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Pathogens
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Rubella Virus Pathogenesis
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Rubella Virus Pathogenesis

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Viral Pathogens".

Deadline for manuscript submissions: closed (28 February 2023) | Viewed by 6800

Special Issue Editor

Dr. Claudia Claus

E-Mail Website
Guest Editor
Institute of Virology, University Clinics and Medical Faculty, University of Leipzig, Leipzig, Germany
Interests: (immuno)metabolism; innate immunity; host–virus interaction; infectious disease; iPSCs and iPSC-derived cell cultures

Special Issue Information

Dear Colleagues,

Rubella virus remains endemic in some parts of the world which lack sufficient coverage with the highly effective attenuated vaccine. Rubella is a mild and in many cases asymptomatic childhood disease. In contrast to the course of postnatal infections, serious consequences may arise from primary infections of susceptible women during the first trimester of pregnancy. The resulting developmental alterations are summarized in the term congenital rubella syndrome. The main defects are noted in the heart (patent ductus arteriosus, interventricular septal defects), eye (cataract, microphthalmia), and ear (deafness) in addition to vascular lesions. A special aspect of rubella pathogenesis is noted under conditions of primary immunodeficiency (emergence of infectious vaccine-derived rubella virus) or in immune privileged organs such as the eye (rubella virus-associated uveitis). Cell culture models based on human induced pluripotent stem cells address the human-specific alterations induced early during embryogenesis. Rubella virus replicates in pluripotent stem cells with an impact on their potential to differentiate into primary germ layer cells, which could contribute to the aforementioned developmental defects of congenital rubella.

We invite the submission of original articles and reviews on basic and clinical research to follow up on and extend our current understanding of rubella pathogenicity and teratogenicity. This Special Issue aims at aspects covering the interaction of rubella virus with its host cells, elucidation of pathogenic alterations, modulation of (innate) immune response mechanisms, and the identification of molecular and cellular markers up to biological differences among rubella virus strains that could affect disease progression after prenatal as well as postnatal infection. Novel and innovative approaches and methodologies on this important human-specific viral teratogen are highly welcome. Further understanding of its teratogenic potential and mode of persistence could serve as a blueprint for how pathogens affect very early human development and how RNA viruses and vaccine-derived viruses could persist under certain conditions.    

Dr. Claudia Claus
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pathogens is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Virus strains and RNA editing
  • Congenital rubella syndrome and developmental defects
  • Angiogenesis and endothelial cells
  • Embryonic and fetal development
  • Immune cells and innate immunity
  • Rubella vaccine and infectious vaccine-derived virus

Published Papers (3 papers)

