scholarly journals Analysis of Simian Hemorrhagic Fever Virus (SHFV) Subgenomic RNAs, Junction Sequences, and 5′ Leader

Virology ◽  
1995 ◽  
Vol 207 (2) ◽  
pp. 543-548 ◽  
Author(s):  
L. Zeng ◽  
E.K. Godeny ◽  
S.L. Methven ◽  
M.A. Brinton
Keyword(s):  
Hemorrhagic Fever ◽  
Fever Virus ◽  
Simian Hemorrhagic Fever Virus ◽  
Hemorrhagic Fever Virus ◽  
Subgenomic Rnas

scholarly journals Identification of the Leader-Body Junctions for the Viral Subgenomic mRNAs and Organization of the Simian Hemorrhagic Fever Virus Genome: Evidence for Gene Duplication during Arterivirus Evolution

1998 ◽  
Vol 72 (1) ◽  
pp. 862-867 ◽  
Author(s):  
E. K. Godeny ◽  
A. A. F. de Vries ◽  
X. C. Wang ◽  
S. L. Smith ◽  
R. J. de Groot
Keyword(s):  
Consensus Sequence ◽  
Hemorrhagic Fever ◽  
Comparative Sequence Analysis ◽  
The Body ◽  
Fever Virus ◽  
The Other ◽  
Pcr Analysis ◽  
Virus Family ◽  
Simian Hemorrhagic Fever Virus ◽  
Hemorrhagic Fever Virus

ABSTRACT Simian hemorrhagic fever virus (SHFV) was recently reclassified and assigned to the new virus family Arteriviridae. During replication, arteriviruses produce a 3′ coterminal, nested set of subgenomic mRNAs (sgRNAs). These sgRNAs arise by discontinuous transcription, and each contains a 5′ leader sequence which is joined to the body of the mRNA through a conserved junction sequence. Only the 5′-most open reading frame (ORF) is believed to be transcribed from each sgRNA. The SHFV genome encodes nine ORFs that are presumed to be expressed from sgRNAs. However, reverse transcription-PCR analysis with leader- and ORF-specific primers identified only eight sgRNA species. The consensus sequence 5′-UCNUUAACC-3′ was identified as the junction motif. Our data suggest that sgRNA 2 may be bicistronic, expressing both ORF 2a and ORF 2b. SHFV encodes three more ORFs on its genome than the other arteriviruses. Comparative sequence analysis suggested that SHFV ORFs 2a, 2b, and 3 are related to ORFs 2 through 4 of the other arteriviruses. Evidence which suggests that SHFV ORFs 4 through 6 are related to ORFs 2a through 3 and may have resulted from a recombination event during virus evolution is presented.

scholarly journals Functional Analyses of the Three Simian Hemorrhagic Fever Virus Nonstructural Protein 1 Papain-Like Proteases

2014 ◽  
Vol 88 (16) ◽  
pp. 9129-9140 ◽  
Author(s):  
H. A. Vatter ◽  
H. Di ◽  
E. F. Donaldson ◽  
G. U. Radu ◽  
T. R. Maines ◽  
...  
Keyword(s):  
Nonstructural Protein ◽  
Hemorrhagic Fever ◽  
Fever Virus ◽  
Simian Hemorrhagic Fever Virus ◽  
Hemorrhagic Fever Virus ◽  
Nonstructural Protein 1 ◽  
Functional Analyses

Simian Hemorrhagic Fever Virus: A New Togavirus

1975 ◽  
Vol 150 (3) ◽  
pp. 707-711 ◽  
Author(s):  
M. D. Trousdale ◽  
D. W. Trent ◽  
A. Shelokov
Keyword(s):  
Hemorrhagic Fever ◽  
Fever Virus ◽  
Simian Hemorrhagic Fever Virus ◽  
Hemorrhagic Fever Virus

scholarly journals Clinical Characterization of Host Response to Simian Hemorrhagic Fever Virus Infection in Permissive and Refractory Hosts: A Model for Determining Mechanisms of VHF Pathogenesis

