Congenital Zika syndrome: association between the gestational trimester of maternal infection, severity of brain computed tomography findings and microcephaly at birth

Mendes, Ana Karolina Torres; Ribeiro, Marizélia Rodrigues Costa; Lamy-Filho, Fernando; Amaral, Gláucio Andrade; Borges, Marcella Costa Ribeiro; Costa, Luciana Cavalcante; Cavalcante, Tamires Barradas; Batista, Rosângela Fernandes Lucena; Sousa, Patrícia da Silva; Silva, Antônio Augusto Moura da

doi:10.1590/s1678-9946202062056

Cited by 13 publications

(11 citation statements)

References 23 publications

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“…WSLV was detected throughout the foetal brains in neuronal progenitor cells and differentiated cells: neurons, oligodendrocytes, microglia and astrocytes. WSLV infection early in gestation could lead to more severe neurological complications in a manner similar to what is reported for ZIKV [307][308][309] . ZIKV causes congenital disease by infection of the neural progenitor cells associated with persistent inflammatory responses 310,311 .…”

Section: Question 3 How Does Gestational Age Affect the Outcome Of Asupporting

confidence: 60%

“…Gestational age is an important determinant of the outcome of infection by vertically transmitting arboviruses. Several cohort studies have demonstrated a strong relationship between maternal infection with ZIKV early in pregnancy with more severe brain abnormalities compared to maternal infection late in pregnancy 307,308 . Additionally, a recent cohort of children with a normal baseline neurologic examination whose mothers were infected with ZIKV during pregnancy were found to be more likely to experience developmental delays if infection had occurred during the third trimester compared to those exposed during the first or second trimester 309 .…”

Section: Question 3 How Does Gestational Age Affect the Outcome Of Amentioning

confidence: 99%

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Crossing barriers : How neglected arboviruses journey through the placenta

Oymans¹

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The medical importance of arboviruses Over 500 species of viruses that are spread by arthropod vectors such as mosquitoes, midges, ticks, and sandflies are known. These viruses, belonging to 14 different virus families, are called arthropod-borne viruses, or arboviruses 1. Most arboviruses are not pathogenic to humans or animals, however more than 100 species have been described to cause human or animal disease 1,2. Virtually all viruses that are pathogenic to humans or animals belong to the families Flaviviridae, Togaviridae, Reoviridae and multiple families within the order Bunyavirales. Although these viruses differ greatly genetically and phenotypically, there are striking similarities in their lifecycles. Chapter 1 12 viral RNPs (vRNPs) into the cytosol 41-43. At the cytoplasm the vRNPs direct synthesis of mRNA and of complementary viral RNA (cRNA) 44. Progeny vRNPs, traffic by yet unknown mechanisms to the Trans-golgi-Network where newly produced glycoproteins assemble into virions and the RNPs are packaged 43,45. Rift Valley fever virus RVFV, a phlebovirus from the family Phenuiviridae, was first isolated during an outbreak among sheep on the shores of lake Naivasha in the Rift Valley of Kenya 46. The virus caused heavy mortality among the newborn lambs on the farm. Moreover, a high mortality rate of adult animals was observed as well as an increased rate of abortions 47. RVFV proved to be a zoonotic virus as laboratory workers became ill after exposure 48. Since the discovery of RVFV it has become apparent that RVFV is widespread in Africa, with occasionally major epidemics such as in 1951 in several states in South Africa 49. Many farmers lost a large proportion of their sheep and nearly all of their lambs, while the losses of cattle were less significant 50,51. Since then RVFV has remained endemic to South Africa, occasionally causing major epidemics with severe losses of sheep and cattle as a result, but also affecting humans 52,53. RVFV was reported in Egypt for the first time in 1977 after completion of the Aswan dam, which created a new breeding ground for mosquitoes 54. This outbreak was unique due to the large number of humans that were infected, which was estimated at 200,000 with 598 reported deaths 55-57. In 1987, RVFV outbreaks were reported for the first time in East Africa in Mauritania and Senegal 58,59. In the year 2000, the first incursion of RVFV outside of the African continent was reported, when two simultaneous outbreaks occurred on the Arabian Peninsula, one in northern Yemen and the other in Gazan 60. Nowadays, RVFV is endemic throughout the whole African continent and the Arabian Peninsula, occasionally causing major epidemics and epizootics 57. The history of these RVFV outbreaks, together with genomic analysis of RVFV strains from different regions suggest that RVFV is able to spread over long distances and is able to cause epizootics and epidemics after a single introduction 61. General introduction 13 often accompanied by jaundice and oedema. Haemorrhages can occur in the heart...

