Simian hemorrhagic fever virus infection of rhesus macaques as a model of viral hemorrhagic fever: Clinical characterization and risk factors for severe disease

Johnson, Reed F.; Dodd, Lori E.; Yellayi, Srikanth; Gu, Wenjuan; Cann, Jennifer A.; Jett, Catherine; Bernbaum, John G.; Ragland, Dan R.; Claire, Marisa St.; Byrum, Russell; Paragas, Jason; Blaney, Joseph E.; Jahrling, Peter B.

doi:10.1016/j.virol.2011.09.016

Cited by 32 publications

(60 citation statements)

References 36 publications

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“…In addition, inoculation of grivet Vero E6 (ATCC CRL-1586) cells under MA-104 growth conditions (SHFV and KRCV-1 grow only in MA-104 or MA-104-derived cells) with such challenge stocks did not result in cytopathic effects. Titers of SHFV stocks were determined by plaque assay on MA-104 cells as previously described (43,44).…”

Section: Methodsmentioning

confidence: 99%

Within-Host Evolution of Simian Arteriviruses in Crab-Eating Macaques

Moncla

Weiler²,

Barry³

et al. 2017

J Virol

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Simian arteriviruses are a diverse clade of viruses infecting captive and wild nonhuman primates. We recently reported that Kibale red colobus virus 1 (KRCV-1) causes a mild and self-limiting disease in experimentally infected crabeating macaques, while simian hemorrhagic fever virus (SHFV) causes lethal viral hemorrhagic fever. Here we characterize how these viruses evolved during replication in cell culture and in experimentally infected macaques. During passage in cell culture, 68 substitutions that were localized in open reading frames (ORFs) likely associated with host cell entry and exit became fixed in the KRCV-1 genome. However, we did not detect any strong signatures of selection during replication in macaques. We uncovered patterns of evolution that were distinct from those observed in surveys of wild red colobus monkeys, suggesting that these species may exert different adaptive challenges for KRCV-1. During SHFV infection, we detected signatures of selection on ORF 5a and on a small subset of sites in the genome. Overall, our data suggest that patterns of evolution differ markedly among simian arteriviruses and among host species.IMPORTANCE Certain RNA viruses can cross species barriers and cause disease in new hosts. Simian arteriviruses are a diverse group of related viruses that infect captive and wild nonhuman primates, with associated disease severity ranging from apparently asymptomatic infections to severe, viral hemorrhagic fevers. We infected nonhuman primate cell cultures and then crab-eating macaques with either simian hemorrhagic fever virus (SHFV) or Kibale red colobus virus 1 (KRCV-1) and assessed within-host viral evolution. We found that KRCV-1 quickly acquired a large number of substitutions in its genome during replication in cell culture but that evolution in macaques was limited. In contrast, we detected selection focused on SHFV ORFs 5a and 5, which encode putative membrane proteins. These patterns suggest that in addition to diverse pathogenic phenotypes, these viruses may also exhibit distinct patterns of within-host evolution both in vitro and in vivo.KEYWORDS evolution, simian arterivirus, simian hemorrhagic fever virus, virology, within-host diversity I n 1964, acute outbreaks of a highly lethal viral hemorrhagic fever caused by a previously unknown agent swept through captive nonhuman primate research facilities in the former Soviet Union and the United States (1-4). Although the origin and

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Section: Methodsmentioning

confidence: 99%

Within-Host Evolution of Simian Arteriviruses in Crab-Eating Macaques

Moncla

Weiler²,

Barry³

et al. 2017

J Virol

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“…Infection of macaques with simian hemorrhagic fever virus offered a BSL-2 model of viral hemorrhagic fevers caused by pathogenic filoviruses and LASV [141]. SHEV is an arterivirus discovered in 1964 as a cause of hemorrhagic fevers in macaques at research facilities.…”

Section: Surrogate Models Of Lfmentioning

confidence: 99%

The search for animal models for Lassa fever vaccine development

Lukashevich

2013

Expert Review of Vaccines

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Lassa virus (LASV) is the most prevalent arenavirus in West Africa and is responsible for several hundred thousand infections and thousands of deaths annually. The sizeable disease burden, numerous imported cases of Lassa fever (LF) and the possibility that LASV can be used as an agent of biological warfare make a strong case for vaccine development. Currently there is no licensed LF vaccine and research and devlopment is hampered by the high cost of nonhuman primate animal models and by biocontainment requirements (BSL-4). In addition, a successful LF vaccine has to induce a strong cell-mediated cross-protective immunity against different LASV lineages. All of these challenges will be addressed in this review in the context of available and novel animal models recently described for evaluation of LF vaccine candidates.

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“…Additionally, increased expression of IL-10, an anti-inflammatory cytokine which we also found to have elevated levels in DMVV-1-infected vervets (albeit to nonsignificant levels), is associated with a reduction in virulence for both simian and nonsimian arteriviruses (56)(57)(58). Macaques infected with SHFV have increased plasma concentrations of proinflammatory cytokines but not increased levels of IL-10, possibly suggesting that IL-10 may be a host factor that protects African monkeys from simian arterivirus pathogenesis and SHF (59,60).…”

Section: Discussionmentioning

confidence: 52%

Arteriviruses, Pegiviruses, and Lentiviruses Are Common among Wild African Monkeys

Bailey

Lauck

Ghai

et al. 2016

J Virol

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Nonhuman primates (NHPs) are a historically important source of zoonotic viruses and are a gold-standard model for research on many human pathogens. However, with the exception of simian immunodeficiency virus (SIV) (family Retroviridae), the blood-borne viruses harbored by these animals in the wild remain incompletely characterized. Here, we report the discovery and characterization of two novel simian pegiviruses (family Flaviviridae) and two novel simian arteriviruses (family Arteriviridae) in wild African green monkeys from Zambia (malbroucks [Chlorocebus cynosuros]) and South Africa (vervet monkeys [Chlorocebus pygerythrus]). We examine several aspects of infection, including viral load, genetic diversity, evolution, and geographic distribution, as well as host factors such as age, sex, and plasma cytokines. In combination with previous efforts to characterize blood-borne RNA viruses in wild primates across sub-Saharan Africa, these discoveries demonstrate that in addition to SIV, simian pegiviruses and simian arteriviruses are widespread and prevalent among many African cercopithecoid (i.e., Old World) monkeys. IMPORTANCEPrimates are an important source of viruses that infect humans and serve as an important laboratory model of human virus infection. Here, we discover two new viruses in African green monkeys from Zambia and South Africa. In combination with previous virus discovery efforts, this finding suggests that these virus types are widespread among African monkeys. Our analysis suggests that one of these virus types, the simian arteriviruses, may have the potential to jump between different primate species and cause disease. In contrast, the other virus type, the pegiviruses, are thought to reduce the disease caused by human immunodeficiency virus (HIV) in humans. However, we did not observe a similar protective effect in SIV-infected African monkeys coinfected with pegiviruses, possibly because SIV causes little to no disease in these hosts.

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Simian hemorrhagic fever virus infection of rhesus macaques as a model of viral hemorrhagic fever: Clinical characterization and risk factors for severe disease

Cited by 32 publications

References 36 publications

Within-Host Evolution of Simian Arteriviruses in Crab-Eating Macaques

Within-Host Evolution of Simian Arteriviruses in Crab-Eating Macaques

The search for animal models for Lassa fever vaccine development

Arteriviruses, Pegiviruses, and Lentiviruses Are Common among Wild African Monkeys

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