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Viruses
Special Issues
Pathogenesis of Flavivirus Infections
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Pathogenesis of Flavivirus Infections

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "General Virology".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 1966

Special Issue Editor

Dr. Juarez Quaresma

E-Mail Website
Guest Editor
Department of Pathology, Tropical Medicine Center, Federal University of Pará, Belém 66055-190, PA, Brazil
Interests: pathology; immunopathology and public health of arboviruses
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Flavivirus infections provide an in-depth analysis of the interaction between flaviviruses and the human and animal host, exploring the mechanisms by which these viruses cause cell lesions and diseases. By providing an overview of flaviviruses, this Special Issue discusses their viral structure, ecology, and transmission, as well as their immune and genetic diversity that contributes to their pathogenicity. The Special Issue specifically addresses viral infection and replication, detailing how flaviviruses invade and replicate within host cells, as well as the complex relationship between flaviviruses and the immune system, revealing how the immune response can influence the pathogenesis of these infections. Papers that exhaustively describe aspects of pathogenesis and immunopathogenesis related to the clinical manifestations of diseases caused by flaviviruses, including severe complications (such as encephalitis and haemorrhagic syndromes), are welcome. We also encourage the submission of silico study papers using computer simulation tools and related areas (such as artificial intelligence technologies). Finally, available therapeutic and prevention strategies, including antivirals, vaccines, and public health practices, essential for addressing diseases caused by flaviviruses, are also important topics that are covered in this Special Issue. This Special Issue offers a comprehensive and up-to-date overview of the pathogenesis of these viruses, providing fundamental information for the diagnosis, treatment, and effective control of diseases caused by them.

Dr. Juarez Quaresma
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. Viruses 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 2600 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

  • pathogenesis
  • immunopathogenesis
  • immune response
  • clinical outcomes
  • vaccines
  • diagnostic
  • public health
  • one health
  • molecular biology
  • flavivirus
  • computer simulation
  • artificial intelligence

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

18 pages, 5699 KiB  
Article
Histopathological Changes and Immune Response Profile in the Brains of Non-Human Primates Naturally Infected with Yellow Fever Virus
by Suzana Ribeiro de Melo Oliveira, Ermelinda do Rosário Moutinho da Cruz, Nelielma Garcia de Oliveira Prestes, Fábio Silva da Silva, Marialva Tereza Ferreira de Araújo, Orlando Pereira Amador Neto, Maria de Lourdes Gomes Lima, Bianca Nascimento de Alcântara, Daniel Damous Dias, Jorge Rodrigues de Sousa, Arnaldo Jorge Martins Filho, Livia Medeiros Neves Casseb and Daniele Barbosa de Almeida Medeiros
Viruses 2025, 17(3), 386; https://doi.org/10.3390/v17030386 - 7 Mar 2025
Viewed by 735
Abstract
In the history of yellow fever (YF) outbreaks in Brazil, howler monkeys (Alouatta sp.) and marmosets (Callithrix sp.) have been among the most affected genera, exhibiting significant hepatic injuries similar to those seen in humans. However, limited information exists regarding yellow [...] Read more.
In the history of yellow fever (YF) outbreaks in Brazil, howler monkeys (Alouatta sp.) and marmosets (Callithrix sp.) have been among the most affected genera, exhibiting significant hepatic injuries similar to those seen in humans. However, limited information exists regarding yellow fever virus (YFV) infection in their central nervous system (CNS). To address this gap, an epidemiological study was conducted to assess tissue changes, viral detection, and cytokine profiles in the brains of both neotropical primate species when they are naturally infected with YFV. A total of 22 brain samples from these species (8 from Alouatta sp. and 14 from Callithrix sp.) showing infection with YFV in the liver via immunohistochemistry (IHC) were selected. From them, YFV antigen detection occurred in 35.7% (5/14) of Callithrix sp. brain samples and 87.5% (7/8) of Alouatta sp. samples, with a higher frequency of viral antigen quantification in Callithrix sp. Both species exhibited similar CNS lesions, characterized by congestion, low hemorrhage, limited inflammatory infiltration interstitial and perivascular edema associated with neuronal degeneration, neurophagy, and higher cell death (necrosis and apoptosis) quantification. Pro- and anti-inflammatory cytokine profiles were balanced, with TNF-α and IL-1β playing a key role in inflammation, while IL-10 and IL-13 exhibited a prominent role in immunomodulation, suggesting an anti-inflammatory modulation typical of flaviviruses occurs. This study demonstrates that YFV can induce CNS lesions in neotropical primates, establishing it as a secondary target of viral tropism. These findings highlight the importance of collecting nervous tissue during epizootics, particularly in Callithrix sp., as such tissue is often overlooked despite its critical role in disease monitoring. Full article
(This article belongs to the Special Issue Pathogenesis of Flavivirus Infections)
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10 pages, 19203 KiB  
Article
Analysis of MLKL, RIP1 and RIP3 Immunostaining Markers in Human Liver Tissue from Fatal Yellow Fever Cases: Insights into Necroptosis
by Vanessa do Socorro Cabral Miranda, Luiz Fabio Magno Falcão, Hellen Thais Fuzii, Marcos Luiz Gaia Carvalho, Jeferson da Costa Lopes, Arnaldo Jorge Martins Filho, Ana Cecilia Ribeiro Cruz, Raimunda do Socorro da Silva Azevedo, Jorge Rodrigues de Sousa, Mayumi Duarte Wakimoto, Pedro Fernando da Costa Vasconcelos and Juarez Antônio Simões Quaresma
Viruses 2025, 17(1), 3; https://doi.org/10.3390/v17010003 - 24 Dec 2024
Viewed by 801
Abstract
Necroptosis is a regulated form of cell death implicated in several pathological conditions, including viral infections. In this study, we investigated the expression and correlation of necroptosis markers MLKL, RIP1 and RIP3 in human liver tissue from fatal cases of yellow fever (YF) [...] Read more.
Necroptosis is a regulated form of cell death implicated in several pathological conditions, including viral infections. In this study, we investigated the expression and correlation of necroptosis markers MLKL, RIP1 and RIP3 in human liver tissue from fatal cases of yellow fever (YF) using immunohistochemistry (IHC). The liver samples were obtained from 21 YF-positive individuals and five flavivirus-negative controls with preserved liver parenchymal architecture. The cases underwent histopathological analysis, followed by tissue immunostaining with the immunohistochemical method of streptavidin–biotin peroxidase. Using the in situ method, we evaluated the centrilobular zone (Z3), midzonal zone (Z2), periportal zone and portal tract (PT) of human liver parenchyma with markers for necroptosis, RIPK1, RIPK3 and MLKL. A quantitative analysis revealed a significantly higher expression of MLKL, RIP1 and RIP3 in the liver parenchyma of YF cases compared to controls in different zones (Z3, Z2, Z1) and portal tracts (PTs) of the liver, especially in zone 2. Immunostaining confirmed the localization of MLKL, RIP1 and RIP3 in hepatocytes and inflammatory infiltrates, highlighting their involvement in the pathogenesis of YF. A Pearson correlation analysis demonstrated significant correlations among necroptosis markers, which indicates their coordinated regulation during YF-induced liver injury. Full article
(This article belongs to the Special Issue Pathogenesis of Flavivirus Infections)
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