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Section: Question 3 How Does Gestational Age Affect the Outcome Of Asupporting

confidence: 60%

Section: Question 3 How Does Gestational Age Affect the Outcome Of Amentioning

confidence: 99%

Crossing barriers : How neglected arboviruses journey through the placenta

Oymans¹

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“…Likewise, Mendes et al proposed a classification of brain damage based on head CT findings in ZIKV exposed infants, establishing correlations between the most severe brain findings with trimester of ZIKV infection and severity of microcephaly at birth (Hoen et al, 2018). Thus, timing of ZIKV infection is a variable that has been consistently reported as being a determinant in the severity of clinical outcomes (Hoen et al, 2018;Karolina et al, 2020;Pool et al, 2019). However, because there are few infections outside of first trimester in our cohort, differences by trimester of infection were not able to be assessed.…”

Section: Discussionmentioning

confidence: 99%

Clinical and neurodevelopmental outcomes based on brain imaging studies in a Colombian cohort of children with probable antenatal Zika virus exposure

Daza¹,

Mercado

Moore

et al. 2021

Birth Defects Research

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Background: Our aim was to describe the neuroimaging and clinical evaluations of children with antenatal Zika-virus (ZIKV) exposure. Methods: The Colombian National Institute of Health performed serial clinical evaluations of children with probable antenatal ZIKV exposure (i.e., born to ZIKV symptomatic mothers or born with birth defects compatible with ZIKV infection, regardless of laboratory results) over 2 years that included head circumference (HC), eye examination, and neurodevelopmental assessments. Clinical neuroimaging studies (head computed tomography and/or brain magnetic resonance imaging) were analyzed for abnormalities, twodimensional measurements were made of the right and left frontal and occipital cortical thickness. Two abnormal patterns were defined: Pattern 1 (sum of four areas of cortex <6 cm) and Pattern 2 (sum of four areas of cortex ≥6 cm and < 10 cm).The findings and conclusions in this report are those of the authors and do not necessarily represent the official position of the Centers for Disease Control and Prevention.

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“…Such resistance, however, may vary in efficacy by gestational age. To this latter point, several virus infections have been demonstrated to exert more dramatic fetal effects when infection occurs early in pregnancy [ 107 , 108 , 109 , 110 ]. While a comprehensive review of the mechanisms involved in trophoblast-specific responses to infection are beyond the specific purview of this review, we would like to highlight studies from our own work that suggest that the STB from early and late gestation may have inherent and diametrically opposed susceptibilities to a variety of pathogens.…”

Section: Immune Interactions At Stb Interfacesmentioning

confidence: 99%

The Immunology of Syncytialized Trophoblast

Schust

Bonney

Sugimoto

et al. 2021

IJMS

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Multinucleate syncytialized trophoblast is found in three forms in the human placenta. In the earliest stages of pregnancy, it is seen at the invasive leading edge of the implanting embryo and has been called primitive trophoblast. In later pregnancy, it is represented by the immense, multinucleated layer covering the surface of placental villi and by the trophoblast giant cells found deep within the uterine decidua and myometrium. These syncytia interact with local and/or systemic maternal immune effector cells in a fine balance that allows for invasion and persistence of allogeneic cells in a mother who must retain immunocompetence for 40 weeks of pregnancy. Maternal immune interactions with syncytialized trophoblast require tightly regulated mechanisms that may differ depending on the location of fetal cells and their invasiveness, the nature of the surrounding immune effector cells and the gestational age of the pregnancy. Some specifically reflect the unique mechanisms involved in trophoblast cell–cell fusion (aka syncytialization). Here we will review and summarize several of the mechanisms that support healthy maternal–fetal immune interactions specifically at syncytiotrophoblast interfaces.

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Congenital Zika syndrome: association between the gestational trimester of maternal infection, severity of brain computed tomography findings and microcephaly at birth

Abstract: This is an open-access article distributed under the terms of the Creative Commons Attribution License.

Cited by 13 publications

References 23 publications

Crossing barriers : How neglected arboviruses journey through the placenta

Crossing barriers : How neglected arboviruses journey through the placenta

Clinical and neurodevelopmental outcomes based on brain imaging studies in a Colombian cohort of children with probable antenatal Zika virus exposure

The Immunology of Syncytialized Trophoblast

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