Disease Manifestations of Canine Distemper Virus Infection in Ferrets Are Modulated by Vitamin A Status ,

Rodeheffer, Carey; Messling, Véronika von; Milot, Sylvain; Lépine, François; Manges, Amee R.; Ward, Brian J.

doi:10.1093/jn/137.8.1916

Cited by 27 publications

(12 citation statements)

References 45 publications

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“…Our current studies do not address the timing of retinoid treatment during clinical MeV infection however. A small animal model is required to investigate the role of RIG-I during established MeV infection [61].…”

Section: Discussionmentioning

confidence: 99%

RIG-I Is Required for the Inhibition of Measles Virus by Retinoids

et al. 2011

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Vitamin A can significantly decrease measles-associated morbidity and mortality. Vitamin A can inhibit the replication of measles virus (MeV) in vitro through an RARα- and type I interferon (IFN)-dependent mechanism. Retinoid-induced gene I (RIG-I) expression is induced by retinoids, activated by MeV RNA and is important for IFN signaling. We hypothesized that RIG-I is central to retinoid-mediated inhibition of MeV in vitro. We demonstrate that RIG-I expression is increased in cells treated with retinoids and infected with MeV. The central role of RIG-I in the retinoid-anti-MeV effect was demonstrated in the Huh-7/7.5 model; the latter cells having non-functional RIG-I. RAR-dependent retinoid signaling was required for the induction of RIG-I by retinoids and MeV. Retinoid signaling was also found to act in combination with IFN to induce high levels of RIG-I expression. RIG-I promoter activation required both retinoids and MeV, as indicated by markers of active chromatin. IRF-1 is known to be regulated by retinoids and MeV, but we found recruitment of IRF-1 to the RIG-I promoter by retinoids alone. Using luciferase expression constructs, we further demonstrated that the IRF-1 response element of RIG-I was required for RIG-I activation by retinoids or IFN. These results reveal that retinoid treatment and MeV infection induces significant RIG-I. RIG-I is required for the retinoid-MeV antiviral response. The induction is dependent on IFN, retinoids and IRF-1.

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Section: Discussionmentioning

confidence: 99%

RIG-I Is Required for the Inhibition of Measles Virus by Retinoids

et al. 2011

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“…Many viruses are known to interfere with type I IFN signaling at different steps, and ATRA has been shown to inhibit at least one other virus (vesicular stomatitis virus) in an IFN-independent manner (20). We have recently demonstrated that ferrets infected with an otherwise lethal canine distemper virus strain survive when given retinol supplements (55). Furthermore, we have preliminary evidence that mumps virus replication can be inhibited by retinoids in vitro in an IFN-dependent manner similar to that of MeV (unpublished results).…”

Section: Discussionmentioning

confidence: 99%

Retinoids inhibit measles virus through a type I IFN‐dependent bystander effect

et al. 2009

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Measles-associated mortality can be decreased in response to treatment with vitamin A. Our goal was to understand the mechanism by which vitamin A and other retinoids reduce measles virus (MeV) replication in vitro. MeV is known to inhibit type I interferon (IFN) signaling, and retinoids are increasingly implicated in modulating innate immunity. Type I IFN blocking antibodies abrogated the inhibitory effects of all-trans retinoic acid (ATRA) on MeV replication (EC(50) of ATRA: 3.17 x 10(-8) M). IFN-stimulated genes (ISGs) are up-regulated by ATRA in MeV-infected U937 cell cultures starting at 12 h and reaching a plateau at 24 h postinfection when compared to either treatment or infection alone. We found that this increased gene expression occurs in uninfected cells by using a transwell system where the uninfected cells were separated from infected cells by a membrane with 0.02-muM pores. Uninfected bystander cells from the ATRA-treated transwells did not support substantial viral replication when subsequently infected with MeV. In the absence of ATRA, the cells from the uninfected chamber did not up-regulate ISG expression and were not protected from subsequent challenge with virus. These results demonstrate that retinoids inhibit MeV replication by up-regulating elements of the innate immune response in uninfected bystander cells, making them refractory to productive infection during subsequent rounds of viral replication.

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“…The nutritional status of domestic dogs is thought to play a role in the outcome of infection (Appel, 1970), and recent studies with CDV in ferrets have suggested that vitamin A status may modulate the clinical presentation of infection (Rodeheffer et al, 2007). Jackals on the Namibian coast are highly dependent on the seals as a food source (Hiscocks and Perrin, 1987) and are restricted to killing young seal pups, before they grow too large, or to scavenging seals.…”

Section: Discussionmentioning

confidence: 99%

Epidemiology, Pathology, and Genetic Analysis of a Canine Distemper Epidemic in Namibia

Gowtage-Sequeira

Banyard

Barrett

et al. 2009

Journal of Wildlife Diseases

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ABSTRACT:Severe population declines have resulted from the spillover of canine distemper virus (CDV) into susceptible wildlife, with both domestic and wild canids being involved in the maintenance and transmission of the virus. This study (March 2001 to October 2003 collated case data, serologic, pathologic, and molecular data to describe the spillover of CDV from domestic dogs (Canis familiaris) to black-backed jackals (Canis mesomelas) during an epidemic on the Namibian coast. Antibody prevalence in jackals peaked at 74.1%, and the clinical signs and histopathologic observations closely resembled those observed in domestic dog cases. Viral RNA was isolated from the brain of a domestic dog from the outbreak area. Sequence data from the phosphoprotein (P) gene and the hemagglutinin (H) genes were used for phylogenetic analyses. The P gene sequence from the domestic dog shared 98% identity with the sequence data available for other CDV isolates of African carnivores. For the H gene, the two sequences available from the outbreak that decimated the lion population in Tanzania in 1994 were the closest match with the Namibian sample, being 94% identical across 1,122 base pairs (bp). Phylogenetic analyses based on this region clustered the Namibian sample with the CDV that is within the morbilliviruses. This is the first description of an epidemic involving black-backed jackals in Namibia, demonstrating that this species has the capacity for rapid and large-scale dissemination of CDV. This work highlights the threat posed to endangered wildlife in Namibia by the spillover of CDV from domestic dog populations. Very few sequence data are currently available for CDV isolates from African carnivores, and this work provides the first sequence data from a Namibian CDV isolate.

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Disease Manifestations of Canine Distemper Virus Infection in Ferrets Are Modulated by Vitamin A Status ,

Cited by 27 publications

References 45 publications

RIG-I Is Required for the Inhibition of Measles Virus by Retinoids

RIG-I Is Required for the Inhibition of Measles Virus by Retinoids

Retinoids inhibit measles virus through a type I IFN‐dependent bystander effect

Epidemiology, Pathology, and Genetic Analysis of a Canine Distemper Epidemic in Namibia

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