Rift Valley Fever Epidemiology, Pathogenesis and Host Response

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Human Virology and Viral Diseases".

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 3447

Special Issue Editors


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Guest Editor
1. Department of Diagnostic Medicine/Pathobiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS, USA
2. Department of Paraclinical Sciences, Faculty of Veterinary Sciences, University of Pretoria, Pretoria, South Africa
Interests: emerging and zoonotic viral diseases; tissue based assays; biospecimen preservation; veterinary pathology and microbiology
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Guest Editor
Department of Paraclinical Sciences, Faculty of Veterinary Science, University of Pretoria, Pretoria, South Africa
Interests: viral hemorrhagic fever viruses; viral zoonotic diseases; veterinary pathology and histopathology; pathogenesis of disease; immunohistochemistry and other specialized diagnostic methods involving FFPE tissues

Special Issue Information

Dear Colleagues,

Rift Valley fever phlebovirus is an arthropod-borne RNA virus that causes disease in a wide range of domestic and wild cloven-hoofed animals, camelids, and humans. Humans may become fatally infected by consuming or handling products from sick animals, including slaughtering sick livestock and handling dead fetuses.

In affected countries, Rift Valley fever (RVF) causes huge economic losses and extremely high mortality rates, especially in sheep. Epidemics are characterized by trimester-independent, near-simultaneous abortions or fetal loss in pregnant animals. In humans, vertical transmission of RVFV to the fetus correlates with an increased risk of miscarriage.

Outbreaks of RVF occur virtually every year in Africa in one or more countries. In some areas of Africa, serological data suggests that the virus circulates continuously year after year, with occasional occurrence of disease missed. The movement of virus out of areas endemic for the disease is thought to cause the occasional epidemic with marked spill-over outbreaks in humans. Livestock trade might contribute to the spread of the disease into disease-free areas. However, on numerous occasions RVFV from the same lineage has been shown to spread over long distances, sometimes at fast rates that cannot be explained by livestock trade. This heightens the concern that this emerging disease may spread beyond its initial area of endemicity into the rest of Asia, Europe, or the Americas.

A complete understanding of RVF pathogenesis and host response to infection is also still lacking. Direct tissue injury (i.e., liver, kidneys, adrenal cortex), failure of the adaptive immune response (likely exacerbated by marked loss of lymphocytes), and various innate immune responses (i.e., tissue factor synthesis) have been demonstrated. However, our understanding of the diversity of forms RVF presents across species, age groups, and individuals is woefully incomplete. Usually, human infections present as an acute self-limiting febrile illness, but some patients develop severe or fatal disease that can include hepatic disease, widespread hemorrhages, renal impairment, encephalitis, and ocular lesions. Intriguingly, while encephalitis has been experimentally reproduced in mice, rats, marmosets, and African green monkeys, it has not been described in any natural cases in ruminants.

To this Special Issue of Viruses, we invite research and review articles focused on improving our understanding of Rift Valley fever epidemiology, pathogenesis and host response including manuscripts detailing the application of new techniques and methodologies to these topics.

Dr. A. Sally Davis
Dr. Lieza Odendaal
Guest Editors

Manuscript Submission Information

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Keywords

  • rift valley fever phlebovirus
  • epidemiology
  • pathogenesis
  • host response
  • transboundary and emerging diseases
  • zoonoses
  • arbovirus

Published Papers (2 papers)

