Advances in Alphavirus and Flavivirus Research, 3rd Edition

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Human Virology and Viral Diseases".

Deadline for manuscript submissions: 31 December 2026 | Viewed by 2340

Special Issue Editors


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Guest Editor
1. Centre for Human Genetics, Division of Structural Biology, University of Oxford, Roosevelt Drive, Oxford OX3 7BN, UK
2. Oxford Vaccine Group, Department of Paediatrics, University of Oxford, Oxford OX3 7LE, UK
Interests: alphaviruses; flaviviruses; bacteria; vaccines; diagnostics; immunology; immunoassays
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
1. The Jenner Institute, ORCRB, Nuffield Department of Medicine, University of Oxford, Roosevelt Drive, Oxford OX3 7DQ, UK
2. Instituto Politécnico Nacional, IPN, Av. Luis Enrique Erro s/n, Unidad Adolfo López Mateos, Mexico City, Mexico
Interests: Plasmodium vivax; pre-erythrocytic malaria vaccines; flavivirus vaccines; alphavirus-based vaccines; Zika vaccines; Dengue vaccines; Chikungunya vaccines; VLP; recombinant viral vectors; chimpanzee adenovirus (ChAdOx); MVA
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous Special Issues, titled “Advances in Alphavirus and Flavivirus Research” (https://www.mdpi.com/journal/viruses/special_issues/alphavirus_flavivirus_research) and “Advances in Alphavirus and Flavivirus Research, 2nd Edition” (https://www.mdpi.com/journal/viruses/special_issues/alphavirus_flavivirus_V2).

As we have seen during the last decade and the most recent pandemics, the emergence or re-emergence of zoonotic viral diseases has become one of the most important public health concerns globally. In particular, mosquito-borne viruses, such as Dengue (DENV), Zika (ZIKV), and Chikungunya (CHIKV), have emerged in recent decades, affecting millions of people worldwide. These alphaviruses and flaviviruses can be classified into a broader category of arboviruses. Moreover, they cause significant disease burdens and public health concerns. This Special Issue, titled “Advances in Alphavirus and Flavivirus Research”, is devoted to publishing advances made in the field of alphavirus and flavivirus research.

We welcome submissions of all types of articles, including short reports, original research, and reviews. We look forward to receiving your contributions.

Dr. Young Chan Kim
Dr. Arturo Reyes-Sandoval
Guest Editors

Manuscript Submission Information

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Keywords

  • arbovirus
  • alphavirus
  • flavivirus
  • Chikungunya
  • Mayaro
  • Zika
  • dengue
  • diagnostics
  • surveillance
  • vaccine
  • antivirals
  • animal models

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Published Papers (3 papers)