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Research

20 pages, 3594 KiB  
Article
Exogenous Rubella Virus Capsid Proteins Enhance Virus Genome Replication
by Min-Hsin Chen, Cara C. Burns, Emily Abernathy, Adaeze A. Ogee-Nwankwo and Joseph P. Icenogle
Pathogens 2022, 11(6), 683; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens11060683 - 14 Jun 2022
Viewed by 1779
Abstract
Enhanced replication of rubella virus (RuV) and replicons by de novo synthesized viral structural proteins has been previously described. Such enhancement can occur by viral capsid proteins (CP) alone in trans. It is not clear whether the CP in the virus particles, i.e., [...] Read more.
Enhanced replication of rubella virus (RuV) and replicons by de novo synthesized viral structural proteins has been previously described. Such enhancement can occur by viral capsid proteins (CP) alone in trans. It is not clear whether the CP in the virus particles, i.e., the exogenous CP, modulate viral genome replication. In this study, we found that exogenous RuV CP also enhanced viral genome replication, either when used to package replicons or when mixed with RNA during transfection. We demonstrated that CP does not affect the translation efficiency from genomic (gRNA) or subgenomic RNA (sgRNA), the intracellular distribution of the non-structural proteins (NSP), or sgRNA synthesis. Significantly active RNA replication was observed in transfections supplemented with recombinant CP (rCP), which was supported by accumulated genomic negative-strand RNA. rCP was found to restore replication of a few mutants in NSP but failed to fully restore replicons known to have defects in the positive-strand RNA synthesis. By monitoring the amount of RuV RNA following transfection, we found that all RuV replicon RNAs were well-retained in the presence of rCP within 24 h of post-transfection, compared to non-RuV RNA. These results suggest that the exogenous RuV CP increases efficiency of early viral genome replication by modulating the stage(s) prior to and/or at the initiation of negative-strand RNA synthesis, possibly through a general mechanism such as protecting viral RNA. Full article
(This article belongs to the Special Issue Rubella Virus Pathogenesis)
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14 pages, 3746 KiB  
Article
Interferon Signaling-Dependent Contribution of Glycolysis to Rubella Virus Infection
by Erik Schilling, Maria Elisabeth Wald, Juliane Schulz, Lina Emilia Werner and Claudia Claus
Pathogens 2022, 11(5), 537; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens11050537 - 03 May 2022
Cited by 2 | Viewed by 1756
Abstract
Interferons (IFNs) are an essential part of innate immunity and contribute to adaptive immune responses. Here, we employed a loss-of-function analysis with human A549 respiratory epithelial cells with a knockout (KO) of the type I IFN receptor (IFNAR KO), either solely or together [...] Read more.
Interferons (IFNs) are an essential part of innate immunity and contribute to adaptive immune responses. Here, we employed a loss-of-function analysis with human A549 respiratory epithelial cells with a knockout (KO) of the type I IFN receptor (IFNAR KO), either solely or together with the receptor of type III IFN (IFNAR/IFNLR1 KO). The course of rubella virus (RuV) infection on the IFNAR KO A549 cells was comparable to the control A549. However, on the IFNAR/IFNLR1 KO A549 cells, both genome replication and the synthesis of viral proteins were significantly enhanced. The generation of IFN β during RuV infection was influenced by type III IFN signaling. In contrast to IFNAR KO A549, extracellular IFN β was not detected on IFNAR/IFNLR1 KO A549. The bioenergetic profile of RuV-infected IFNAR/IFNLR1 KO A549 cells generated by extracellular flux analysis revealed a significant increase in glycolysis, whereas mitochondrial respiration was comparable between all three cell types. Moreover, the application of the glucose analogue 2-deoxy-D-glucose (2-DG) significantly increased viral protein synthesis in control A549 cells, while no effect was noted on IFNAR/IFNLR KO A549. In conclusion, we identified a positive signaling circuit of type III IFN signaling on the generation of IFN β during RuV infection and an IFN signaling-dependent contribution of glycolysis to RuV infection. This study on epithelial A549 cells emphasizes the interaction between glycolysis and antiviral IFN signaling and notably, the antiviral activity of type III IFNs against RuV infection, especially in the absence of both type I and III IFN signaling, the RuV replication cycle was enhanced. Full article
(This article belongs to the Special Issue Rubella Virus Pathogenesis)
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12 pages, 2144 KiB  
Article
Drug Sensitivity of Vaccine-Derived Rubella Viruses and Quasispecies Evolution in Granulomatous Lesions of Two Ataxia-Telangiectasia Patients Treated with Nitazoxanide
by Raeesa Faisthalab, Suganthi Suppiah, Morna Dorsey, Kathleen E. Sullivan, Joseph Icenogle and Ludmila Perelygina
Pathogens 2022, 11(3), 338; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens11030338 - 11 Mar 2022
Cited by 4 | Viewed by 1796
Abstract
A strong association between rubella virus (RuV) and chronic granulomas, in individuals with inborn errors of immunity, has been recently established. Both the RA27/3 vaccine and wild-type RuV strains were highly sensitive to a broad-spectrum antiviral drug, nitazoxanide (NTZ), in vitro. However, NTZ [...] Read more.
A strong association between rubella virus (RuV) and chronic granulomas, in individuals with inborn errors of immunity, has been recently established. Both the RA27/3 vaccine and wild-type RuV strains were highly sensitive to a broad-spectrum antiviral drug, nitazoxanide (NTZ), in vitro. However, NTZ treatment, used as a salvage therapy, resulted in little or no improvements of RuV-associated cutaneous granulomas in patients. Here, we report investigations of possible causes of treatment failures in two ataxia-telangiectasia patients. Although a reduction in RuV RNA in skin lesions was detected by real-time RT-PCR, live immunodeficiency-related vaccine-derived rubella viruses (iVDRV) were recovered from granulomas, before and after the treatments. Tizoxanide, an active NTZ metabolite, inhibited replications of all iVDRVs in cultured A549 cells, but the 50% and 90% inhibitory concentrations were 10–40 times higher than those for the RA27/3 strain. There were no substantial differences in iVDRV sensitivities, neither before nor after treatments. Analysis of quasispecies in the E1 gene, a suspected NTZ target, showed no effect of NTZ treatments on quasispecies’ complexity in lesions. Thus, failures of NTZ therapies were likely due to low sensitivities of iVDRVs to the drug, and not related to the emergence of resistance, following long-term NTZ treatments. Full article
(This article belongs to the Special Issue Rubella Virus Pathogenesis)
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