Special Issue "Viral Pathogenesis"

A special issue of Pathogens (ISSN 2076-0817).

Deadline for manuscript submissions: closed (29 February 2016).

Special Issue Editor

Dr. Thomas E. "Tem" Morrison
Website
Guest Editor
Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045, USA
Interests: molecular pathogenesis of RNA virus infections; immunological responses to RNA virus infections; mosquito-transmitted viruses; chikungunya virus, Ross River virus, and related arthritogenic alphaviruses

Special Issue Information

Dear Colleagues,

Viral pathogenesis is a complex set of events and processes that occurs following infection of a host with a virus. These virus-host interactions result in outcomes ranging from asymptomatic to severe, fatal infections. The molecular mechanisms that underlay viral pathogenesis are challenging to unravel, as the broad range of outcomes of virus infections are influenced by various factors, including the viral species, the host species, viral and host genetic variation, host immune and health status, host age, and many others. Nevertheless, researchers investigating the pathogenesis of a multitude of evolutionarily diverse viruses have made tremendous progress, revealing both common and unique molecular mechanisms that contribute to the outcome of viral infections. For this Special Issue of Pathogens, we invite you to submit a review or article related to viral pathogenesis, and we look forward to your contribution.

Dr. Thomas E. "Tem" Morrison
Guest Editor

Keywords

  • Virus
  • Pathogenesis
  • Acute infection
  • Chronic infection
  • Viral immunity
  • Immunopathology
  • Virus-host interactions
  • Virus infection
  • Animal models

Published Papers (4 papers)

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Research

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Open AccessArticle
Experimental West Nile Virus Infection in Rabbits: An Alternative Model for Studying Induction of Disease and Virus Control
Pathogens 2015, 4(3), 529-558; https://doi.org/10.3390/pathogens4030529 - 14 Jul 2015
Cited by 10
Abstract
The economic impact of non-lethal human and equine West Nile virus (WNV) disease is substantial, since it is the most common presentation of the infection. Experimental infection with virulent WNV strains in the mouse and hamster models frequently results in severe neural infection [...] Read more.
The economic impact of non-lethal human and equine West Nile virus (WNV) disease is substantial, since it is the most common presentation of the infection. Experimental infection with virulent WNV strains in the mouse and hamster models frequently results in severe neural infection and moderate to high mortality, both of which are not representative features of most human and equine infections. We have established a rabbit model for investigating pathogenesis and immune response of non-lethal WNV infection. Two species of rabbits, New Zealand White (Oryctolagus cuniculus) and North American cottontail (Sylvilagus sp.), were experimentally infected with virulent WNV and Murray Valley encephalitis virus strains. Infected rabbits exhibited a consistently resistant phenotype, with evidence of low viremia, minimal-absent neural infection, mild-moderate neuropathology, and the lack of mortality, even though productive virus replication occurred in the draining lymph node. The kinetics of anti-WNV neutralizing antibody response was comparable to that commonly seen in infected horses and humans. This may be explained by the early IFNα/β and/or γ response evident in the draining popliteal lymph node. Given this similarity to the human and equine disease, immunocompetent rabbits are, therefore, a valuable animal model for investigating various aspects of non-lethal WNV infections. Full article
(This article belongs to the Special Issue Viral Pathogenesis)
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Review

