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Prof. Reed Johnson
National Institute of Allergy and Infectious Diseases, Bethesda, United States

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0 Pathogenesis
0 Host response
0 SHFV
0 Simarterivirus
0 Simian hemorrhagic fever

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Pathogenesis
SHFV
Simian hemorrhagic fever
Viral hemorrhagic fever
Host response
Simarterivirus

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Journal article
Published: 09 August 2021 in Viruses
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Hemorrhagic smallpox, caused by variola virus (VARV), was a rare but nearly 100% lethal human disease manifestation. Hemorrhagic smallpox is frequently characterized by secondary bacterial infection, coagulopathy, and myocardial and subendocardial hemorrhages. Previous experiments have demonstrated that intravenous (IV) cowpox virus (CPXV) exposure of macaques mimics human hemorrhagic smallpox. The goal of this experiment was to further understand the onset, nature, and severity of cardiac pathology and how it may contribute to disease. The findings support an acute late-stage myocarditis with lymphohistiocytic infiltrates in the CPXV model of hemorrhagic smallpox.

ACS Style

Reed Johnson; Lauren Keith; Timothy Cooper; Srikanth Yellayi; Nicole Josleyn; Krisztina Janosko; James Pettitt; David Thomasson; Katie Hagen; Robin Gross; John Bernbaum; Debbie Douglas; Jeffrey Solomon; Mark Martinez; Kurt Cooper; Marisa St. Claire; Danny Ragland; Peter Jahrling; Jens Kuhn; Andrew Arai. Acute Late-Stage Myocarditis in the Crab-Eating Macaque Model of Hemorrhagic Smallpox. Viruses 2021, 13, 1571 .

AMA Style

Reed Johnson, Lauren Keith, Timothy Cooper, Srikanth Yellayi, Nicole Josleyn, Krisztina Janosko, James Pettitt, David Thomasson, Katie Hagen, Robin Gross, John Bernbaum, Debbie Douglas, Jeffrey Solomon, Mark Martinez, Kurt Cooper, Marisa St. Claire, Danny Ragland, Peter Jahrling, Jens Kuhn, Andrew Arai. Acute Late-Stage Myocarditis in the Crab-Eating Macaque Model of Hemorrhagic Smallpox. Viruses. 2021; 13 (8):1571.

Chicago/Turabian Style

Reed Johnson; Lauren Keith; Timothy Cooper; Srikanth Yellayi; Nicole Josleyn; Krisztina Janosko; James Pettitt; David Thomasson; Katie Hagen; Robin Gross; John Bernbaum; Debbie Douglas; Jeffrey Solomon; Mark Martinez; Kurt Cooper; Marisa St. Claire; Danny Ragland; Peter Jahrling; Jens Kuhn; Andrew Arai. 2021. "Acute Late-Stage Myocarditis in the Crab-Eating Macaque Model of Hemorrhagic Smallpox." Viruses 13, no. 8: 1571.

Journal article
Published: 07 April 2021 in Viruses
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Simian hemorrhagic fever virus (SHFV) causes acute, lethal disease in macaques. We developed a single-plasmid cDNA-launch infectious clone of SHFV (rSHFV) and modified the clone to rescue an enhanced green fluorescent protein-expressing rSHFV-eGFP that can be used for rapid and quantitative detection of infection. SHFV has a narrow cell tropism in vitro, with only the grivet MA-104 cell line and a few other grivet cell lines being susceptible to virion entry and permissive to infection. Using rSHFV-eGFP, we demonstrate that one cricetid rodent cell line and three ape cell lines also fully support SHFV replication, whereas 55 human cell lines, 11 bat cell lines, and three rodent cells do not. Interestingly, some human and other mammalian cell lines apparently resistant to SHFV infection are permissive after transfection with the rSHFV-eGFP cDNA-launch plasmid. To further demonstrate the investigative potential of the infectious clone system, we introduced stop codons into eight viral open reading frames (ORFs). This approach suggested that at least one ORF, ORF 2b’, is dispensable for SHFV in vitro replication. Our proof-of-principle experiments indicated that rSHFV-eGFP is a useful tool for illuminating the understudied molecular biology of SHFV.

