Vector and Host C-Type Lectin Receptor (CLR)–Fc Fusion Proteins as a Cross-Species Comparative Approach to Screen for CLR–Rift Valley Fever Virus Interactions

Schön, Kathleen; Lindenwald, Dimitri; Monteiro, João Tiago Silva; Glanz, Julien; Jung, Klaus; Becker, Stefanie; Lepenies, Bernd

doi:10.3390/ijms23063243

Cited by 6 publications

(3 citation statements)

References 79 publications

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“…Therefore, different glycans may impact correct antigen folding and stability in a pathogen-specific manner. Further evidence supporting this is that RVFV derived from insect cells has been suggested to interact with C-type lectin receptors (CLR) differently to those grown in mammalian cells [43].…”

Section: Discussionmentioning

confidence: 99%

Pathogenesis of Rift Valley Fever Virus in a BALB/c Mouse Model Is Affected by Virus Culture Conditions and Sex of the Animals

Graham,

Easterbrook,

Kennedy

et al. 2023

Viruses

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Rift Valley fever virus (RVFV) is a mosquito-borne zoonotic pathogen causing disease in livestock and humans. Whilst initially restricted to the African continent, recent spread to the Arabian Peninsula has highlighted the likelihood of entry into new regions. Due to the absence of a regulatory-approved human vaccine, work is ongoing to develop and assess countermeasures. As such, small animal models play a pivotal role in providing information on disease pathogenesis and elucidating which intervention strategies confer protection. To develop and establish the BALB/c mouse model, we challenged mice with RVFV grown from two separate cell lines: one derived from mosquitoes (C6/36) and the other mammalian derived (Vero E6). Following infection, we assessed the clinical course of disease progression at days 1 and 3 post-challenge and evaluated viral tropism and immune analytes. The results demonstrated that RVFV infection was affected by the cell line used to propagate the challenge virus, with those grown in insect cells resulting in a more rapid disease progression. The lowest dose that caused uniform severe disease remained the same across both virus preparations. In addition, to demonstrate reproducibility, the lowest dose was used for a subsequent infection study using male and female animals. The results further demonstrated that male mice succumbed to infection more rapidly than their female counterparts. Our results establish an RVFV mouse model and key parameters that affect the course of disease progression in BALB/c mice.

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Section: Discussionmentioning

confidence: 99%

Pathogenesis of Rift Valley Fever Virus in a BALB/c Mouse Model Is Affected by Virus Culture Conditions and Sex of the Animals

Graham,

Easterbrook,

Kennedy

et al. 2023

Viruses

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“…Macrophage inducible C-type lectin (Mincle) recognizes glucose residues and GlcCer, among other glycolipids (Nagata et al, 2017). In addition, this lectin has recently been shown to bind the phenuivirus RVFV and La Crosse virus, a peribunyavirus similar to GERV (Monteiro et al, 2019; Schön et al, 2022). Further investigations will be needed, not only to determine whether Mincle is an attachment factor or receptor for UUKV and other viruses carrying GlcCer molecules in their envelope, but also to identify the receptors that can capture enveloped viruses through GlcCer.…”

Section: Discussionmentioning

confidence: 99%

The glycolipid GlcCer is recruited into the viral envelope to promote phenuivirus binding to host cells

Uckeley

Mazelier

Luechtenborg

et al. 2022

Preprint

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Virus-receptor interactions largely contribute to the tropism and outcome of an infection. Here, we found that the glycolipid glucosylceramide (GlcCer) is a major component of Uukuniemi phenuivirus and allows viral binding to host cells. A lipidomic analysis with mass spectrometry revealed the lipidome of UUKV particles and indicated that GlcCer was enriched in both infected cells and viral particles. In addition, the infectivity of UUKV depended on the conversion of ceramide (Cer) into GlcCer in the Golgi network of producer cells. In contrast, depletion of GlcCer in virions profoundly impaired the attachment of UUKV and other related viruses to target cells. Furthermore, competing GlcCer ligands prevented virus binding to various cell types. Altogether, our results demonstrate that glycolipids are essential structural determinants of the virions necessary for virus attachment to host cells and have strong implications for future work on the identification of virus receptors.

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“…However, the conservation of LRP1 protein sequence is relatively low in humans and some RVFV-sensitive animals, suggesting the existence of other receptors in these animals. In mice, sheep, and Aedes aegypti , homologs of C-type lectin receptors (CLRs) have been proposed as potential attachment factors or entry receptors in various species ( 84 ).…”

Section: Conclusion and Prospectmentioning

confidence: 99%

Natural hosts and animal models for Rift Valley fever phlebovirus

Xu,

Wang,

Jiang

et al. 2023

Front. Vet. Sci.

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Rift Valley fever phlebovirus (RVFV) is a zoonotic mosquito-transmitted arbovirus, presenting a serious threat to humans and animals. Susceptible hosts are of great significance for the prevention of RVFV. Appropriate animal models are helpful to better understand the onset and development of diseases, as well as the control measures and vaccine research. This review focuses on the role of animal hosts in the maintenance of the virus, and summarizes the host range of RVFV. We list some common animal models in the process of RVFV research, which would provide some important insights into the prevention and treatment of RVFV, as well as the study of Rift Valley fever (RVF) pathogenesis and vaccines.

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Vector and Host C-Type Lectin Receptor (CLR)–Fc Fusion Proteins as a Cross-Species Comparative Approach to Screen for CLR–Rift Valley Fever Virus Interactions

Cited by 6 publications

References 79 publications

Pathogenesis of Rift Valley Fever Virus in a BALB/c Mouse Model Is Affected by Virus Culture Conditions and Sex of the Animals

Pathogenesis of Rift Valley Fever Virus in a BALB/c Mouse Model Is Affected by Virus Culture Conditions and Sex of the Animals

The glycolipid GlcCer is recruited into the viral envelope to promote phenuivirus binding to host cells

Natural hosts and animal models for Rift Valley fever phlebovirus

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