytokines, and apoptotic markers belonging to the extrinsic and intrinsic pathways are suggested to be involved in fatal cases of ZIKV-induced microcephaly, their exact roles and associations are unclear. To address this, brain tissue samples were collected from 10 individuals, five of whom were diagnosed as ZIKV-positive with microcephaly and a further five were flavivirus-negative controls that died because of other causes. Examination of material from the fatal cases of microcephaly revealed lesions in the cerebral cortex, edema, vascular proliferation, neuronal necrosis, gliosis, neuronophagy, calcifications, apoptosis, and neuron loss. The expression of various apoptosis markers in the neural parenchyma, including FASL, FAS, BAX, BCL2, and Caspase 3 differed between ZIKV-positive cases and controls. Further investigation of Th1 and Th2 cytokines confirmed a greater anti-inflammatory response in fatal ZIKV-associated microcephaly cases. Finally, an analysis of the linear correlation between tumor necrosis facor-α, interleukin (IL)-1β, IL-4, IL-10, transforming growth factor-β, and IL-33 expression, and various apoptotic markers, suggested that the immune response may be associated with the apoptotic phenomenon observed in ZIKV-induced microcephaly.

___

Footnote: P.F.C.V and J.A.S.Q contributed equally.

Disclosures: None declared.

Funding: Supported by grants from the Ministry of Science, Technology and Innovation/National Council for Scientific and Technological Development CNPQ/Brazil (grant numbers: 303999/2016-0, 439971/2016-0, 440405/2016-5) and CAPES (Zika Fast-track) awarded to P.F.C.V.

© 2018 Published by Elsevier Inc. on behalf of the American Society for Investigative Pathology.

Keywords: Zika Virus; Microcephaly; Viral Pathogenesis.

——

#Zika might not be acting alone: Using an #ecological study approach to investigate potential co-acting #risk #factors for an unusual #pattern of #microcephaly in #Brazil (PLoS One, abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

PLoS One. 2018 Aug 15;13(8):e0201452. doi: 10.1371/journal.pone.0201452. eCollection 2018.

Zika might not be acting alone: Using an ecological study approach to investigate potential co-acting risk factors for an unusual pattern of microcephaly in Brazil.

Campos MC1, Dombrowski JG2, Phelan J1, Marinho CRF2, Hibberd M1, Clark TG1,3, Campino S1.

Author information: 1 Faculty of Infectious and Tropical Diseases, London School of Hygiene & Tropical Medicine, London, United Kingdom. 2 Department of Parasitology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil. 3 Faculty of Epidemiology and Population Health, London School of Hygiene & Tropical Medicine, London, United Kingdom.

 

Abstract

Zika virus infections can cause a range of neurologic disorders including congenital microcephaly. However, while Zika infections have been notified across all regions in Brazil, there has been an unusual number of congenital microcephaly case notifications concentrated in the Northeast of the country. To address this observation, we investigated epidemiological data (2014-2016) on arbovirus co-distribution, environmental and socio-economic factors for each region in Brazil. Data on arbovirus reported cases and microcephaly were collected from several Brazilian Ministry of Health databases for each Federal unit. These were complemented by environmental management, social economic and Aedes aegypti infestation index data, extracted from multiple databases. Spatial time “ecological” analysis on the number of arboviruses transmitted by Aedes mosquitoes in Brazil show that the distribution of dengue and Zika was widespread in the whole country, with higher incidence in the West-Central region. However, reported chikungunya cases were higher in the Northeast, the region also with the highest number of microcephaly cases registered. Social economic factors (human development index and poverty index) and environmental management (water supply/storage and solid waste management) pointed the Northeast as the less wealthy region. The Northeast is also the region with the highest risk of Aedes aegypti house infestation due to the man-made larval habitats. In summary, the results of our ecological analysis support the hypothesis that the unusual distribution of microcephaly might not be due to Zika infection alone and could be accentuated by poverty and previous or co-infection with other pathogens. Our study reinforces the link between poverty and the risk of disease and the need to understand the effect on pathogenesis of sequential exposure to arboviruses and co-viral infections. Comprehensive large-scale cohort studies are required to corroborate our findings. We recommend that the list of infectious diseases screened, particularly during pregnancy, be regularly updated to include and effectively differentiate all viruses from ongoing outbreaks.

PMID: 30110370 DOI: 10.1371/journal.pone.0201452

Keywords: Zika Virus; Microcephaly; Chikungunya Fever; Poverty; Society.

——