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Research

12 pages, 1224 KiB  
Article
Rift Valley Fever Virus Non-Structural Protein S Is Associated with Nuclear Translocation of Active Caspase-3 and Inclusion Body Formation
by Lukas Mathias Michaely, Melanie Rissmann, Federico Armando, Felicitas von Arnim, Markus Keller, Martin Eiden, Rebecca König, Benjamin Gutjahr, Wolfgang Baumgärtner, Martin H. Groschup and Reiner Ulrich
Viruses 2022, 14(11), 2487; https://doi.org/10.3390/v14112487 - 10 Nov 2022
Cited by 4 | Viewed by 1307
Abstract
Rift Valley fever phlebovirus (RVFV) causes Rift Valley fever (RVF), an emerging zoonotic disease that causes abortion storms and high mortality rates in young ruminants as well as severe or even lethal complications in a subset of human patients. This study investigates the [...] Read more.
Rift Valley fever phlebovirus (RVFV) causes Rift Valley fever (RVF), an emerging zoonotic disease that causes abortion storms and high mortality rates in young ruminants as well as severe or even lethal complications in a subset of human patients. This study investigates the pathomechanism of intranuclear inclusion body formation in severe RVF in a mouse model. Liver samples from immunocompetent mice infected with virulent RVFV 35/74, and immunodeficient knockout mice that lack interferon type I receptor expression and were infected with attenuated RVFV MP12 were compared to livers from uninfected controls using histopathology and immunohistochemistry for RVFV nucleoprotein, non-structural protein S (NSs) and pro-apoptotic active caspase-3. Histopathology of the livers showed virus-induced, severe hepatic necrosis in both mouse strains. However, immunohistochemistry and immunofluorescence revealed eosinophilic, comma-shaped, intranuclear inclusions and an intranuclear (co-)localization of RVFV NSs and active caspase-3 only in 35/74-infected immunocompetent mice, but not in MP12-infected immunodeficient mice. These results suggest that intranuclear accumulation of RVFV 35/74 NSs is involved in nuclear translocation of active caspase-3, and that nuclear NSs and active caspase-3 are involved in the formation of the light microscopically visible inclusion bodies. Full article
(This article belongs to the Special Issue Rift Valley Fever Epidemiology, Pathogenesis and Host Response)
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14 pages, 1516 KiB  
Article
Intranasal Exposure to Rift Valley Fever Virus Live-Attenuated Strains Leads to High Mortality Rate in Immunocompetent Mice
by Sandra Lacote, Carole Tamietti, Mehdi Chabert, Marie-Pierre Confort, Laurine Conquet, Coralie Pulido, Noémie Aurine, Camille Baquerre, Adrien Thiesson, Bertrand Pain, Marcelo De Las Heras, Marie Flamand, Xavier Montagutelli, Philippe Marianneau, Maxime Ratinier and Frédérick Arnaud
Viruses 2022, 14(11), 2470; https://doi.org/10.3390/v14112470 - 08 Nov 2022
Cited by 1 | Viewed by 1610
Abstract
Rift Valley fever virus (RVFV) is a pathogenic arthropod-borne virus that can cause serious illness in both ruminants and humans. The virus can be transmitted by an arthropod bite or contact with contaminated fluids or tissues. Two live-attenuated veterinary vaccines—the Smithburn (SB) and [...] Read more.
Rift Valley fever virus (RVFV) is a pathogenic arthropod-borne virus that can cause serious illness in both ruminants and humans. The virus can be transmitted by an arthropod bite or contact with contaminated fluids or tissues. Two live-attenuated veterinary vaccines—the Smithburn (SB) and Clone 13 (Cl.13)—are currently used during epizootic events in Africa. However, their residual pathogenicity (i.e., SB) or potential of reversion (i.e., Cl.13) causes important adverse effects, strongly limiting their use in the field. In this study, we infected immunocompetent mice with SB or Cl.13 by a subcutaneous or an intranasal inoculation. Interestingly, we found that, unlike the subcutaneous infection, the intranasal inoculation led to a high mortality rate. In addition, we detected high titers and viral N antigen levels in the brain of both the SB- and Cl.13-infected mice. Overall, we unveil a clear correlation between the pathogenicity and the route of administration of both SB and Cl.13, with the intranasal inoculation leading to a stronger neurovirulence and higher mortality rate than the subcutaneous infection. Full article
(This article belongs to the Special Issue Rift Valley Fever Epidemiology, Pathogenesis and Host Response)
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