Advances in Zika Virus–Host Cell Interaction: Current Knowledge and Future Perspectives

Lee, Jae Kwan; Shin, Ok Sarah

doi:10.3390/ijms20051101

Cited by 46 publications

(43 citation statements)

References 120 publications

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“…In particular, the effect of neurotropic virus infection on hNPCs has been well demonstrated through extensive research. Zika virus, in particular, directly infects human neural progenitor cells and results in transcriptional dysregulation and attenuated cell growth, in addition to cytotoxic effects, leading to the abrogation of neurogenesis [31][32][33][34].…”

Section: Discussionmentioning

confidence: 99%

Coxsackievirus B3 Infection of Human Neural Progenitor Cells Results in Distinct Expression Patterns of Innate Immune Genes

Gim

Lee

et al. 2020

Viruses

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Coxsackievirus B3 (CVB3), a member of Picornaviridae family, is an important human pathogen that causes a wide range of diseases, including myocarditis, pancreatitis, and meningitis. Although CVB3 has been well demonstrated to target murine neural progenitor cells (NPCs), gene expression profiles of CVB3-infected human NPCs (hNPCs) has not been fully explored. To characterize the molecular signatures and complexity of CVB3-mediated host cellular responses in hNPCs, we performed QuantSeq 3′ mRNA sequencing. Increased expression levels of viral RNA sensors (RIG-I, MDA5) and interferon-stimulated genes, such as IFN-β, IP-10, ISG15, OAS1, OAS2, Mx2, were detected in response to CVB3 infection, while IFN-γ expression level was significantly downregulated in hNPCs. Consistent with the gene expression profile, CVB3 infection led to enhanced secretion of inflammatory cytokines and chemokines, such as interleukin-6 (IL-6), interleukin-8 (IL-8), and monocyte chemoattractant protein-1 (MCP-1). Furthermore, we show that type I interferon (IFN) treatment in hNPCs leads to significant attenuation of CVB3 RNA copy numbers, whereas, type II IFN (IFN-γ) treatment enhances CVB3 replication and upregulates suppressor of cytokine signaling 1/3 (SOCS) expression levels. Taken together, our results demonstrate the distinct molecular patterns of cellular responses to CVB3 infection in hNPCs and the pro-viral function of IFN-γ via the modulation of SOCS expression.

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Section: Discussionmentioning

confidence: 99%

Coxsackievirus B3 Infection of Human Neural Progenitor Cells Results in Distinct Expression Patterns of Innate Immune Genes

Gim

Lee

et al. 2020

Viruses

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“…The ZIKV genome is comprised of three structural (C, prM, and E) and seven non-structural (NS) proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5) [6,7]. Flaviviruses utilize diverse strategies involving NS proteins to suppress interferon (IFN)-mediated pathways.…”

Section: Introductionmentioning

confidence: 99%

Zika Virus-Induction of the Suppressor of Cytokine Signaling 1/3 Contributes to the Modulation of Viral Replication

2020

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Zika virus (ZIKV) is a mosquito-borne flavivirus that has emerged and caused global outbreaks since 2007. Although ZIKV proteins have been shown to suppress early anti-viral innate immune responses, little is known about the exact mechanisms. This study demonstrates that infection with either the African or Asian lineage of ZIKV leads to a modulated expression of suppressor of cytokine signaling (SOCS) genes encoding SOCS1 and SOCS3 in the following cell models: A549 human lung adenocarcinoma cells; JAr human choriocarcinoma cells; human neural progenitor cells. Studies of viral gene expression in response to SOCS1 or SOCS3 demonstrated that the knockdown of these SOCS proteins inhibited viral NS5 or ZIKV RNA expression, whereas overexpression resulted in an increased expression. Moreover, the overexpression of SOCS1 or SOCS3 inhibited the retinoic acid-inducible gene-I-like receptor-mediated activation of both type I and III interferon pathways. These results imply that SOCS upregulation following ZIKV infection modulates viral replication, possibly via the regulation of anti-viral innate immune responses.

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“…Clinical observation of birth defects during the recent epidemic has also emphasized ZIKV as an important threat to public health in the Americas. ZIKV is a mosquito-borne flavivirus that can undergo vertical transmission to cause serious fetal defects, including microcephaly and abnormal central nervous system development [63,64]. Previous reports have confirmed ZIKV RNA in the human fetal brain and amniotic fluid [65,66].…”

Section: Viral Infections During Pregnancymentioning

confidence: 99%

Recent Updates on Research Models and Tools to Study Virus–Host Interactions at the Placenta

Lee

Park

et al. 2019

Viruses

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The placenta is a unique mixed organ, composed of both maternal and fetal tissues, that is formed only during pregnancy and serves as the key physiological and immunological barrier preventing maternal–fetal transmission of pathogens. Several viruses can circumvent this physical barrier and enter the fetal compartment, resulting in miscarriage, preterm birth, and birth defects, including microcephaly. The mechanisms underlying viral strategies to evade the protective role of placenta are poorly understood. Here, we reviewed the role of trophoblasts and Hofbauer cells in the placenta and have highlighted characteristics of vertical and perinatal infections caused by a wide range of viruses. Moreover, we explored current progress and future opportunities in cellular targets, pathogenesis, and underlying biological mechanisms of congenital viral infections, as well as novel research models and tools to study the placenta.

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Advances in Zika Virus–Host Cell Interaction: Current Knowledge and Future Perspectives

Cited by 46 publications

References 120 publications

Coxsackievirus B3 Infection of Human Neural Progenitor Cells Results in Distinct Expression Patterns of Innate Immune Genes

Coxsackievirus B3 Infection of Human Neural Progenitor Cells Results in Distinct Expression Patterns of Innate Immune Genes

Zika Virus-Induction of the Suppressor of Cytokine Signaling 1/3 Contributes to the Modulation of Viral Replication

Recent Updates on Research Models and Tools to Study Virus–Host Interactions at the Placenta

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