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Pathogens
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Vector Born and Zoonotic Disease Pathogenesis and Immunopathogenesis
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Vector Born and Zoonotic Disease Pathogenesis and Immunopathogenesis

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

Deadline for manuscript submissions: closed (15 October 2021) | Viewed by 7475

Special Issue Editor

Dr. Juarez Antônio Simões Quaresma

E-Mail Website
Guest Editor
Instituto Evandro Chagas Ananindeua, Brazil
Interests: Immunopathology and Immunology of Infectious diseases; Infectious diseases

Special Issue Information

Dear Colleagues,

Arboviruses are diseases caused by a group of viruses that include dengue, zika, chikungunya, and yellow fever. The arbovirus classification encompasses all those transmitted by arthropods, i.e., insects and arachnids (such as spiders and ticks). There are 545 arbovirus species, 150 of which cause disease in humans. Arbovirus infections may develop with symptoms consisting of fever, skin rash, jaundice, encephalitis, or haemorrhagic fever. The pathogenic mechanisms of infection by major arboviruses are accompanied by an immune response against the virus that can, secondarily, compromise various organs of the host, causing damage to tissues, such as liver, kidney, brain, lung, and blood vessel. For this Special Issue of Pathogens, we invite you to submit research articles, reviews, short notes, or communications related to pathogenesis and immunopathogenesis of arbovirus infections in humans and experimental models, especially molecular and immunological aspects, virus–host interactions, and vaccine development. We look forward to your contribution.

Dr. Juarez Antônio Simões 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. 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

  • Arboviruses
  • virulence factor
  • innate immunity
  • adaptive immunity
  • vaccine
  • animal models

Published Papers (3 papers)

