ArticleViruses2019
Host Immune Response to ZIKV in an Immunocompetent Embryonic Mouse Model of Intravaginal Infection.
Article in Viruses, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- FVB/NJ strain as a mouse model for cutaneous leishmaniasis by Leishmania (L.) amazonensis.Memorias do Instituto Oswaldo Cruz · 2024Article
- Neurodevelopment in Children Exposed to ZikaFrontiers in genetics · 2022Review
- From Mosquito Bites to Sexual Transmission: Evaluating Mouse Models of Zika Virus Infection.Viruses · 2021Review
- Characterization of subclinical ZIKV infection in immune-competent guinea pigs and mice.The Journal of general virology · 2021Article
- Animal models of congenital zika syndrome provide mechanistic insight into viral pathogenesis during pregnancy.PLoS neglected tropical diseases · 2020Review
- Beyond HIV infection: Neglected and varied impacts of CCR5 and CCR5Δ32 on viral diseases.Virus research · 2020Review
- Article
- Yellow Fever Vaccination in a Mouse Model Is Associated With Uninterrupted Pregnancies and Viable Neonates Except When Administered at Implantation Period.Frontiers in microbiology · 2020Article
- Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Zika virus (ZIKV) only induces mild symptoms in adults; however, it can cause congenital Zika syndrome (CZS), including microcephaly. Most of the knowledge on ZIKV pathogenesis was gained using immunocompromised mouse models, which do not fully recapitulate human pathology. Moreover, the study of the host immune response to ZIKV becomes challenging in these animals. Thus, the main goal of this study was to develop an immunocompetent mouse model to study the ZIKV spread and teratogeny. FVB/NJ immune competent dams were infected intravaginally with ZIKV during the early stage of pregnancy. We found that the placentae of most fetuses were positive for ZIKV, while the virus was detected in the brain of only about 42% of the embryos. To investigate the host immune response, we measured the expression of several inflammatory factors. Embryos from ZIKV-infected dams had an increased level of inflammatory factors, as compared to Mock. Next, we compared the gene expression levels in embryos from ZIKV-infected dams that were either negative or positive for ZIKV in the brain. The mRNA levels of viral response genes and cytokines were increased in both ZIKV-positive and negative brains. Interestingly, the levels of chemokines associated with microcephaly in humans, including CCL2 and CXCL10, specifically increased in embryos harboring ZIKV in the embryo brains.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.