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Special Issue "Pathogenesis of Emerging and Re-Emerging RNA Viruses"

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

Deadline for manuscript submissions: closed (31 March 2011)

Special Issue Editor

Guest Editor
Prof. Dr. Brian Hjelle

Departments of Pathology, Biology, and Molecular Genetics & Microbiology Center for Infectious Diseases and Immunity Health Sciences Center, 329CRF MSC08 4640, 1 University of New Mexico, Albuquerque, NM 87131, USA
Website | E-Mail
Phone: 505-272-0624
Fax: +1 504 272 4401

Special Issue Information

Dear Colleagues,

The last several decades has witnessed a steady stream of newly-emerged highly pathogenic RNA viruses including Ebola and Marburg viruses, novel New World and Old World arenaviruses, the agents of hantavirus cardiopulmonary syndrome, the SARS coronavirus, Henipaviruses, and the appearance of West Nile virus in the Western Hemisphere. Other RNA viruses such as hepatitis C virus have continued to cause mounting numbers of cases of chronic illness, often with severe consequences.
Recent investigations are revealing in ever-increasing detail the many strategies that viruses use to evade immunity and to interfere with the normal function of cells, creating new potential for the understanding of the basis for pathogenesis by, and prevention and treatment of, RNA viruses and their associated illnesses.

Prof. Dr. Brian Hjelle
Guest Editor

Published Papers (10 papers)