2018 ◽  
Author(s):  
Joseph P. Cornish ◽  
Ian N. Moore ◽  
Donna L. Perry ◽  
Abigail Lara ◽  
Mahnaz Minai ◽  
...  
Keyword(s):  
Rhesus Monkeys ◽  
Host Response ◽  
Severe Disease ◽  
Hemorrhagic Fever ◽  
Fever Virus ◽  
Host Responses ◽  
Viral Hemorrhagic Fever ◽  
Simian Hemorrhagic Fever Virus ◽  
Patas Monkeys ◽  
Hemorrhagic Fever Virus

ABSTRACTSimian hemorrhagic fever virus (SHFV) causes a fulminant and typically lethal viral hemorrhagic fever (VHF) in macaques (Cercopithecinae: Macaca spp.) but causes subclinical infections in patas monkeys (Cercopithecinae: Erythrocebus patas). This difference in disease course offers a unique opportunity to compare host-responses to infection by a VHF-causing virus in biologically similar susceptible and refractory animals. Patas and rhesus monkeys were inoculated side-by-side with SHFV. In contrast to the severe disease observed in rhesus monkeys, patas monkeys developed a limited clinical disease characterized by changes in complete blood counts, serum chemistries, and development of lymphadenopathy. Viremia was measurable 2 days after exposure and its duration varied by species. Infectious virus was detected in terminal tissues of both patas and rhesus monkeys. Varying degrees of overlap in changes in serum concentrations of IFN-γ, MCP-1, and IL-6 were observed between patas and rhesus monkeys, suggesting the presence of common and species-specific cytokine responses to infection. Similarly, quantitative immunohistochemistry of terminal livers and whole blood flow cytometry revealed varying degrees of overlap in changes in macrophages, natural killer cells, and T-cells. The unexpected degree of overlap in host-response suggests that relatively small subsets of a host’s response to infection may be responsible for driving pathogenesis that results in a hemorrhagic fever. Furthermore, comparative SHFV infection in patas and rhesus monkeys offers an experimental model to characterize host-response mechanisms associated with viral hemorrhagic fever and evaluate pan-viral hemorrhagic fever countermeasures.IMPORTANCEHost-response mechanisms involved in pathogenesis of VHFs remain poorly understood. An underlying challenge is separating beneficial, inconsequential, and detrimental host-responses during infection. The comparison of host-responses to infection with the same virus in biologically similar animals that have drastically different disease manifestations allows for the identification of pathogenic mechanisms. SHFV, a surrogate virus for human VHF-causing viruses likely causes subclinical infection in African monkeys such as patas monkeys but can cause severe disease in Asian macaque monkeys. Data from the accompanying article by Buechler et al. support that infection of macaques and baboons with non-SHFV simarteviruses can establish persistent or long-term subclinical infections. Baboons, macaques, and patas monkeys are relatively closely taxonomically related (Cercopithecidae: Cercopithecinae) and therefore offer a unique opportunity to dissect how host-response differences determine disease outcome in VHFs.

scholarly journals Clinical Characterization of Host Response to Simian Hemorrhagic Fever Virus Infection in Permissive and Refractory Hosts: A Model for Determining Mechanisms of VHF Pathogenesis

Viruses ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 67
Author(s):  
Joseph Cornish ◽  
Ian Moore ◽  
Donna Perry ◽  
Abigail Lara ◽  
Mahnaz Minai ◽  
...  
Keyword(s):  
Rhesus Monkeys ◽  
Host Response ◽  
Severe Disease ◽  
Hemorrhagic Fever ◽  
Fever Virus ◽  
Host Responses ◽  
Viral Hemorrhagic Fever ◽  
Simian Hemorrhagic Fever Virus ◽  
Patas Monkeys ◽  
Hemorrhagic Fever Virus

