E-Mail Alert

Add your e-mail address to receive forthcoming issues of this journal:

Journal Browser

Journal Browser

Special Issue "Pathogenesis of Emerging Viral Infections"

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

Deadline for manuscript submissions: 15 September 2019.

Special Issue Editors

Guest Editor
Dr. Jason Kindrachuk

Laboratory of Emerging and Re-Emerging Viruses, Department of Medical Microbiology, University of Manitoba, Winnipeg, MB, Canada
Website | E-Mail
Interests: Molecular pathogenesis of emerging viruses that impact human and animal health
Guest Editor
Dr. Daniel S. Chertow

Critical Care Medicine Department, National Institutes of Health Clinical Center, Laboratory of Immunoregulation, National Institute of Allergy and Infections Diseases, Bethesda, MD, USA
Website | E-Mail
Interests: Pathogenesis and treatment of severe emerging viral infections

Special Issue Information

Dear Colleagues,

Emerging viruses pose a significant threat to global human and animal health, and outbreaks of these pathogens are increasing in frequency due to changing socio-economic, environmental, and ecological factors. In recent years, multiple zoonotic viruses, including Ebola virus, Middle East respiratory syndrome coronavirus, and Zika virus, have emerged or re-emerged as public health threats. In outbreak ‘hotspots’, limitations in resource capacity or control often hamper timely and effective medical and public health response efforts. Further, emerging viral infections often induce severe illness, with few or no available therapies to limit disease morbidity and mortality. Improved insight into the molecular processes that contribute to organ injury and repair is needed to guide optimal care and the development of efficacious therapies. To this end, better integration of basic and clinical research efforts is required to accelerate breakthrough translational research. Detailed molecular investigations of the clinical and pathologic manifestations of emerging viral infections will provide important insight into disease pathogenesis and advance therapeutic discovery.

Dr. Jason Kindrachuk
Dr. Daniel S. Chertow
Guest Editors

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 papers will be 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 1800 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

  • Emerging viruses
  • Viral pathogenesis
  • Disease mechanisms
  • Therapeutic discovery

Published Papers (3 papers)

View options order results:
result details:
Displaying articles 1-3
Export citation of selected articles as:

Research

Open AccessArticle
BK Virus Replication in the Glomerular Vascular Unit: Implications for BK Virus Associated Nephropathy
Viruses 2019, 11(7), 583; https://doi.org/10.3390/v11070583
Received: 3 April 2019 / Revised: 10 June 2019 / Accepted: 25 June 2019 / Published: 27 June 2019
PDF Full-text (5015 KB) | HTML Full-text | XML Full-text
Abstract
Background: BK polyomavirus (BKV) reactivates from latency after immunosuppression in renal transplant patients, resulting in BKV-associated nephropathy (BKVAN). BKVAN has emerged as an important cause of graft dysfunction and graft loss among transplant patients. BKV infection in kidney transplant patients has increased over [...] Read more.
Background: BK polyomavirus (BKV) reactivates from latency after immunosuppression in renal transplant patients, resulting in BKV-associated nephropathy (BKVAN). BKVAN has emerged as an important cause of graft dysfunction and graft loss among transplant patients. BKV infection in kidney transplant patients has increased over recent decades which correlates with the use of more potent immunosuppressive therapies. BKV infection of the Glomerular Vascular Unit (GVU) consisting of podocytes, mesangial cells, and glomerular endothelial cells could lead to glomerular inflammation and contribute to renal fibrosis. The effects of BKV on GVU infectivity have not been reported. methods: We infected GVU cells with the Dunlop strain of BKV. Viral infectivity was analyzed by microscopy, immunofluorescence, Western blot analysis, and quantitative RT-PCR (qRT-PCR). The expression of specific proinflammatory cytokines induced by BKV was analyzed by qRT-PCR. Results: BKV infection of podocytes, mesangial cells, and glomerular endothelial cells was confirmed by qRT-PCR and positive staining with antibodies to the BKV VP1 major capsid protein, or the SV40 Large T-Antigen. The increased transcriptional expression of interferon gamma-induced protein 10 (CXCL10/IP-10) and interferon beta (IFNβ) was detected in podocytes and mesangial cells at 96 h post-infection. conclusions: All cellular components of the GVU are permissive for BKV replication. Cytopathic effects induced by BKV in podocytes and glomerular endothelial cells and the expression of CXCL10 and IFNβ genes by podocytes and mesangial cells may together contribute to glomerular inflammation and cytopathology in BKVAN. Full article
(This article belongs to the Special Issue Pathogenesis of Emerging Viral Infections)
Figures

