scholarly journals Simian Varicella Virus Pathogenesis

2010 ◽  
pp. 309-321 ◽  
Author(s):  
Ravi Mahalingam ◽  
Ilhem Messaoudi ◽  
Don Gilden
Keyword(s):  
Simian Varicella Virus ◽  
Varicella Virus

scholarly journals Intratracheal inoculation of human varicella zoster virus (VZV; MAV strain) vaccine successfully induced VZV IgG antibodies in rhesus monkeys

2021 ◽  
Vol 37 (1) ◽  
Author(s):  
Jong-Min Kim ◽  
Chung-Gyu Park
Keyword(s):  
Rhesus Monkey ◽  
Varicella Zoster Virus ◽  
Humoral Immunity ◽  
Antibody Production ◽  
Rhesus Monkeys ◽  
Igg Antibodies ◽  
Simian Varicella Virus ◽  
Varicella Zoster ◽  
Varicella Virus ◽  
Strain Vaccine

Abstract Background The objective of this study was to investigate whether the use of live attenuated varicella zoster virus (VZV) MAV vaccination can efficiently induce VZV antibody production in naive rhesus monkeys as an approach to prevent simian varicella virus (SVV) reactivation in animals immunosuppressed for transplantation studies. Results Clinically available human VZV vaccine was used to induce the production of anti-VZV antibodies in rhesus monkeys. A vial of the vaccine was subcutaneously injected at 0 week, and the second and third vaccination was performed at 5 and 6 weeks by intratracheal inoculation. The titer of anti-VZV IgG was assessed at 0, 2, 4, 6, and 7 weeks. At 2 weeks, 3/16 were seropositive for VZV IgG. At 6 weeks, 9/16 were shown to be seropositive. At 7 weeks, 16/16 were found to be seropositive. Conclusions The VZV vaccine via intratrachael inoculation was shown to induce VZV IgG humoral immunity in rhesus monkeys and may be important immunosuppressed macaques for transplantation studies. Although the humoral immunity produced is an important finding, further studies will be necessary to confirm possible protection and it could protect probably against SVV infection in rhesus monkey.

scholarly journals Robust pro-inflammatory and lesser anti-inflammatory immune responses during primary simian varicella virus infection and reactivation in rhesus macaques

2014 ◽  
Vol 20 (5) ◽  
pp. 526-530 ◽  
Author(s):  
Vicki Traina-Dorge ◽  
Robert Sanford ◽  
Stephanie James ◽  
Lara A. Doyle-Meyers ◽  
Eileen de Haro ◽  
...  
Keyword(s):  
Virus Infection ◽  
Immune Responses ◽  
Rhesus Macaques ◽  
Simian Varicella Virus ◽  
Varicella Virus ◽  
Anti Inflammatory

Pharmacokinetics and antiviral activity of a novel isonucleoside, BMS-181165, against simian varicella virus infection in African green monkeys

1994 ◽  
Vol 23 (3-4) ◽  
pp. 219-224 ◽  
Author(s):  
K.F. Soike ◽  
J.-L. Huang ◽  
J.W. Russell ◽  
V.J. Whiterock ◽  
J.E. Sundeen ◽  
...  
Keyword(s):  
Virus Infection ◽  
Antiviral Activity ◽  
Simian Varicella Virus ◽  
Varicella Virus ◽  
Green Monkeys

Enhancement of Simian Varicella Virus Infection in African Green Monkeys by Recombinant Human Tumor Necrosis Factor  

1989 ◽  
Vol 159 (2) ◽  
pp. 331-334 ◽  
Author(s):  
K. F. Soike ◽  
C. W. Czarnlecki ◽  
G. Baskin ◽  
J. Blanchard ◽  
D. Liggitt
Keyword(s):  
Tumor Necrosis Factor ◽  
Virus Infection ◽  
Tumor Necrosis ◽  
Human Tumor ◽  
Human Tumor Necrosis Factor ◽  
Simian Varicella Virus ◽  
Varicella Virus ◽  
Necrosis Factor ◽  
Green Monkeys

The genomes of simian varicella virus and varicella zoster virus are colinear

1992 ◽  
Vol 26 (3) ◽  
pp. 255-266 ◽  
Author(s):  
Carla Y. Pumphrey ◽  
Wayne L. Gray
Keyword(s):  
Varicella Zoster Virus ◽  
Simian Varicella Virus ◽  
Varicella Zoster ◽  
Varicella Virus

Investigation of antiviral activity of 1-β-d-arabinofuranosylthymine (ara-T) and 1-β-d-arabinofuranosyl-E-5-(2-bromovinyl)uracil (BV-ara-U) in monkeys infected with simian varicella virus

1984 ◽  
Vol 4 (5) ◽  
pp. 245-257 ◽  
Author(s):  
Kenneth F. Soike ◽  
Gary Baskin ◽  
Connie Cantrell ◽  
Peter Gerone
Keyword(s):  
Antiviral Activity ◽  
Simian Varicella Virus ◽  
Varicella Virus

scholarly journals The ORF61 Protein Encoded by Simian Varicella Virus and Varicella-Zoster Virus Inhibits NF-κB Signaling by Interfering with IκBα Degradation