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Research

13 pages, 1053 KB  
Article
Genetic Characterization of Yellow Fever Virus Strain JSS, the Original South American Strain
by Madison E. Lee, Clairissa A. Hansen, Jill K. Thompson, Haiping Hao, Nigel Bourne and Alan D. T. Barrett
Viruses 2026, 18(5), 564; https://doi.org/10.3390/v18050564 - 15 May 2026
Viewed by 201
Abstract
Yellow fever virus (YFV) is divided into seven genotypes, including West Africa II (WAII) and South America I (SAI). The first wild-type YFVs isolated, Asibi (Ghana/1927) and French Viscerotropic virus ([FVV] Senegal/1927), are members of WAII. The first YFV strain isolated in South [...] Read more.
Yellow fever virus (YFV) is divided into seven genotypes, including West Africa II (WAII) and South America I (SAI). The first wild-type YFVs isolated, Asibi (Ghana/1927) and French Viscerotropic virus ([FVV] Senegal/1927), are members of WAII. The first YFV strain isolated in South America, JSS (Brazil/1935), was associated with the last outbreak of urban YF in Brazil and has been insufficiently studied. We utilized Next Generation Sequencing to compare JSS with Asibi, FVV, and other South American YFV strains. SAI strains, including JSS, had higher genetic diversity than WAII strains. Phylogenetic and phylogeographic studies of YFV in South America have revealed the circulation of five lineages within Brazil, termed 1A-1E. JSS was found to be distinct from the five genetic lineages currently recognized in Brazil, and so we termed JSS as the currently sole member of Brazilian linage 1F. a comparison of JSS with all other Brazilian genomes of YFV suggests that lineage 1F appears to have become extinct. Full article
(This article belongs to the Special Issue Advances in Alphavirus and Flavivirus Research, 3rd Edition)
20 pages, 2724 KB  
Article
CHIKV-Infected Human Dermal Fibroblasts Mount an IFNβ Transcriptional Response Independent of TBK1/IKKε Signaling That Fails to Prevent Lethal Infection
by Meagan M. Taylor, Rosemary W. Roberts and Jonathan O. Rayner
Viruses 2026, 18(5), 503; https://doi.org/10.3390/v18050503 - 28 Apr 2026
Viewed by 433
Abstract
Chikungunya virus (CHIKV) is an alphavirus that infects dermal fibroblasts as a primary target cell during natural mosquito-borne transmission. While primary human dermal fibroblasts (hDFs) have been implicated as a key source of type I interferon (IFN-I) during CHIKV infection, the dynamics of [...] Read more.
Chikungunya virus (CHIKV) is an alphavirus that infects dermal fibroblasts as a primary target cell during natural mosquito-borne transmission. While primary human dermal fibroblasts (hDFs) have been implicated as a key source of type I interferon (IFN-I) during CHIKV infection, the dynamics of this response and its sufficiency for antiviral protection remain incompletely understood. Here, we systematically characterize in vitro CHIKV infection of primary hDFs, evaluating the effects of single-passage viral stock origin (mammalian- vs. mosquito-propagated), donor variability, and multiplicity of infection (MOI) on infection kinetics and innate immune induction. We demonstrate that hDFs support high-titered CHIKV replication at both MOI 1 and 0.01, resulting in universal cell death by 72 hpi despite robust IFNβ transcript induction—reaching up to ~2800-fold over mock—and secretion of pro-inflammatory cytokines, including IFNα2, TNFα, IL-1β, and IL-8. Notably, IFNβ protein levels remained below 10 pg/mL under all infection conditions, revealing a disconnect between transcriptional and translational responses, suggesting CHIKV-mediated translational suppression. Pharmacological inhibition of TBK1/IKKε via amlexanox did not suppress IFNβ transcript induction at any tested concentration, suggesting that canonical PRR signaling through this node—including both RIG-I/MAVS and TLR3/TRIF pathways—is not the major driver of the observed transcriptional response. In contrast, co-inoculation with exogenous IFNβ as low as 20 pg/mL activated IFNAR signaling, robustly upregulated interferon-stimulated genes (ISGs), and fully rescued hDFs from otherwise lethal infection. Together, these findings demonstrate that CHIKV-infected hDFs mount a transcriptionally robust but translationally insufficient innate immune response and that the transcriptional response appears to operate independently of TBK1/IKKε. These results have direct implications for understanding how the skin microenvironment may modulate early CHIKV pathogenesis and suggest that paracrine IFNβ signaling from neighboring cell types may be critical for fibroblast survival during natural infection. Full article
(This article belongs to the Special Issue Advances in Alphavirus and Flavivirus Research, 3rd Edition)
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14 pages, 858 KB  
Article
In Vivo Characterization and Tissue Tropism of a Wild-Type Yellow Fever Virus Isolate from the 2017–2018 Brazilian Outbreak in C57BL/6 IFNAR1−/− Mice
by Ana Luiza Campos Cruz, Natália Lima Pessoa, Ester Maria Paiva Silva, Sabrynna Brito Oliveira, Jéssica Pauline Coelho Souza, Samantha Stephany Fiuza Meneses Viegas, Anna Catarina Dias Soares Guimarães, Pedro Augusto Alves, Cintia Lopes de Brito Magalhães, Thomas P. Monath, Olindo Assis Martins-Filho, Andréa Teixeira-Carvalho, A. Desiree LaBeaud, Nidia Esther Colquehuanca Arias and Betânia Paiva Drumond
Viruses 2025, 17(10), 1325; https://doi.org/10.3390/v17101325 - 29 Sep 2025
Viewed by 1285
Abstract
Yellow fever remains a significant public health concern in endemic regions of South America and Africa, where periodic outbreaks continue to challenge surveillance and control efforts. Despite the widespread use of vaccines and historical YFV strains in experimental settings, there is limited information [...] Read more.
Yellow fever remains a significant public health concern in endemic regions of South America and Africa, where periodic outbreaks continue to challenge surveillance and control efforts. Despite the widespread use of vaccines and historical YFV strains in experimental settings, there is limited information on the pathogenic behavior of contemporary wild-type isolates in animal models. To address this gap, this study aimed to develop and characterize a murine model infected with a wild-type YFV strain isolated in 2018, from Brazil’s largest sylvatic outbreak in decades. In this study, four-week-old male and female C57BL/6 IFNAR1−/− mice were subcutaneously infected with WT YFV. Mice exhibited a nearly 50% survival rate and developed several clinical signs. Viral loads were assessed in serum and some tissues, collected either upon euthanasia of moribund animals or at the end point. YFV RNA was detected in all sampled tissues and serum. Infectious viral particles were identified in the brains of both sexes and in the testis. No statistically significant differences were observed between males and females in survival, clinical signs, or viral loads. Altogether, this study provides a robust and reproducible murine model for wild-type YFV infection, offering a valuable platform for investigating viral pathogenesis, host responses, and potential therapeutic interventions. Full article
(This article belongs to the Special Issue Advances in Alphavirus and Flavivirus Research, 3rd Edition)
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