Zika Virus Vertical Transmission in Children With Confirmed Antenatal Exposure

Brasil, Patrícia; Vasconcelos, Zilton Farias Meira de; Kerin, Tara; Gabaglia, Claudia Raja; Ribeiro, Ieda Pereira; Bonaldo, Myrna C.; Damasceno, Luana; Pone, Marcos Vinícius da Silva; Pone, Sheila Moura; Zin, Andréa; Tsui, Irena; Adachi, Kristina; Pereira, José Paulo; Gaw, Stephanie L.; Carvalho, L. M. de; Cunha, Denise Cotrim da; Guida, Letícia da Cunha; Rocha, Michael S.; Cherry, James D.; Wang, Lulan; Aliyari, Saba R.; Cheng, Genhong; Foo, Suan-Sin; Chen, Weiqiang; Jung, Jae U.; Brickley, Elizabeth B.; Moreira, Maria Elisabeth Lopes; Nielsen‐Saines, Karin

doi:10.1101/2020.02.26.20028399

Cited by 3 publications

(1 citation statement)

References 32 publications

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“…ZIKV is a unique vector-born flavivirus in that it has two additional routes of transmission, sexual (6)(7)(8) and vertical (9)(10)(11)(12)(13). The risk of vertical transmission is as high as 46% in the 1 st trimester of pregnancy, and vertically transmitted ZIKV can infect the developing fetal brain producing CZS in about 9% of babies born to mothers infected in the 1 st trimester (14).…”

Section: Introductionmentioning

confidence: 99%

Zika virus induces mitotic catastrophe in human neural progenitors by triggering unscheduled mitotic entry in the presence of DNA damage while functionally depleting nuclear PNKP

Rychłowska

Agyapong

Weinfeld

et al. 2021

Preprint

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Vertical transmission of Zika virus (ZIKV) leads with high frequency to congenital ZIKV syndrome (CZS), whose worse outcome is microcephaly. However, the mechanisms of congenital ZIKV neurodevelopmental pathologies, including direct cytotoxicity to neural progenitor cells (NPC), placental insufficiency, and immune responses, remain incompletely understood. At the cellular level, microcephaly typically results from death or insufficient proliferation of NPC or cortical neurons. NPCs replicate fast, requiring efficient DNA damage responses to ensure genome stability. Like congenital ZIKV infection, mutations in the polynucleotide 5’-kinase 3’-phosphatase (PNKP) gene, which encodes a critical DNA damage repair enzyme, results in recessive syndromes often characterized by congenital microcephaly with seizures (MCSZ). We thus tested whether there were any links between ZIKV and PNKP. Here we show that a PNKP phosphatase inhibitor inhibits ZIKV replication. PNKP relocalized from the nucleus to the cytoplasm in infected cells, co-localizing with the marker of ZIKV replication factories (RF) NS1 and resulting in functional nuclear PNKP depletion. Although infected NPC accumulated DNA damage, they failed to activate the DNA damage checkpoint kinases Chk1 and Chk2. ZIKV also induced activation of cytoplasmic CycA/CDK1 complexes, which trigger unscheduled mitotic entry. Inhibition of CDK1 activity inhibited ZIKV replication and the formation of RF, supporting a role of cytoplasmic CycA/CDK1 in RF morphogenesis. In brief, ZIKV infection induces mitotic catastrophe resulting from unscheduled mitotic entry in the presence of DNA damage. PNKP and CycA/CDK1 are thus host factors participating in ZIKV replication in NPC, and probably pathogenesis.

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Section: Introductionmentioning

confidence: 99%

Zika virus induces mitotic catastrophe in human neural progenitors by triggering unscheduled mitotic entry in the presence of DNA damage while functionally depleting nuclear PNKP

Rychłowska

Agyapong

Weinfeld

et al. 2021

Preprint

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Fetal Central Nervous System Anomalies According to RT-PCR and Trimester of Maternal Infection with ZIKV. A Prospective Study

et al. 2020

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Perinatal COVID-19 Pandemic: Short- and Long-Term Impacts on the Health of Offspring

Cavalcante¹,

Parente²,

Almeida³

et al. 2022

Contemporary Developments and Perspectives in International Health Security - Volume 3

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Currently, the consequences of coronavirus disease 2019 (COVID-19) in children of mothers affected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection during pregnancy are unknown. In addition to pregnancy risks, the impact of COVID-19 on the health of these children can occur in the short, medium, and long term. Initial data reveal a low risk of vertical transmission during the third trimester of pregnancy and through breastfeeding. However, despite this low risk, cases of neonatal COVID-19 have already been reported in the literature. Historically, other viral infections during pregnancy have been associated with an increased risk of neuropsychiatric diseases in the offspring of affected pregnant women, even in the absence of fetal infection. This study aimed to review the impact of viral infections on the offspring of mothers affected in the perinatal period and discuss and determine measures for the possible consequences of COVID-19 in the offspring of pregnant women infected with SARS-CoV-2.

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Zika Virus Vertical Transmission in Children With Confirmed Antenatal Exposure

Cited by 3 publications

References 32 publications

Zika virus induces mitotic catastrophe in human neural progenitors by triggering unscheduled mitotic entry in the presence of DNA damage while functionally depleting nuclear PNKP

Zika virus induces mitotic catastrophe in human neural progenitors by triggering unscheduled mitotic entry in the presence of DNA damage while functionally depleting nuclear PNKP

Fetal Central Nervous System Anomalies According to RT-PCR and Trimester of Maternal Infection with ZIKV. A Prospective Study

Perinatal COVID-19 Pandemic: Short- and Long-Term Impacts on the Health of Offspring

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