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Research

7 pages, 3263 KiB  
Communication
Endothelium Activation during Severe Yellow Fever Triggers an Intense Cytokine-Mediated Inflammatory Response in the Liver Parenchyma
by Fábio Alves Olímpio, Luiz Fábio Magno Falcão, Marcos Luiz Gaia Carvalho, Jeferson da Costa Lopes, Caio Cesar Henriques Mendes, Arnaldo Jorge Martins Filho, Carlos Augusto Moreira da Silva, Vanessa do Socorro Cabral Miranda, Lais Carneiro dos Santos, Fellipe Souza da Silva Vilacoert, Ana Cecília Ribeiro Cruz, Vanessa Costa Alves Galúcio, Raimunda do Socorro da Silva Azevedo, Lívia Caricio Martins, Maria Irma Seixas Duarte, Jorge Rodrigues de Sousa, Pedro Fernando da Costa Vasconcelos and Juarez Antônio Simões Quaresma
Pathogens 2022, 11(1), 101; https://doi.org/10.3390/pathogens11010101 - 15 Jan 2022
Cited by 5 | Viewed by 1708
Abstract
Yellow fever (YF) is a pansystemic disease caused by the yellow fever virus (YFV), the prototype species of the family Flaviviridae and genus Flavivirus, and has a highly complex host-pathogen relationship, in which endothelial dysfunction reflects viral disease tropism. In this study, [...] Read more.
Yellow fever (YF) is a pansystemic disease caused by the yellow fever virus (YFV), the prototype species of the family Flaviviridae and genus Flavivirus, and has a highly complex host-pathogen relationship, in which endothelial dysfunction reflects viral disease tropism. In this study, the in situ endothelial response was evaluated. Liver tissue samples were collected from 21 YFV-positive patients who died due to the disease and five flavivirus-negative controls who died of other causes and whose hepatic parenchyma architecture was preserved. Immunohistochemical analysis of tissues in the hepatic parenchyma of YF cases showed significantly higher expression of E-selectin, P-selectin, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and very late antigen-4 in YFV-positive cases than in flavivirus-negative controls. These results indicate that endothelium activation aggravates the inflammatory response by inducing the expression of adhesion molecules that contribute to the rolling, recruitment, migration, and construction of the inflammatory process in the hepatic parenchyma in fatal YF cases. Full article
(This article belongs to the Special Issue Vector Born and Zoonotic Disease Pathogenesis and Immunopathogenesis)
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13 pages, 2134 KiB  
Communication
In Vitro Infection Dynamics of Japanese Encephalitis Virus in Established Porcine Cell Lines
by Shakirat A. Adetunji, Dmitriy Smolensky, Dana N. Mitzel, Jeana L. Owens, Carol G. Chitko-McKown, Natalia Cernicchiaro and Leela E. Noronha
Pathogens 2021, 10(11), 1468; https://doi.org/10.3390/pathogens10111468 - 12 Nov 2021
Viewed by 2914
Abstract
Japanese encephalitis virus (JEV) is a zoonotic mosquito-borne pathogen that regularly causes severe neurological disease in humans in Southeast Asia and the Western Pacific region. Pigs are one of the main amplifying hosts of JEV and play a central role in the virus [...] Read more.
Japanese encephalitis virus (JEV) is a zoonotic mosquito-borne pathogen that regularly causes severe neurological disease in humans in Southeast Asia and the Western Pacific region. Pigs are one of the main amplifying hosts of JEV and play a central role in the virus transmission cycle. The objective of this study was to identify in vitro cell systems to investigate early effects of JEV infection including viral replication and host cell death. Here, we demonstrate the susceptibility of several porcine cell lines to the attenuated genotype III JEV strain SA14-14-2. Monolayers of porcine nasal turbinate (PT-K75), kidney (SK-RST), testis (ST), and monocyte-derived macrophage (CΔ2+) cells were infected with SA14-14-2 for up to five days at a multiplicity of infection (MOI) of 0.1. The hamster kidney cell line BHK-21, previously shown to be susceptible to SA14-14-2, was used as a positive control. Culture supernatants and cells were collected between 0 and 120 h post infection (hpi), and monolayers were observed for cytopathic effect (CPE) using brightfield microscopy. The number of infectious virus particles was quantified by plaque assay and cell viability was determined using trypan blue staining. An indirect immunofluorescence assay was used to detect the presence of JEV NS1 antigens in cells infected at 1 MOI. All four porcine cell lines demonstrated susceptibility to SA14-14-2 and produced infectious virus by 12 hpi. Virus titers peaked at 48 hpi in CΔ2+, BHK-21, and SK-RST cells, at 72 hpi in PT-K75, and at 120 hpi in ST cells. CPE was visible in infected CΔ2+ and BHK-21 cells, but not the other three cell lines. The proportion of viable cells, as measured by trypan blue exclusion, declined after 24 hpi in BHK-21 and 48 hpi in CΔ2+ cells, but did not substantially decline in SK-RST, PT-K75 or ST cells. At 48 hpi, JEV NS1 was detected in all infected cell lines by fluorescence microscopy. These findings demonstrate several porcine cell lines which have the potential to serve as useful research tools for investigating JEV infection dynamics and host cell mechanisms in a natural amplifying host species, such as pigs, in vitro. Full article
(This article belongs to the Special Issue Vector Born and Zoonotic Disease Pathogenesis and Immunopathogenesis)
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20 pages, 5856 KiB  
Article
Brazilian Dengue Virus Type 2-Associated Renal Involvement in a Murine Model: Outcomes after Infection by Two Lineages of the Asian/American Genotype
by Fernanda Cunha Jácome, Gabriela Cardoso Caldas, Arthur da Costa Rasinhas, Ana Luisa Teixeira de Almeida, Daniel Dias Coutinho de Souza, Amanda Carlos Paulino, Marcos Alexandre Nunes da Silva, Ortrud Monika Barth, Flávia Barreto dos Santos and Debora Ferreira Barreto-Vieira
Pathogens 2021, 10(9), 1084; https://doi.org/10.3390/pathogens10091084 - 26 Aug 2021
Cited by 4 | Viewed by 2113
Abstract
Dengue virus type 2 (DENV-2) is, traditionally, the most studied serotype due to its association with explosive outbreaks and severe cases. In Brazil, almost 20 years after the first introduction in the 1990s, a new lineage (Lineage II) of the DENV-2 Asian/American genotype [...] Read more.
Dengue virus type 2 (DENV-2) is, traditionally, the most studied serotype due to its association with explosive outbreaks and severe cases. In Brazil, almost 20 years after the first introduction in the 1990s, a new lineage (Lineage II) of the DENV-2 Asian/American genotype emerged and caused an epidemic with severe cases and hospitalizations. Severe dengue includes multiple organ failure, and renal involvement can be potentially related to increased mortality. In order to better understand the role of DENV infection in renal injury, here we aimed to investigate the outcomes of infection with two distinct lineages of DENV-2 Asian/American genotype in the kidney of a murine model. BALB/c mice were infected with Lineages I and II and tissues were submitted to histopathology, immunohistochemistry, histomorphometry and ultrastructural analysis. Blood urea nitrogen (BUN) was detected in blood sample accessed by cardiac puncture. A tendency in kidney weight increase was observed in mice infected with both lineages, but urea levels, on average, were increased only in mice infected with Lineage II. The DENV antigen was detected in the tissue of mice infected with Lineage II and morphological changes were similar to those observed in human dengue cases. Furthermore, the parameters such as organ weight, urea levels and morphometric analysis, showed significant differences between the two lineages in the infected BALB/c, which was demonstrated to be a suitable experimental model for dengue pathophysiology studies in kidneys. Full article
(This article belongs to the Special Issue Vector Born and Zoonotic Disease Pathogenesis and Immunopathogenesis)
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