Persistent Zika virus infection in porcine conceptuses is associated with elevated <i>in utero</i> cortisol levels

Trus, Ivan; Darbellay, Joseph; Huang, Yanyun; Gilmour, Matthew W.; Safronetz, David; Gerdts, Volker; Karniychuk, Uladzimir

doi:10.1080/21505594.2018.1504558

Cited by 18 publications

(53 citation statements)

References 35 publications

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“…Infected plates were incubated (5% CO 2 , +37 • C) until the sampling time point when supernatants were collected, clarified (2,000 g, 5 min) and frozen (−80 • C) for subsequent infectious virus quantification (34)(35)(36)(37). After the supernatant collection, the plate with infected cells was dried and frozen (−20 • C).…”

Section: In Vitro Replication Phenotypes Of Cpg-recoded Zikv Variantsmentioning

confidence: 99%

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CpG-Recoding in Zika Virus Genome Causes Host-Age-Dependent Attenuation of Infection With Protection Against Lethal Heterologous Challenge in Mice

et al. 2020

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Experimental increase of CpG dinucleotides in an RNA virus genome impairs infection providing a promising approach for vaccine development. While CpG recoding is an emerging and promising vaccine approach, little is known about infection phenotypes caused by recoded viruses in vivo. For example, infection phenotypes, immunogenicity, and protective efficacy induced by CpG-recoded viruses in different age groups were not studied yet. This is important, because attenuation of infection phenotypes caused by recoded viruses may depend on the population-based expression of cellular components targeting viral CpG dinucleotides. In the present study, we generated several Zika virus (ZIKV) variants with the increasing CpG content and compared infection in neonatal and adult mice. Increasing the CpG content caused host-age-dependent attenuation of infection with considerable attenuation in neonates and high attenuation in adults. Expression of the zinc-finger antiviral protein (ZAP)-the host protein targeting viral CpG dinucleotides-was also age-dependent. Similar to the wild-type virus, ZIKV variants with the increased CpG content evoked robust cellular and humoral immune responses and protection against lethal challenge. Collectively, the host age should be accounted for in future studies on mechanisms targeting viral CpG dinucleotides, development of safe dinucleotide recoding strategies, and applications of CpG-recoded vaccines.

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Section: In Vitro Replication Phenotypes Of Cpg-recoded Zikv Variantsmentioning

confidence: 99%

“…For quantification of infectious ZIKV loads in cell culture media the endpoint dilution assay was used as described before (34)(35)(36)(37)42). Cell culture media were serially diluted 5-fold in four replicates starting from 1:5, and 50 µl of each dilution was added to confluent VERO cells cultured in 96-well plates.…”

Section: Virus Titrationmentioning

confidence: 99%

CpG-Recoding in Zika Virus Genome Causes Host-Age-Dependent Attenuation of Infection With Protection Against Lethal Heterologous Challenge in Mice

et al. 2020

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“…Pigs have large litters (greater than or equal to 21 piglets) similar to mice but have greater gestational periods of 114 days . Additionally, each porcine fetus possesses an individual placenta and amniotic membrane . These models therefore provide ample number of replicates to study congenital deformities and a long time frame to study the infectivity of the virus in pregnant mothers.…”

Section: Research Models Of Zikv Infectionmentioning

confidence: 68%

“…Porcine‐based models are also gaining recognition as preclinical models since they are closely related to humans with respect to anatomy, physiology, genetics, and immunity . Pigs have large litters (greater than or equal to 21 piglets) similar to mice but have greater gestational periods of 114 days . Additionally, each porcine fetus possesses an individual placenta and amniotic membrane .…”

Section: Research Models Of Zikv Infectionmentioning

confidence: 99%

Zika virus: Molecular responses and tissue tropism in the mammalian host

Shaily

Upadhya

2019

Reviews in Medical Virology

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Zika virus (ZIKV) outbreaks have raised alarm because of reports of congenital Zika virus syndrome in infants. The virus is also known to cause the debilitating Guillain-Barré syndrome in adults. As a result, extensive research has been carried out on the virus over the past few years. To study the molecular responses of viral infectivity in mammals, in vitro two-dimensional and three-dimensional cellular models have been employed. The in vivo models of mouse, pig, chicken, and nonhuman primates are primarily used to investigate the teratogenicity of the virus, to study effects of the virus on specific tissues, and to study the systemic effects of a proposed antiviral agent. The virus exhibits wide tissue tropism in the mammalian host.

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“…Molecular mimicry between host and virus has also been invoked, where numerous short peptide sequences from human proteins, including those involved in microcephaly or other neurological conditions, are shared with ZIKV‐derived ones . Finally, because of the ability of ZIKV to cross the placental barrier, fetal pathogenesis has also been linked with placental inflammatory response and increased in utero levels of cortisol …”

Section: Introduction: Zikv‐mediated Pathogenesismentioning

confidence: 99%

Explaining Pathogenicity of Congenital Zika and Guillain–Barré Syndromes: Does Dysregulation of RNA Editing Play a Role?

2019

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Previous studies of Zika virus (ZIKV) pathogenesis have focused primarily on virus‐driven pathology and neurotoxicity, as well as host‐related changes in cell proliferation, autophagy, immunity, and uterine function. It is now hypothesized that ZIKV pathogenesis arises instead as an (unintended) consequence of host innate immunity, specifically, as the side effect of an otherwise well‐functioning machine. The hypothesis presented here suggests a new way of thinking about the role of host immune mechanisms in disease pathogenesis, focusing on dysregulation of post‐transcriptional RNA editing as a candidate driver of a broad range of observed neurodevelopmental defects and neurodegenerative clinical symptoms in both infants and adults linked with ZIKV infections. The authors collect and synthesize existing evidence of ZIKV‐mediated changes in the expression of adenosine deaminases acting on RNA (ADARs), known links between abnormal RNA editing and pathogenesis, as well as ideas for future research directions, including potential treatment strategies.

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Persistent Zika virus infection in porcine conceptuses is associated with elevated in utero cortisol levels

Cited by 18 publications

References 35 publications

CpG-Recoding in Zika Virus Genome Causes Host-Age-Dependent Attenuation of Infection With Protection Against Lethal Heterologous Challenge in Mice

CpG-Recoding in Zika Virus Genome Causes Host-Age-Dependent Attenuation of Infection With Protection Against Lethal Heterologous Challenge in Mice

Zika virus: Molecular responses and tissue tropism in the mammalian host

Explaining Pathogenicity of Congenital Zika and Guillain–Barré Syndromes: Does Dysregulation of RNA Editing Play a Role?

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