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Host range and specificity of the Drosophila C virus.

ABSTRACT: The Drosophila C virus (DCV) is a common and well-studied Drosophila pathogen. Although natural infections are known from Drosophila melanogaster and D. simulans, and artificial infections have been reported from several Drosophila species and other insects, it remains unclear to date whether DCV infections also occur naturally in other Drosophila species.Using reverse transcription PCR, we detected natural infections in six Drosophila species, which have not been previously known as natural hosts. By subsequent Sanger sequencing we compared DCV haplotypes among eight Drosophila host species. Our data suggest that cross-infections might be frequent both within and among species within the laboratory environment. Moreover, we find that some lines exhibit multiple infections with distinct DCV haplotypes.Our results suggest that the natural host range of DCV is much broader than previously assumed and that cross-infections might be a common phenomenon in the laboratory, even among different Drosophila hosts.

SUBMITTER: Kapun M

PROVIDER: S-EPMC2928731 | biostudies-literature | 2010 Aug

REPOSITORIES: biostudies-literature

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Host range and specificity of the Drosophila C virus.

Kapun Martin M Nolte Viola V Flatt Thomas T Schlötterer Christian C

PloS one 20100826 8

<h4>Background</h4>The Drosophila C virus (DCV) is a common and well-studied Drosophila pathogen. Although natural infections are known from Drosophila melanogaster and D. simulans, and artificial infections have been reported from several Drosophila species and other insects, it remains unclear to date whether DCV infections also occur naturally in other Drosophila species.<h4>Methods/principal findings</h4>Using reverse transcription PCR, we detected natural infections in six Drosophila specie ...[more]

PMID: 20865043

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Project description:Hepatitis C virus (HCV) species tropism is incompletely understood. We have previously shown that at the level of entry, human CD81 and occludin (OCLN) comprise the minimal set of human factors needed for viral uptake into murine cells. As an alternative approach to genetic humanization, species barriers can be overcome by adapting HCV to use the murine orthologues of these entry factors. We previously generated a murine tropic HCV (mtHCV or Jc1/mCD81) strain harboring three mutations within the viral envelope proteins that allowed productive entry into mouse cell lines. In this study, we aimed to characterize the ability of mtHCV to enter and infect mouse hepatocytes in vivo and in vitro Using a highly sensitive, Cre-activatable reporter, we demonstrate that mtHCV can enter mouse hepatocytes in vivo in the absence of any human cofactors. Viral entry still relied on expression of mouse CD81 and SCARB1 and was more efficient when mouse CD81 and OCLN were overexpressed. HCV entry could be significantly reduced in the presence of anti-HCV E2 specific antibodies, suggesting that uptake of mtHCV is dependent on viral glycoproteins. Despite mtHCV's ability to enter murine hepatocytes in vivo, we did not observe persistent infection, even in animals with severely blunted type I and III interferon signaling and impaired adaptive immune responses. Altogether, these results establish proof of concept that the barriers limiting HCV species tropism can be overcome by viral adaptation. However, additional viral adaptations will likely be needed to increase the robustness of a murine model system for hepatitis C. IMPORTANCE:At least 150 million individuals are chronically infected with HCV and are at risk of developing serious liver disease. Despite the advent of effective antiviral therapy, the frequency of chronic carriers has only marginally decreased. A major roadblock in developing a vaccine that would prevent transmission is the scarcity of animal models that are susceptible to HCV infection. It is poorly understood why HCV infects only humans and chimpanzees. To develop an animal model for hepatitis C, previous efforts focused on modifying the host environment of mice, for example, to render them more susceptible to HCV infection. Here, we attempted a complementary approach in which a laboratory-derived HCV variant was tested for its ability to infect mice. We demonstrate that this engineered HCV strain can enter mouse liver cells but does not replicate efficiently. Thus, additional adaptations are likely needed to construct a robust animal model for HCV.

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Host range and specificity of the Drosophila C virus.

Publications

Host range and specificity of the Drosophila C virus.

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