Fetal Brain Infection Is Not a Unique Characteristic of Brazilian Zika Viruses

Setoh, Yin Xiang; Peng, Nias Y. G.; Nakayama, Eri; Amarilla, Alberto A.; Prow, Natalie A.; Suhrbier, Andreas; Khromykh, Alexander A.

doi:10.3390/v10100541

Cited by 15 publications

(19 citation statements)

References 35 publications

(47 reference statements)

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“…Likewise, intracranial inoculation of neonatal mice confirmed a similar neurovirulence phenotype across ZIKV lineages. A recent study identified the potential capacity of an ancestral Asian strain to cause fetal brain infection after maternal infection in mice [39]; that study used a cloned virus created from reverse genetics that corresponded to a publicly available consensus ZIKV genome sequence. To our knowledge, our study is the first to assess a low-passage African isolate, or the S139N substitution, in a vertical transmission model.…”

Section: Discussionmentioning

confidence: 99%

Zika viruses of African and Asian lineages cause fetal harm in a mouse model of vertical transmission

et al. 2019

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Congenital Zika virus (ZIKV) infection was first linked to birth defects during the American outbreak in 2015/2016. It has been proposed that mutations unique to the Asian/American-genotype explain, at least in part, the ability of Asian/American ZIKV to cause congenital Zika syndrome (CZS). Recent studies identified mutations in ZIKV infecting humans that arose coincident with the outbreak in French Polynesia and were stably maintained during subsequent spread to the Americas. Here we show that African ZIKV can infect and harm fetuses and that the S139N substitution that has been associated with the American outbreak is not essential for fetal harm. Our findings, in a vertical transmission mouse model, suggest that ZIKV will remain a threat to pregnant women for the foreseeable future, including in Africa, Southeast Asia, and the Americas. Additional research is needed to better understand the risks associated with ZIKV infection during pregnancy, both in areas where the virus is newly endemic and where it has been circulating for decades.

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Section: Discussionmentioning

confidence: 99%

Zika viruses of African and Asian lineages cause fetal harm in a mouse model of vertical transmission

et al. 2019

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“…Viral replication rate between resistant CC001 and highly susceptible CC071 mice was investigated as a plausible mechanism for the differences in susceptibility between these two strains. MEFs are a semi-permanent source of cells which have been extensively used to assess viral replication (73, 74) including with ZIKV (75, 76). Although not the primary target of ZIKV infection, macrophages are also a relevant cell type to investigate ZIKV replication and innate responses (77).…”

Section: Discussionmentioning

confidence: 99%

Genetic diversity of Collaborative Cross mice controls viral replication, clinical severity and brain pathology induced by Zika virus infection, independently of Oas1b

Manet¹,

Simon‐Lorière

Jouvion

et al. 2019

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1The explosive spread of Zika virus (ZIKV) has been associated with major variations in severe 2 disease and congenital afflictions among infected populations, suggesting an influence of host 3 genes. We investigated how genome-wide variants could impact susceptibility to ZIKV infection 4 in mice. We first describe that the susceptibility of Ifnar1 knockout mice is largely influenced by 5 their genetic background. We then show that the broad genetic diversity of Collaborative Cross 6 mice, which receptor to type I interferon (IFNAR) was blocked by anti-IFNAR antibody, 7 expressed phenotypes ranging from complete resistance to severe symptoms and death with large 8 variations in the peak and rate of decrease of plasma viral load, in brain viral load, in brain 9 histopathology and in viral replication rate in infected cells. Differences of susceptibility 701 Wakimoto M, Rabello RS,

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“…Furthermore, reverse substitution of N139S in Asian strains did not alter infectivity or rates of resorption, suggesting that the S139 substitution is not principally required for fetal harm, at least in a mouse model [ 47 ]. Thus, CZS might not be a novel syndrome caused by a new ZIKV variant, but rather a preexisting disease that was recognized due to the large-scale outbreak in South America [ 50 ].…”

Section: Other Rodentsmentioning

confidence: 99%

Animal models of congenital zika syndrome provide mechanistic insight into viral pathogenesis during pregnancy

et al. 2020

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In utero Zika virus (ZIKV; family Flaviviridae ) infection causes a distinct pattern of birth defects and disabilities in the developing fetus and neonate that has been termed congenital zika syndrome (CZS). Over 8,000 children were affected by the 2016 to 2017 ZIKV outbreak in the Americas, many of whom developed CZS as a result of in utero exposure. To date, there is no consensus about how ZIKV causes CZS; animal models, however, are providing mechanistic insights. Using nonhuman primates, immunocompromised mice, immunocompetent mice, and other animal models (e.g., pigs, sheep, guinea pigs, and hamsters), studies are showing that maternal immunological responses, placental infection and inflammation, as well as viral genetic factors play significant roles in predicting the downstream consequences of in utero ZIKV infection on the development of CZS in offspring. There are thousands of children suffering from adverse consequences of CZS. Therefore, the animal models developed to study ZIKV-induced adverse outcomes in offspring could provide mechanistic insights into how other viruses, including influenza and hepatitis C viruses, impact placental viability and fetal growth to cause long-term adverse outcomes in an effort to identify therapeutic treatments.

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Fetal Brain Infection Is Not a Unique Characteristic of Brazilian Zika Viruses

Cited by 15 publications

References 35 publications

Zika viruses of African and Asian lineages cause fetal harm in a mouse model of vertical transmission

Zika viruses of African and Asian lineages cause fetal harm in a mouse model of vertical transmission

Genetic diversity of Collaborative Cross mice controls viral replication, clinical severity and brain pathology induced by Zika virus infection, independently of Oas1b

Animal models of congenital zika syndrome provide mechanistic insight into viral pathogenesis during pregnancy

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