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Review

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Open AccessReview Filoviral Immune Evasion Mechanisms
Viruses 2011, 3(9), 1634-1649; doi:10.3390/v3091634
Received: 11 August 2011 / Accepted: 15 August 2011 / Published: 7 September 2011
Cited by 37 | PDF Full-text (642 KB)
Abstract
The Filoviridae family of viruses, which includes the genera Ebolavirus (EBOV) and Marburgvirus (MARV), causes severe and often times lethal hemorrhagic fever in humans. Filoviral infections are associated with ineffective innate antiviral responses as a result of virally encoded immune antagonists, which render
[...] Read more.
The Filoviridae family of viruses, which includes the genera Ebolavirus (EBOV) and Marburgvirus (MARV), causes severe and often times lethal hemorrhagic fever in humans. Filoviral infections are associated with ineffective innate antiviral responses as a result of virally encoded immune antagonists, which render the host incapable of mounting effective innate or adaptive immune responses. The Type I interferon (IFN) response is critical for establishing an antiviral state in the host cell and subsequent activation of the adaptive immune responses. Several filoviral encoded components target Type I IFN responses, and this innate immune suppression is important for viral replication and pathogenesis. For example, EBOV VP35 inhibits the phosphorylation of IRF-3/7 by the TBK-1/IKKε kinases in addition to sequestering viral RNA from detection by RIG-I like receptors. MARV VP40 inhibits STAT1/2 phosphorylation by inhibiting the JAK family kinases. EBOV VP24 inhibits nuclear translocation of activated STAT1 by karyopherin-α. The examples also represent distinct mechanisms utilized by filoviral proteins in order to counter immune responses, which results in limited IFN-α/β production and downstream signaling. Full article
(This article belongs to the Special Issue Pathogenesis of Emerging and Re-Emerging RNA Viruses)
Open AccessReview Intracellular Events and Cell Fate in Filovirus Infection
Viruses 2011, 3(8), 1501-1531; doi:10.3390/v3081501
Received: 7 June 2011 / Revised: 9 August 2011 / Accepted: 15 August 2011 / Published: 24 August 2011
Cited by 25 | PDF Full-text (4936 KB)
Abstract
Marburg and Ebola viruses cause a severe hemorrhagic disease in humans with high fatality rates. Early target cells of filoviruses are monocytes, macrophages, and dendritic cells. The infection spreads to the liver, spleen and later other organs by blood and lymph flow. A
[...] Read more.
Marburg and Ebola viruses cause a severe hemorrhagic disease in humans with high fatality rates. Early target cells of filoviruses are monocytes, macrophages, and dendritic cells. The infection spreads to the liver, spleen and later other organs by blood and lymph flow. A hallmark of filovirus infection is the depletion of non-infected lymphocytes; however, the molecular mechanisms leading to the observed bystander lymphocyte apoptosis are poorly understood. Also, there is limited knowledge about the fate of infected cells in filovirus disease. In this review we will explore what is known about the intracellular events leading to virus amplification and cell damage in filovirus infection. Furthermore, we will discuss how cellular dysfunction and cell death may correlate with disease pathogenesis. Full article
(This article belongs to the Special Issue Pathogenesis of Emerging and Re-Emerging RNA Viruses)
Open AccessReview T Cells and Pathogenesis of Hantavirus Cardiopulmonary Syndrome and Hemorrhagic Fever with Renal Syndrome
Viruses 2011, 3(7), 1059-1073; doi:10.3390/v3071059
Received: 31 March 2011 / Revised: 30 June 2011 / Accepted: 1 July 2011 / Published: 6 July 2011
Cited by 32 | PDF Full-text (214 KB)
Abstract
We previously hypothesized that increased capillary permeability observed in both hantavirus cardiopulmonary syndrome (HCPS) and hemorrhagic fever with renal syndrome (HFRS) may be caused by hantavirus-specific cytotoxic T cells attacking endothelial cells presenting viral antigens on their surface based on clinical observations and
[...] Read more.
We previously hypothesized that increased capillary permeability observed in both hantavirus cardiopulmonary syndrome (HCPS) and hemorrhagic fever with renal syndrome (HFRS) may be caused by hantavirus-specific cytotoxic T cells attacking endothelial cells presenting viral antigens on their surface based on clinical observations and in vitro experiments. In HCPS, hantavirus-specific T cell responses positively correlated with disease severity. In HFRS, in one report, contrary to HCPS, T cell responses negatively correlated with disease severity, but in another report the number of regulatory T cells, which are thought to suppress T cell responses, negatively correlated with disease severity. In rat experiments, in which hantavirus causes persistent infection, depletion of regulatory T cells helped infected rats clear virus without inducing immunopathology. These seemingly contradictory findings may suggest delicate balance in T cell responses between protection and immunopathogenesis. Both too strong and too weak T cell responses may lead to severe disease. It is important to clarify the role of T cells in these diseases for better treatment (whether to suppress T cell functions) and protection (vaccine design) which may need to take into account viral factors and the influence of HLA on T cell responses. Full article
(This article belongs to the Special Issue Pathogenesis of Emerging and Re-Emerging RNA Viruses)
Open AccessReview Correlates of Immunity to Filovirus Infection
Viruses 2011, 3(7), 982-1000; doi:10.3390/v3070982
Received: 14 April 2011 / Revised: 14 June 2011 / Accepted: 16 June 2011 / Published: 27 June 2011
Cited by 14 | PDF Full-text (173 KB)
Abstract
Filoviruses can cause severe, often fatal hemorrhagic fever in humans. Recent advances in vaccine and therapeutic drug development have provided encouraging data concerning treatment of these infections. However, relatively little is known about immune responses in fatal versus non-fatal filovirus infection. This review
[...] Read more.
Filoviruses can cause severe, often fatal hemorrhagic fever in humans. Recent advances in vaccine and therapeutic drug development have provided encouraging data concerning treatment of these infections. However, relatively little is known about immune responses in fatal versus non-fatal filovirus infection. This review summarizes the published literature on correlates of immunity to filovirus infection, and highlights deficiencies in our knowledge on this topic. It is likely that there are several types of successful immune responses, depending on the type of filovirus, and the presence and timing of vaccination or drug treatment. Full article
(This article belongs to the Special Issue Pathogenesis of Emerging and Re-Emerging RNA Viruses)
Open AccessReview West Nile Virus: Immunity and Pathogenesis
Viruses 2011, 3(6), 811-828; doi:10.3390/v3060811
Received: 3 April 2011 / Revised: 26 May 2011 / Accepted: 27 May 2011 / Published: 15 June 2011
Cited by 37 | PDF Full-text (336 KB)
Abstract
West Nile virus (WNV) is a neurotropic, arthropod-borne flavivirus that is maintained in an enzootic cycle between mosquitoes and birds, but can also infect and cause disease in horses and humans. WNV is endemic in parts of Africa, Europe, the Middle East, and
[...] Read more.
West Nile virus (WNV) is a neurotropic, arthropod-borne flavivirus that is maintained in an enzootic cycle between mosquitoes and birds, but can also infect and cause disease in horses and humans. WNV is endemic in parts of Africa, Europe, the Middle East, and Asia, and since 1999 has spread to North America, Mexico, South America, and the Caribbean. WNV infects the central nervous system (CNS) and can cause severe disease in a small minority of infected humans, mostly immunocompromised or the elderly. This review discusses some of the mechanisms by which the immune system can limit dissemination of WNV infection and elaborates on the mechanisms involved in pathogenesis. Reasons for susceptibility to WNV-associated neuroinvasive disease in less than 1% of cases remain unexplained, but one favored hypothesis is that the involvement of the CNS is associated with a weak immune response allowing robust WNV replication in the periphery and spread of the virus to the CNS. Full article
(This article belongs to the Special Issue Pathogenesis of Emerging and Re-Emerging RNA Viruses)
Open AccessReview The Role of Interferon Antagonist, Non-Structural Proteins in the Pathogenesis and Emergence of Arboviruses
Viruses 2011, 3(6), 629-658; doi:10.3390/v3060629
Received: 5 April 2011 / Revised: 4 May 2011 / Accepted: 7 May 2011 / Published: 1 June 2011
Cited by 12 | PDF Full-text (750 KB)
Abstract
A myriad of factors favor the emergence and re-emergence of arthropod-borne viruses (arboviruses), including migration, climate change, intensified livestock production, an increasing volume of international trade and transportation, and changes to ecosystems (e.g., deforestation and loss of biodiversity). Consequently, arboviruses are distributed worldwide
[...] Read more.
A myriad of factors favor the emergence and re-emergence of arthropod-borne viruses (arboviruses), including migration, climate change, intensified livestock production, an increasing volume of international trade and transportation, and changes to ecosystems (e.g., deforestation and loss of biodiversity). Consequently, arboviruses are distributed worldwide and represent over 30% of all emerging infectious diseases identified in the past decade. Although some arboviral infections go undetected or are associated with mild, flu-like symptoms, many are important human and veterinary pathogens causing serious illnesses such as arthritis, gastroenteritis, encephalitis and hemorrhagic fever and devastating economic loss as a consequence of lost productivity and high mortality rates among livestock. One of the most consistent molecular features of emerging arboviruses, in addition to their near exclusive use of RNA genomes, is the inclusion of viral, non-structural proteins that act as interferon antagonists. In this review, we describe these interferon antagonists and common strategies that arboviruses use to counter the host innate immune response. In addition, we discuss the complex interplay between host factors and viral determinants that are associated with virus emergence and re-emergence, and identify potential targets for vaccine and anti-viral therapies. Full article
(This article belongs to the Special Issue Pathogenesis of Emerging and Re-Emerging RNA Viruses)
Figures