Figure 1

Open AccessArticle
A Stillborn Multiple Organs’ Investigation from a Maternal DENV-4 Infection: Histopathological and Inflammatory Mediators Characterization
Viruses 2019, 11(4), 319; https://doi.org/10.3390/v11040319
Received: 15 January 2019 / Revised: 18 February 2019 / Accepted: 20 February 2019 / Published: 2 April 2019
PDF Full-text (9976 KB) | HTML Full-text | XML Full-text
Abstract
Dengue virus (DENV) is an emerging virus involved in outbreaks in Brazil. The association between the virus and vertical transmission, with disorders in the placenta, has raised a worldwide concern. On the 29th gestational week, a pregnant woman presented severe complications due to [...] Read more.
Dengue virus (DENV) is an emerging virus involved in outbreaks in Brazil. The association between the virus and vertical transmission, with disorders in the placenta, has raised a worldwide concern. On the 29th gestational week, a pregnant woman presented severe complications due to a DENV infection leading to maternal and fetus death. Postmortem analysis of fetal organs demonstrated the presence of DENV using reverse transcriptase polymerase chain reaction (RT-PCR) in the fetal brain and DENV non-structural protein 3 (NS3) staining in placenta and several peripheral fetal tissues, such as the brain, liver, lungs, and spleen. Histological analysis of the placenta and fetal organs revealed different types of tissue abnormalities, which included inflammation, hemorrhage, edema, and necrosis in placenta and tissue disorganization in the fetus, such as spongiform parenchyma, microglial inflammation, steatosis, hyalinose arteriolar, inflammatory cells in the alveolar septa, and disorganization of the lymphoid follicle. Increased cellularity (macrophage, Hofbauer cells and TCD8+ lymphocytes) and up-regulation of inflammatory mediators such as IFN-γ, TNF-α, RANTES/CCL5, MCP1/CCL2, and VEGF/R2 were detected in the liver, lung, spleen, brain, and placenta, supporting placental and fetus peripheral tissues inflammation. Maternal infection leading to the production of those vascular mediators may alter the vascular permeability, facilitating the virus entry and tissue and barrier dysfunction. Full article
(This article belongs to the Special Issue Pathogenesis of Emerging Viral Infections)
Figures

Figure 1

Open AccessArticle
Clinical, Histopathologic, and Immunohistochemical Characterization of Experimental Marburg Virus Infection in A Natural Reservoir Host, the Egyptian Rousette Bat (Rousettus aegyptiacus)
Viruses 2019, 11(3), 214; https://doi.org/10.3390/v11030214
Received: 5 February 2019 / Revised: 26 February 2019 / Accepted: 27 February 2019 / Published: 2 March 2019
PDF Full-text (2704 KB) | HTML Full-text | XML Full-text
Abstract
Egyptian rousette bats (Rousettus aegyptiacus) are natural reservoir hosts of Marburg virus (MARV), and Ravn virus (RAVV; collectively called marburgviruses) and have been linked to human cases of Marburg virus disease (MVD). We investigated the clinical and pathologic effects of experimental [...] Read more.
Egyptian rousette bats (Rousettus aegyptiacus) are natural reservoir hosts of Marburg virus (MARV), and Ravn virus (RAVV; collectively called marburgviruses) and have been linked to human cases of Marburg virus disease (MVD). We investigated the clinical and pathologic effects of experimental MARV infection in Egyptian rousettes through a serial euthanasia study and found clear evidence of mild but transient disease. Three groups of nine, captive-born, juvenile male bats were inoculated subcutaneously with 10,000 TCID50 of Marburg virus strain Uganda 371Bat2007, a minimally passaged virus originally isolated from a wild Egyptian rousette. Control bats (n = 3) were mock-inoculated. Three animals per day were euthanized at 3, 5–10, 12 and 28 days post-inoculation (DPI); controls were euthanized at 28 DPI. Blood chemistry analyses showed a mild, statistically significant elevation in alanine aminotransferase (ALT) at 3, 6 and 7 DPI. Lymphocyte and monocyte counts were mildly elevated in inoculated bats after 9 DPI. Liver histology revealed small foci of inflammatory infiltrate in infected bats, similar to lesions previously described in wild, naturally-infected bats. Liver lesion severity scores peaked at 7 DPI, and were correlated with both ALT and hepatic viral RNA levels. Immunohistochemical staining detected infrequent viral antigen in liver (3–8 DPI, n = 8), spleen (3–7 DPI, n = 8), skin (inoculation site; 3–12 DPI, n = 20), lymph nodes (3–10 DPI, n = 6), and oral submucosa (8–9 DPI, n = 2). Viral antigen was present in histiocytes, hepatocytes and mesenchymal cells, and in the liver, antigen staining co-localized with inflammatory foci. These results show the first clear evidence of very mild disease caused by a filovirus in a reservoir bat host and provide support for our experimental model of this virus-reservoir host system. Full article
(This article belongs to the Special Issue Pathogenesis of Emerging Viral Infections)
Figures

Figure 1

Viruses EISSN 1999-4915 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top