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Open AccessReview
The Role of Gammaherpesviruses in Cancer Pathogenesis
Pathogens 2016, 5(1), 18; https://doi.org/10.3390/pathogens5010018 - 06 Feb 2016
Cited by 45
Abstract
Worldwide, one fifth of cancers in the population are associated with viral infections. Among them, gammaherpesvirus, specifically HHV4 (EBV) and HHV8 (KSHV), are two oncogenic viral agents associated with a large number of human malignancies. In this review, we summarize the current understanding [...] Read more.
Worldwide, one fifth of cancers in the population are associated with viral infections. Among them, gammaherpesvirus, specifically HHV4 (EBV) and HHV8 (KSHV), are two oncogenic viral agents associated with a large number of human malignancies. In this review, we summarize the current understanding of the molecular mechanisms related to EBV and KSHV infection and their ability to induce cellular transformation. We describe their strategies for manipulating major cellular systems through the utilization of cell cycle, apoptosis, immune modulation, epigenetic modification, and altered signal transduction pathways, including NF-kB, Notch, Wnt, MAPK, TLR, etc. We also discuss the important EBV latent antigens, namely EBNA1, EBNA2, EBNA3’s and LMP’s, which are important for targeting these major cellular pathways. KSHV infection progresses through the engagement of the activities of the major latent proteins LANA, v-FLIP and v-Cyclin, and the lytic replication and transcription activator (RTA). This review is a current, comprehensive approach that describes an in-depth understanding of gammaherpes viral encoded gene manipulation of the host system through targeting important biological processes in viral-associated cancers. Full article
(This article belongs to the Special Issue Viral Pathogenesis)
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Open AccessReview
Nonhuman Primate Models of Chikungunya Virus Infection and Disease (CHIKV NHP Model)
Pathogens 2015, 4(3), 662-681; https://doi.org/10.3390/pathogens4030662 - 16 Sep 2015
Cited by 19
Abstract
Chikungunya virus (CHIKV) is a positive-sense RNA virus transmitted by Aedes mosquitoes. CHIKV is a reemerging Alphavirus that causes acute febrile illness and severe and debilitating polyarthralgia of the peripheral joints. Huge epidemics and the rapid spread of CHIKV seen in India and [...] Read more.
Chikungunya virus (CHIKV) is a positive-sense RNA virus transmitted by Aedes mosquitoes. CHIKV is a reemerging Alphavirus that causes acute febrile illness and severe and debilitating polyarthralgia of the peripheral joints. Huge epidemics and the rapid spread of CHIKV seen in India and the Indian Ocean region established CHIKV as a global health concern. This concern was further solidified by the recent incursion of the virus into the Western hemisphere, a region without pre-existing immunity. Nonhuman primates (NHPs) serve as excellent animal models for understanding CHIKV pathogenesis and pre-clinical assessment of vaccines and therapeutics. NHPs present advantages over rodent models because they are a natural amplification host for CHIKV and they share significant genetic and physiological homology with humans. CHIKV infection in NHPs results in acute fever, rash, viremia and production of type I interferon. NHPs develop CHIKV-specific B and T-cells, generating neutralizing antibodies and CHIKV-specific CD4+ and CD8+ T-cells. CHIKV establishes a persistent infection in NHPs, particularly in cynomolgus macaques, because infectious virus could be recovered from spleen, liver, and muscle as late as 44 days post infection. NHPs are valuable models that are useful in preclinical testing of vaccines and therapeutics and uncovering the details of CHIKV pathogenesis. Full article
(This article belongs to the Special Issue Viral Pathogenesis)
Open AccessReview
Human Hemorrhagic Fever Causing Arenaviruses: Molecular Mechanisms Contributing to Virus Virulence and Disease Pathogenesis
Pathogens 2015, 4(2), 283-306; https://doi.org/10.3390/pathogens4020283 - 21 May 2015
Cited by 23
Abstract
Arenaviruses include multiple human pathogens ranging from the low-risk lymphocytic choriomeningitis virus (LCMV) to highly virulent hemorrhagic fever (HF) causing viruses such as Lassa (LASV), Junin (JUNV), Machupo (MACV), Lujo (LUJV), Sabia (SABV), Guanarito (GTOV), and Chapare (CHPV), for which there are limited [...] Read more.
Arenaviruses include multiple human pathogens ranging from the low-risk lymphocytic choriomeningitis virus (LCMV) to highly virulent hemorrhagic fever (HF) causing viruses such as Lassa (LASV), Junin (JUNV), Machupo (MACV), Lujo (LUJV), Sabia (SABV), Guanarito (GTOV), and Chapare (CHPV), for which there are limited preventative and therapeutic measures. Why some arenaviruses can cause virulent human infections while others cannot, even though they are isolated from the same rodent hosts, is an enigma. Recent studies have revealed several potential pathogenic mechanisms of arenaviruses, including factors that increase viral replication capacity and suppress host innate immunity, which leads to high viremia and generalized immune suppression as the hallmarks of severe and lethal arenaviral HF diseases. This review summarizes current knowledge of the roles of each of the four viral proteins and some known cellular factors in the pathogenesis of arenaviral HF as well as of some human primary cell-culture and animal models that lend themselves to studying arenavirus-induced HF disease pathogenesis. Knowledge gained from these studies can be applied towards the development of novel therapeutics and vaccines against these deadly human pathogens. Full article
(This article belongs to the Special Issue Viral Pathogenesis)
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