Open AccessReview The Pathogenesis of Rift Valley Fever
Viruses 2011, 3(5), 493-519; doi:10.3390/v3050493
Received: 31 March 2011 / Revised: 26 April 2011 / Accepted: 2 May 2011 / Published: 6 May 2011
Cited by 82 | PDF Full-text (421 KB)
Abstract
Rift Valley fever (RVF) is an emerging zoonotic disease distributed in sub-Saharan African countries and the Arabian Peninsula. The disease is caused by the Rift Valley fever virus (RVFV) of the family Bunyaviridae and the genus Phlebovirus. The virus is transmitted by
[...] Read more.
Rift Valley fever (RVF) is an emerging zoonotic disease distributed in sub-Saharan African countries and the Arabian Peninsula. The disease is caused by the Rift Valley fever virus (RVFV) of the family Bunyaviridae and the genus Phlebovirus. The virus is transmitted by mosquitoes, and virus replication in domestic ruminant results in high rates of mortality and abortion. RVFV infection in humans usually causes a self-limiting, acute and febrile illness; however, a small number of cases progress to neurological disorders, partial or complete blindness, hemorrhagic fever, or thrombosis. This review describes the pathology of RVF in human patients and several animal models, and summarizes the role of viral virulence factors and host factors that affect RVFV pathogenesis. Full article
(This article belongs to the Special Issue Pathogenesis of Emerging and Re-Emerging RNA Viruses)
Open AccessReview Hantaviruses in the Americas and Their Role as Emerging Pathogens
Viruses 2010, 2(12), 2559-2586; doi:10.3390/v2122559
Received: 25 October 2010 / Revised: 15 November 2010 / Accepted: 24 November 2010 / Published: 25 November 2010
Cited by 39 | PDF Full-text (598 KB)
Abstract
The continued emergence and re-emergence of pathogens represent an ongoing, sometimes major, threat to populations. Hantaviruses (family Bunyaviridae) and their associated human diseases were considered to be confined to Eurasia, but the occurrence of an outbreak in 1993–94 in the southwestern United States
[...] Read more.
The continued emergence and re-emergence of pathogens represent an ongoing, sometimes major, threat to populations. Hantaviruses (family Bunyaviridae) and their associated human diseases were considered to be confined to Eurasia, but the occurrence of an outbreak in 1993–94 in the southwestern United States led to a great increase in their study among virologists worldwide. Well over 40 hantaviral genotypes have been described, the large majority since 1993, and nearly half of them pathogenic for humans. Hantaviruses cause persistent infections in their reservoir hosts, and in the Americas, human disease is manifest as a cardiopulmonary compromise, hantavirus cardiopulmonary syndrome (HCPS), with case-fatality ratios, for the most common viral serotypes, between 30% and 40%. Habitat disturbance and larger-scale ecological disturbances, perhaps including climate change, are among the factors that may have increased the human caseload of HCPS between 1993 and the present. We consider here the features that influence the structure of host population dynamics that may lead to viral outbreaks, as well as the macromolecular determinants of hantaviruses that have been regarded as having potential contribution to pathogenicity. Full article
(This article belongs to the Special Issue Pathogenesis of Emerging and Re-Emerging RNA Viruses)
Open AccessReview Pathogenesis of Noroviruses, Emerging RNA Viruses
Viruses 2010, 2(3), 748-781; doi:10.3390/v2030748
Received: 18 November 2009 / Revised: 15 March 2010 / Accepted: 15 March 2010 / Published: 23 March 2010
Cited by 59 | PDF Full-text (406 KB) | HTML Full-text | XML Full-text
Abstract
Human noroviruses in the family Caliciviridae are a major cause of epidemic gastroenteritis. They are responsible for at least 95% of viral outbreaks and over 50% of all outbreaks worldwide. Transmission of these highly infectious plus-stranded RNA viruses occurs primarily through contaminated food
[...] Read more.
Human noroviruses in the family Caliciviridae are a major cause of epidemic gastroenteritis. They are responsible for at least 95% of viral outbreaks and over 50% of all outbreaks worldwide. Transmission of these highly infectious plus-stranded RNA viruses occurs primarily through contaminated food or water, but also through person-to-person contact and exposure to fomites. Norovirus infections are typically acute and self-limited. However, disease can be much more severe and prolonged in infants, elderly, and immunocompromised individuals. Norovirus outbreaks frequently occur in semi-closed communities such as nursing homes, military settings, schools, hospitals, cruise ships, and disaster relief situations. Noroviruses are classified as Category B biodefense agents because they are highly contagious, extremely stable in the environment, resistant to common disinfectants, and associated with debilitating illness. The number of reported norovirus outbreaks has risen sharply since 2002 suggesting the emergence of more infectious strains. There has also been increased recognition that noroviruses are important causes of childhood hospitalization. Moreover, noroviruses have recently been associated with multiple clinical outcomes other than gastroenteritis. It is unclear whether these new observations are due to improved norovirus diagnostics or to the emergence of more virulent norovirus strains. Regardless, it is clear that human noroviruses cause considerable morbidity worldwide, have significant economic impact, and are clinically important emerging pathogens. Despite the impact of human norovirus-induced disease and the potential for emergence of highly virulent strains, the pathogenic features of infection are not well understood due to the lack of a cell culture system and previous lack of animal models. This review summarizes the current understanding of norovirus pathogenesis from the histological to the molecular level, including contributions from new model systems. Full article
(This article belongs to the Special Issue Pathogenesis of Emerging and Re-Emerging RNA Viruses)

