scholarly journals Histopathological Analysis of Adrenal Glands after Simian Varicella Virus Infection

Viruses ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1245
Author(s):  
Christy S. Niemeyer ◽  
Teresa Mescher ◽  
Rocio Griggs ◽  
David J. Orlicky ◽  
Gregory K. Wilkerson ◽  
...  
Keyword(s):  
Adrenal Glands ◽  
Immunohistochemical Analysis ◽  
Nerve Fibers ◽  
Histopathological Analysis ◽  
Polymorphonuclear Cells ◽  
Simian Varicella Virus ◽  
Varicella Zoster ◽  
Varicella Virus ◽  
Bilateral Adrenal Hemorrhage ◽  
Specific Association

Latent varicella zoster virus (VZV) has been detected in human adrenal glands, raising the possibility of virus-induced adrenal damage and dysfunction during primary infection or reactivation. Rare cases of bilateral adrenal hemorrhage and insufficiency associated with VZV reactivation have been reported. Since there is no animal model for VZV infection of adrenal glands, we obtained adrenal glands from two non-human primates (NHPs) that spontaneously developed varicella from primary simian varicella virus (SVV) infection, the NHP VZV homolog. Histological and immunohistochemical analysis revealed SVV antigen and DNA in the adrenal medulla and cortex of both animals. Adrenal glands were observed to have Cowdry A inclusion bodies, cellular necrosis, multiple areas of hemorrhage, and varying amounts of polymorphonuclear cells. No specific association of SVV antigen with βIII-tubulin-positive nerve fibers was found. Overall, we found that SVV can productively infect NHP adrenal glands, and is associated with inflammation, hemorrhage, and cell death. These findings suggest that further studies are warranted to examine the contribution of VZV infection to human adrenal disease. This study also suggests that VZV infection may present itself as acute adrenal dysfunction with “long-hauler” symptoms of fatigue, weakness, myalgias/arthralgias, and hypotension.

scholarly journals Viral gene expression during acute simian varicella virus infection

2002 ◽  
Vol 83 (4) ◽  
pp. 841-846 ◽  
Author(s):  
Wayne L. Gray ◽  
Lisa Mullis ◽  
Kenneth F. Soike
Keyword(s):  
Gene Expression ◽  
Viral Antigen ◽  
Immunohistochemical Analysis ◽  
Antigen Expression ◽  
Pcr Analysis ◽  
Viral Gene ◽  
Vervet Monkeys ◽  
Simian Varicella Virus ◽  
Varicella Zoster ◽  
Varicella Virus

Simian varicella virus (SVV) causes a natural varicella-like disease in nonhuman primates. Outbreaks of simian varicella occur sporadically in primate facilities. Simian varicella is used as a model for investigation of varicella-zoster virus (VZV) pathogenesis and latency. In this study, SVV gene expression and histopathology were analysed in tissues of acutely infected vervet monkeys. RT–PCR analysis demonstrated expression of specific SVV immediate early, early and late genes in the skin, lung, liver and ganglia tissues of acutely infected monkeys. Viral antigen expression and histopathology, including necrosis and inflammation, were detected in the skin, lungs, liver and spleen of infected monkeys by immunohistochemical analysis. Viral antigen expression, but little or no histopathology, was evident in the neural ganglia, the eventual site of viral latency. The study provides a foundation for further investigation on the role of viral genes in varicella pathogenesis and latency.

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.

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

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.

Immunization of monkeys with varicella-zoster virus glycoprotein antigens and their response to challenge with simian varicella virus

1987 ◽  
Vol 22 (4) ◽  
pp. 307-313 ◽  
Author(s):  
Kenneth F. Soike ◽  
Paul M. Keller ◽  
Ronald W. Ellis
Keyword(s):  
Varicella Zoster Virus ◽  
Simian Varicella Virus ◽  
Varicella Zoster ◽  
Virus Glycoprotein ◽  
Varicella Virus

scholarly journals Naturally Acquired Simian Varicella Virus Infection in African Green Monkeys

2002 ◽  
Vol 76 (17) ◽  
pp. 8548-8550 ◽  
Author(s):  
Ravi Mahalingam ◽  
Vicki Traina-Dorge ◽  
Mary Wellish ◽  
John Smith ◽  
Donald H. Gilden
Keyword(s):  
Virus Infection ◽  
Dna Analysis ◽  
Experimental System ◽  
Varicella Zoster Virus Infection ◽  
Varicella Infection ◽  
Simian Varicella Virus ◽  
Varicella Zoster ◽  
Varicella Virus ◽  
Dna And Rna ◽  
Multiple Levels

ABSTRACT Simian varicella virus (SVV) infection of primates shares clinical, pathological, immunological, and virological features with varicella-zoster virus infection of humans. Natural varicella infection was simulated by exposing four SVV-seronegative monkeys to monkeys inoculated intratracheally with SVV, in which viral DNA and RNA persist in multiple tissues for more than 1 year (T. M. White, R. Mahalingam, V. Traina-Dorge, and D. H. Gilden, J. Neurovirol. 8:191-205, 2002). The four naturally exposed monkeys developed mild varicella 10 to 14 days later, and skin scrapings taken at the time of the rash contained SVV DNA. Analysis of multiple ganglia, liver, and lung tissues from the four naturally exposed monkeys sacrificed 6 to 8 weeks after resolution of the rash revealed SVV DNA in ganglia at multiple levels of the neuraxis but not in the lung or liver tissue of any of the four monkeys. This animal model provides an experimental system to gain information about varicella latency with direct relevance to the human disease.

scholarly journals Simian Varicella Virus Infection of Rhesus Macaques Recapitulates Essential Features of Varicella Zoster Virus Infection in Humans

2009 ◽  
Vol 5 (11) ◽  
pp. e1000657 ◽  
Author(s):  
Ilhem Messaoudi ◽  
Alexander Barron ◽  
Mary Wellish ◽  
Flora Engelmann ◽  
Alfred Legasse ◽  
...  
Keyword(s):  
Virus Infection ◽  
Varicella Zoster Virus ◽  
Rhesus Macaques ◽  
Varicella Zoster Virus Infection ◽  
Simian Varicella Virus ◽  
Varicella Zoster ◽  
Varicella Virus
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