Ultrastructural study of Rift Valley fever virus in the mouse model

Reed, Christopher; Steele, Keith; Honko, Anna N.; Shamblin, Joshua D.; Hensley, Lisa E.; Smith, Darci R.

doi:10.1016/j.virol.2012.05.012

Cited by 32 publications

(28 citation statements)

References 35 publications

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“…In order to test the effect of RVFV infection upon the level of ␤-catenin in vivo, the presence of ␤-catenin was analyzed in the liver and brain of mice that were either noninfected or infected with the ⌬NSs or ZH strain. Of note, the liver and brain are two main organs targeted during RVFV infection (60). Mice were euthanized at days 3 and 5 p.i., and the liver and brain were removed; one half of each organ was used for total protein purification and Western blot analysis, and the other half was used for RNA purification and RT-qPCR analysis.…”

Section: Licl Treatment Enhances Constitutive Ifn-␤ Gene Expressionmentioning

confidence: 99%

β-Catenin Upregulates the Constitutive and Virus-Induced Transcriptional Capacity of the Interferon Beta Promoter through T-Cell Factor Binding Sites

Marcato

Luron

Laqueuvre

et al. 2016

Molecular and Cellular Biology

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. Rapid upregulation of IFN-␤ gene expression occurs after recognition of viral nucleic acids by pattern recognition receptors (PRRs) consisting of either cytosolic receptors, such as retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated antigen 5 (MDA-5), or membrane-associated Toll-like receptors, such as Toll-like receptor 3 (TLR3) (3). After sensing single-or doublestranded RNA of viral origin, these receptors activate signaling pathways, implicating the phosphorylation and nuclear translocation of several transcription factors, among which is interferon regulatory factor 3 (IRF3), rapidly leading downstream to a robust activation of expression of the IFN-␤ gene. After being secreted, the IFN-␤ protein binds to the type I interferon receptor and triggers the JAK-STAT1/2 signal transduction pathway. This pathway leads to the activation and inhibition of the expression of a large set of genes that constitute the type I IFN response mounted to antagonize viral infection at different levels (4).Mice lacking IFN-␤ (5) or the subunit of the type I interferon receptor (6, 7) are highly susceptible to viral infections. They succumb to sublethal doses of a variety of viruses, thus confirming the main role of IFN-␤ in the establishment of an innate antiviral response. However, beyond the antiviral response, IFN-␤ affects a wide range of other biological functions; for the most part, these are related to modulation of the immune (innate and adaptive) and inflammatory responses as well as to cell proliferation and differentiation. Even though IFN-␤ has been described to have an anti-inflammatory benefit, it has also been implicated in the development of several inflammatory and autoimmune diseases (8-10). Hence, the beneficial or detrimental outcome of IFN-␤ expression for the organism depends on the timing and kinetics of IFN-␤ synthesis and the amount of IFN-␤ being synthesized (11,12). If a marked activation of IFN-␤ gene expression is required to efficiently set up the appropriate response to an external aggression, such as virus infection, this response needs to be adjusted in order to limit its pathological side effects.As expected for a gene with pleiotropic functions, its transcriptional state is regulated at different levels. At the cellular level, only a stochastic fraction of the infected cells produces 14) as a way to avoid an exacerbated and uncontrolled IFN response. At the nuclear level, one IFN-␤ allele localizes within interchromosomal regions rich in NF-B DNA binding sites before and after infection (15), whereas the other allele localizes next to pericentromeric heterochromatin (PCH) clusters in the absence of infection and dissociates from PCH clusters during infection (16). The monoallelic characteristic of these particular subnuclear localizations suggests that a yet undeciphered regulatory mechanism exists at the chromosome level. Finally, at the promoter level, the coordinated action of several transcription factors and chromatin-remodeling complexes (17-21) regulates the...

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Section: Licl Treatment Enhances Constitutive Ifn-␤ Gene Expressionmentioning

confidence: 99%

β-Catenin Upregulates the Constitutive and Virus-Induced Transcriptional Capacity of the Interferon Beta Promoter through T-Cell Factor Binding Sites

Marcato

Luron

Laqueuvre

et al. 2016

Molecular and Cellular Biology

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“…Vacuolar degeneration, lipid droplet accumulation and numerous phagolysosomes were apparent in the examined specimens. In consistent, Reed et al 25 found that RVFV-infected mice maintained many fat vacuoles, pale cytoplasm and numerous phagolysosomes. Examination of mitochondria revealed mitochondrial damage, mostly, in the form of cisternal segmentation and vesiculation 25.…”

Section: Discussionmentioning

confidence: 66%

“…In consistent, Reed et al 25 found that RVFV-infected mice maintained many fat vacuoles, pale cytoplasm and numerous phagolysosomes. Examination of mitochondria revealed mitochondrial damage, mostly, in the form of cisternal segmentation and vesiculation 25. In this context, Narayanan et al 27 reported that the RVF viral protein accumulated in the mitochondria of RVFV-infected hepatocytes and contributed to mitochondrial damage and production of ROS.…”

Section: Discussionmentioning

confidence: 66%

“…Additions to the presence of viral particles, large inclusion bodies consisting of electron-lucent large bodies with electron-dense aggregates in intact hepatocytes were seen. The presence of these inclusions in intact hepatocytes indicates an early infection of these cells 25. Ellis et al 26 reported that RVF's inclusions formed of either fine or coarse materials.…”

Section: Discussionmentioning

confidence: 99%

“…RVF viral particles were reported to be rarely seen in hepatic tissues. This may be due to that hepatocytes undergo abortive infection or apoptosis before release of mature RVF virions 25. Additions to the presence of viral particles, large inclusion bodies consisting of electron-lucent large bodies with electron-dense aggregates in intact hepatocytes were seen.…”

Section: Discussionmentioning

confidence: 99%

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Ultrastructural pathology of human liver in Rift Valley fever

et al. 2016

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Rift Valley fever (RVF) is a zoonotic disease that primarily affects ruminant animals and can also cause fatal disease in humans. In the current report, we present the ultrastructural changes in the liver of a man aged 60 years who died from RVF in the Aseer Central Hospital, Abha, Saudi Arabia. The main hepatic changes by transmission electron microscopy included the presence of 95-115 nm electron-dense particles consistent with RVF virions, nuclear condensation, vacuolar degeneration, lipid droplet accumulation and mitochondrial damage and dilation. There were also viral inclusion bodies with electron-dense aggregates, dilation of intercellular spaces, damage of sinusoidal microvilli with widening of space of Disse, dilation of bile canaliculi and increasing number of phagolysosomes.

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