Other

Jump to: Review

Open AccessShort Note Meta-Analysis of High-Throughput Datasets Reveals Cellular Responses Following Hemorrhagic Fever Virus Infection
Viruses 2011, 3(5), 613-619; doi:10.3390/v3050613
Received: 2 April 2011 / Accepted: 20 April 2011 / Published: 12 May 2011
Cited by 5 | PDF Full-text (191 KB)
Abstract
The continuing use of high-throughput assays to investigate cellular responses to infection is providing a large repository of information. Due to the large number of differentially expressed transcripts, often running into the thousands, the majority of these data have not been thoroughly investigated.
[...] Read more.
The continuing use of high-throughput assays to investigate cellular responses to infection is providing a large repository of information. Due to the large number of differentially expressed transcripts, often running into the thousands, the majority of these data have not been thoroughly investigated. Advances in techniques for the downstream analysis of high-throughput datasets are providing additional methods for the generation of additional hypotheses for further investigation. The large number of experimental observations, combined with databases that correlate particular genes and proteins with canonical pathways, functions and diseases, allows for the bioinformatic exploration of functional networks that may be implicated in replication or pathogenesis. Herein, we provide an example of how analysis of published high-throughput datasets of cellular responses to hemorrhagic fever virus infection can generate additional functional data. We describe enrichment of genes involved in metabolism, post-translational modification and cardiac damage; potential roles for specific transcription factors and a conserved involvement of a pathway based around cyclooxygenase-2. We believe that these types of analyses can provide virologists with additional hypotheses for continued investigation. Full article
(This article belongs to the Special Issue Pathogenesis of Emerging and Re-Emerging RNA Viruses)

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