Simian hemorrhagic fever virus (SHFV) causes a fulminant and typically lethal viral hemorrhagic fever (VHF) in macaques (Cercopithecinae: Macaca spp.) but causes subclinical infections in patas monkeys (Cercopithecinae: Erythrocebus patas). This difference in disease course offers a unique opportunity to compare host responses to infection by a VHF-causing virus in biologically similar susceptible and refractory animals. Patas and rhesus monkeys were inoculated side-by-side with SHFV. Unlike the severe disease observed in rhesus monkeys, patas monkeys developed a limited clinical disease characterized by changes in complete blood counts, serum chemistries, and development of lymphadenopathy. Viral RNA was measurable in circulating blood 2 days after exposure, and its duration varied by species. Infectious virus was detected in terminal tissues of both patas and rhesus monkeys. Varying degrees of overlap in changes in serum concentrations of interferon (IFN)-γ, monocyte chemoattractant protein (MCP)-1, and interleukin (IL)-6 were observed between patas and rhesus monkeys, suggesting the presence of common and species-specific cytokine responses to infection. Similarly, quantitative immunohistochemistry of livers from terminal monkeys and whole blood flow cytometry revealed varying degrees of overlap in changes in macrophages, natural killer cells, and T-cells. The unexpected degree of overlap in host response suggests that relatively small subsets of a host’s response to infection may be responsible for driving hemorrhagic fever pathogenesis. Furthermore, comparative SHFV infection in patas and rhesus monkeys offers an experimental model to characterize host–response mechanisms associated with viral hemorrhagic fever and evaluate pan-viral hemorrhagic fever countermeasures.

scholarly journals Simian Hemorrhagic Fever Virus Cell Entry Is Dependent on CD163 and Uses a Clathrin-Mediated Endocytosis-Like Pathway

2014 ◽  
Vol 89 (1) ◽  
pp. 844-856 ◽  
Author(s):  
Yíngyún Caì ◽  
Elena N. Postnikova ◽  
John G. Bernbaum ◽  
Shuǐqìng Yú ◽  
Steven Mazur ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Life Cycle ◽  
Cell Surface ◽  
Hemorrhagic Fever ◽  
Low Ph ◽  
Fever Virus ◽  
Target Cells ◽  
Simian Hemorrhagic Fever Virus ◽  
Hemorrhagic Fever Virus ◽  
Ph Dependent

ABSTRACTSimian hemorrhagic fever virus (SHFV) causes a severe and almost uniformly fatal viral hemorrhagic fever in Asian macaques but is thought to be nonpathogenic for humans. To date, the SHFV life cycle is almost completely uncharacterized on the molecular level. Here, we describe the first steps of the SHFV life cycle. Our experiments indicate that SHFV enters target cells by low-pH-dependent endocytosis. Dynamin inhibitors, chlorpromazine, methyl-β-cyclodextrin, chloroquine, and concanamycin A dramatically reduced SHFV entry efficiency, whereas the macropinocytosis inhibitors EIPA, blebbistatin, and wortmannin and the caveolin-mediated endocytosis inhibitors nystatin and filipin III had no effect. Furthermore, overexpression and knockout study and electron microscopy results indicate that SHFV entry occurs by a dynamin-dependent clathrin-mediated endocytosis-like pathway. Experiments utilizing latrunculin B, cytochalasin B, and cytochalasin D indicate that SHFV does not hijack the actin polymerization pathway. Treatment of target cells with proteases (proteinase K, papain, α-chymotrypsin, and trypsin) abrogated entry, indicating that the SHFV cell surface receptor is a protein. Phospholipases A2 and D had no effect on SHFV entry. Finally, treatment of cells with antibodies targeting CD163, a cell surface molecule identified as an entry factor for the SHFV-related porcine reproductive and respiratory syndrome virus, diminished SHFV replication, identifying CD163 as an important SHFV entry component.IMPORTANCESimian hemorrhagic fever virus (SHFV) causes highly lethal disease in Asian macaques resembling human illness caused by Ebola or Lassa virus. However, little is known about SHFV's ecology and molecular biology and the mechanism by which it causes disease. The results of this study shed light on how SHFV enters its target cells. Using electron microscopy and inhibitors for various cellular pathways, we demonstrate that SHFV invades cells by low-pH-dependent, actin-independent endocytosis, likely with the help of a cellular surface protein.

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