2015 ◽  
Vol 89 (17) ◽  
pp. 8687-8700 ◽  
Author(s):  
Travis Whitmer ◽  
Daniel Malouli ◽  
Luke S. Uebelhoer ◽  
Victor R. DeFilippis ◽  
Klaus Früh ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Varicella Zoster Virus ◽  
Primary Infection ◽  
Rhesus Macaques ◽  
Innate Immune ◽  
Simian Varicella Virus ◽  
Varicella Zoster ◽  
Varicella Virus

ABSTRACTVaricella-zoster virus (VZV) causes chickenpox upon primary infection and establishes latency in ganglia. Reactivation from latency causes herpes zoster, which may be complicated by postherpetic neuralgia. Innate immunity mediated by interferon and proinflammatory cytokines represents the first line of immune defense upon infection and reactivation. VZV is known to interfere with multiple innate immune signaling pathways, including the central transcription factor NF-κB. However, the role of these inhibitory mechanismsin vivois unknown. Simian varicella virus (SVV) infection of rhesus macaques recapitulates key aspects of VZV pathogenesis, and this model thus permits examination of the role of immune evasion mechanismsin vivo. Here, we compare SVV and VZV with respect to interference with NF-κB activation. We demonstrate that both viruses prevent ubiquitination of the NF-κB inhibitor IκBα, whereas SVV additionally prevents IκBα phosphorylation. We show that the ORF61 proteins of VZV and SVV are sufficient to prevent IκBα ubiquitination upon ectopic expression. We further demonstrate that SVV ORF61 interacts with β-TrCP, a subunit of the SCF ubiquitin ligase complex that mediates the degradation of IκBα. This interaction seems to inactivate SCF-mediated protein degradation in general, since the unrelated β-TrCP target Snail is also stabilized by ORF61. In addition to ORF61, SVV seems to encode additional inhibitors of the NF-κB pathway, since SVV with ORF61 deleted still prevented IκBα phosphorylation and degradation. Taken together, our data demonstrate that SVV interferes with tumor necrosis factor alpha (TNF-α)-induced NF-κB activation at multiple levels, which is consistent with the importance of these countermechanisms for varicella virus infection.IMPORTANCEThe role of innate immunity during the establishment of primary infection, latency, and reactivation by varicella-zoster virus (VZV) is incompletely understood. Since infection of rhesus macaques by simian varicella virus (SVV) is used as an animal model of VZV infection, we characterized the molecular mechanism by which SVV interferes with innate immune activation. Specifically, we studied how SVV prevents activation of the transcription factor NF-κB, a central factor in eliciting proinflammatory responses. The identification of molecular mechanisms that counteract innate immunity might ultimately lead to better vaccines and treatments for VZV, since overcoming these mechanisms, either by small-molecule inhibition or by genetic modification of vaccine strains, is expected to reduce the pathogenic potential of VZV. Moreover, using SVV infection of rhesus macaques, it will be possible to study how increasing the vulnerability of varicella viruses to innate immunity will impact viral pathogenesis.

scholarly journals Simian Varicella Virus Induces Apoptosis in Monkey Kidney Cells by the Intrinsic Pathway and Involves Downregulation of Bcl-2 Expression

2009 ◽  
Vol 83 (18) ◽  
pp. 9273-9282 ◽  
Author(s):  
Subbiah Pugazhenthi ◽  
Donald H. Gilden ◽  
Sreekala Nair ◽  
Anne McAdoo ◽  
Mary Wellish ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Active Form ◽  
Vero Cells ◽  
Monkey Kidney ◽  
Kidney Cells ◽  
Intrinsic Pathway ◽  
Caspase 9 ◽  
Simian Varicella Virus ◽  
Varicella Virus ◽  
Infected Cells

ABSTRACT Simian varicella virus (SVV) causes varicella in primates, becomes latent in ganglionic neurons, and reactivates to produce zoster. SVV produces a cytopathic effect in monkey kidney cells in tissue culture. To study the mechanism by which SVV-infected cells die, we examined markers of apoptosis 24 to 64 h postinfection (hpi). Western blot analysis of virus-infected cell lysates revealed a significant increase in the levels of the cleaved active form of caspase-3, accompanied by a parallel increase in caspase-3 activity at 40 to 64 hpi. Caspase-9, a marker for the intrinsic pathway, was activated significantly in SVV-infected cells at all time points, whereas trace levels of the active form of caspase-8, an extrinsic pathway marker, was detected only at 64 hpi. Bcl-2 expression at the mRNA and protein levels was decreased by 50 to 70% throughout the course of virus infection. Release of cytochrome c, an activator of caspase-9, from mitochondria into the cytoplasm was increased by 200% at 64 hpi. Analysis of Vero cells infected with SVV expressing green fluorescent protein (SVV-GFP) at 64 hpi revealed colocalization of the active forms of caspase-3 and caspase-9 and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) staining with GFP. A significant decrease in the bcl-2 mRNA levels along with an abundance of mRNA specific for SVV genes 63, 40, and 21 was seen in the fraction of Vero cells that were infected with SVV-GFP. Together, these findings indicate that SVV induces apoptosis in cultured Vero cells through the intrinsic pathway in which Bcl-2 is downregulated.

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