Zika Virus Infection in the Developing Mouse Produces Dramatically Different Neuropathology Dependent on Viral Strain

Noguchi, Kevin K.; Swiney, Brant S.; Williams, Sasha L.; Huffman, Jacob; Lucas, Katherine; Wang, Sophie H.; Kapral, Kayla M.; Li, Amber; Dikranian, Krikor

doi:10.1523/jneurosci.1376-19.2019

Cited by 19 publications

(21 citation statements)

References 61 publications

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“…Animal models of postnatal ZIKV infection have the potential to be highly informative, considering the paucity of studies in children. Postnatally ZIKV-infected neonatal mice demonstrate extensive apoptotic degeneration in several brain regions, including the hippocampus, with activation being followed by the fragmentation of the microglia [ 67 ]. Impairments in motor and cognitive functions were also found in mice infected with ZIKV postnatally [ 68 ].…”

Section: Preclinical Models Of Postnatal Zika Virus Infectionmentioning

confidence: 99%

Clinical and Preclinical Evidence for Adverse Neurodevelopment after Postnatal Zika Virus Infection

Raper

Chahroudi

2021

TropicalMed

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Although the Zika virus (ZIKV) typically causes mild or no symptoms in adults, during the 2015−2016 outbreak, ZIKV infection in pregnancy resulted in a spectrum of diseases in infants, including birth defects and neurodevelopmental disorders identified in childhood. While intense clinical and basic science research has focused on the neurodevelopmental outcomes of prenatal ZIKV infection, less is known about the consequences of infection during early life. Considering the neurotropism of ZIKV and the rapidly-developing postnatal brain, it is important to understand how infection during infancy may disrupt neurodevelopment. This paper reviews the current knowledge regarding early postnatal ZIKV infection. Emerging clinical evidence supports the hypothesis that ZIKV infection during infancy can result in negative neurologic consequences. However, clinical data regarding postnatal ZIKV infection in children are limited; as such, animal models play an important role in understanding the potential complications of ZIKV infection related to the vulnerable developing brain. Preclinical data provide insight into the potential behavioral, cognitive, and motor domains that clinical studies should examine in pediatric populations exposed to ZIKV during infancy.

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Section: Preclinical Models Of Postnatal Zika Virus Infectionmentioning

confidence: 99%

Clinical and Preclinical Evidence for Adverse Neurodevelopment after Postnatal Zika Virus Infection

Raper

Chahroudi

2021

TropicalMed

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“…In the first model, Zika crosses the placenta barrier resulting in fetal infection and CNS damage and residual intrauterine growth, in more severe cases the infection resulted in fetal death, in the second case, after treatment with anti-interferon (IFN)-AB antibodies in the placenta, infection of the developing embryo occurred but was less severe and did not cause the death of the fetus. Furthermore, in Noguchi et al's 2019 [34] study, the effect of the Zika virus infection on the brain and the CNS of the mouse are presented-resulting in massive neurodegeneration of infected regions. The Brazilian Zika virus stain is also reported in the research and produces particularly devastating neuropathology in the fetal brain opposed to the viral French Polynesia stain.…”

Section: Resultsmentioning

confidence: 99%

“…No research had a score of 9 because all studies had a negative response to criterion5 (Table 1). [34] Notes: 1. Representative exposure sample, 2. selection of non-exposed, 3. exposure finding, 4. outcome did not precede the study, 5. adaptation for educational level, 6. adaptation for additional confounding factor, 7. outcome evaluation, 8. adequate monitoring time, 9. non-bias of wear.…”

Section: Methodsmentioning

confidence: 99%

Zika Virus and the Risk of Developing Microcephaly in Infants: A Systematic Review

Antoniou

Orovou

Sarella

et al. 2020

IJERPH

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The global epidemic of Zika virus has been a major public health problem affecting pregnant women and their infants. Zika virus causes a viral disease transmitted to humans mainly by the infected Aedes mosquito bite. The infection is not severe in most cases; however, there is evidence that infection during pregnancy may be associated with fetal genetic abnormalities (including microcephaly). In addition to microcephaly and other malformations, some specific lesions in the central nervous system have been reported. The aim of this systematic review was to determine the risk of developing microcephaly in infants whose mothers were infected with Zika virus in pregnancy. Epidemiological studies and case reports were incorporated in our review, finally including 15 articles from an initial pool of 355 related papers. Most studies have linked maternal infection during pregnancy to the development of neonatal microcephaly. The period considered most dangerous is the first trimester and the beginning or the whole of the second trimester. In order to understand the relationship between Zika virus and microcephaly in infants, a cohort study will be able to estimate the time from the onset of Zika infection and the full spectrum of adverse pregnancy outcomes.

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“…Previous studies demonstrated that the African strain of ZIKV causes more severe infection, including in utero [ 55 , 56 ]. In vivo studies in which mice were infected with different strains of ZIKV also demonstrate variation in tissues tropism [ 57 ], neuropathology [ 58 ] and innate immune response [ 59 ]. Comparative studies with multiple strains of ZIKV are critical for defining genetic variation that may contribute to differences in immune response, pathology, and forward transmission potential.…”

Section: Discussionmentioning

confidence: 99%

Three Immunocompetent Small Animal Models That Do Not Support Zika Virus Infection

et al. 2021

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Zika virus (ZIKV) is a mosquito-borne flavivirus that is primarily transmitted to humans through the bite of an infected mosquito. ZIKV causes disease in infected humans with added complications of Guillain-Barré syndrome and birth defects in infants born to mothers infected during pregnancy. There are several large immunocompetent animal models for ZIKV including non-human primates (NHPs). NHP models closely reflect human infection; however, due to sample size restrictions, investigations into the effects of transmission route and the impacts on disease dynamics have been understudied. Mice have been widely used for modeling ZIKV infection, yet there are few ZIKV-susceptible immunocompetent mouse models and none of these have been used to investigate sexual transmission. In an effort to identify a small immunocompetent animal model to characterize sexual transmission of ZIKV, we attempt experimental infection of multimammate mice, New Zealand white rabbits, and Hartley guinea pigs. The multimammate mouse is the natural reservoir of Lassa fever virus and has been identified to harbor other human pathogens. Likewise, while NZW rabbits are susceptible to West Nile virus, they have not yet been examined for their susceptibility to infection with ZIKV. Guinea pigs have been successfully used as models for ZIKV infection, but only in immunocompromised life stages (young or pregnant). Here, it was found that the multimammate mouse and New Zealand White (NZW) rabbits are not susceptible ZIKV infection as determined by a lack viral RNA in tissues and fluids collected. Sexually mature male Hartley guinea pigs were inoculated subcutaneously and by mosquito bite, but found to be refractory to ZIKV infection, contrary to findings of other studies in young and pregnant guinea pigs. Interestingly, here it is shown that adult male guinea pigs are not susceptible to ZIKV infection, even when infected by natural route (e.g., mosquito bite). Although a new small animal model for the sexual transmission for ZIKV was not established through this study, these findings provide information on outbred animal species that are not permissive to infection (NZW rabbits and multimammate mice) and new information surrounding limitations of a previously established animal model (guinea pigs).

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Zika Virus Infection in the Developing Mouse Produces Dramatically Different Neuropathology Dependent on Viral Strain

Cited by 19 publications

References 61 publications

Clinical and Preclinical Evidence for Adverse Neurodevelopment after Postnatal Zika Virus Infection

Clinical and Preclinical Evidence for Adverse Neurodevelopment after Postnatal Zika Virus Infection

Zika Virus and the Risk of Developing Microcephaly in Infants: A Systematic Review

Three Immunocompetent Small Animal Models That Do Not Support Zika Virus Infection

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