ACS Style

Yingyun Cai; Shuiqing Yu; Ying Fang; Laura Bollinger; Yanhua Li; Michael Lauck; Elena Postnikova; Steven Mazur; Reed Johnson; Courtney Finch; Sheli Radoshitzky; Gustavo Palacios; Thomas Friedrich; Tony Goldberg; David O’Connor; Peter Jahrling; Jens Kuhn. Development and Characterization of a cDNA-Launch Recombinant Simian Hemorrhagic Fever Virus Expressing Enhanced Green Fluorescent Protein: ORF 2b’ Is Not Required for In Vitro Virus Replication. Viruses 2021, 13, 632 .

AMA Style

Yingyun Cai, Shuiqing Yu, Ying Fang, Laura Bollinger, Yanhua Li, Michael Lauck, Elena Postnikova, Steven Mazur, Reed Johnson, Courtney Finch, Sheli Radoshitzky, Gustavo Palacios, Thomas Friedrich, Tony Goldberg, David O’Connor, Peter Jahrling, Jens Kuhn. Development and Characterization of a cDNA-Launch Recombinant Simian Hemorrhagic Fever Virus Expressing Enhanced Green Fluorescent Protein: ORF 2b’ Is Not Required for In Vitro Virus Replication. Viruses. 2021; 13 (4):632.

Chicago/Turabian Style

Yingyun Cai; Shuiqing Yu; Ying Fang; Laura Bollinger; Yanhua Li; Michael Lauck; Elena Postnikova; Steven Mazur; Reed Johnson; Courtney Finch; Sheli Radoshitzky; Gustavo Palacios; Thomas Friedrich; Tony Goldberg; David O’Connor; Peter Jahrling; Jens Kuhn. 2021. "Development and Characterization of a cDNA-Launch Recombinant Simian Hemorrhagic Fever Virus Expressing Enhanced Green Fluorescent Protein: ORF 2b’ Is Not Required for In Vitro Virus Replication." Viruses 13, no. 4: 632.

Preprint content
Published: 14 May 2020
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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is causing an exponentially increasing number of coronavirus disease 19 (COVID-19) cases globally. Prioritization of medical countermeasures for evaluation in randomized clinical trials is critically hindered by the lack of COVID-19 animal models that enable accurate, quantifiable, and reproducible measurement of COVID-19 pulmonary disease free from observer bias. We first used serial computed tomography (CT) to demonstrate that bilateral intrabronchial instillation of SARS-CoV-2 into crab-eating macaques (Macaca fascicularis) results in mild-to-moderate lung abnormalities qualitatively characteristic of subclinical or mild-to-moderate COVID-19 (e.g., ground-glass opacities with or without reticulation, paving, or alveolar consolidation, peri-bronchial thickening, linear opacities) at typical locations (peripheral>central, posterior and dependent, bilateral, multi-lobar). We then used positron emission tomography (PET) analysis to demonstrate increased FDG uptake in the CT-defined lung abnormalities and regional lymph nodes. PET/CT imaging findings appeared in all macaques as early as 2 days post-exposure, variably progressed, and subsequently resolved by 6–12 days post-exposure. Finally, we applied operator-independent, semi-automatic quantification of the volume and radiodensity of CT abnormalities as a possible primary endpoint for immediate and objective efficacy testing of candidate medical countermeasures.

ACS Style

Courtney L. Finch; Ian Crozier; Ji Hyun Lee; Russ Byrum; Timothy K. Cooper; Janie Liang; Kaleb Sharer; Jeffrey Solomon; Philip J. Sayre; Gregory Kocher; Christopher Bartos; Nina M. Aiosa; Marcelo Castro; Peter A. Larson; Ricky Adams; Brett Beitzel; Nicholas Di Paola; Jeffrey R. Kugelman; Jonathan R. Kurtz; Tracey Burdette; Martha C. Nason; Irwin M. Feuerstein; Gustavo Palacios; Marisa C. St. Claire; Matthew G. Lackemeyer; Reed F. Johnson; Katarina M. Braun; Mitchell D. Ramuta; Jiro Wada; Connie S. Schmaljohn; Thomas C. Friedrich; David H. O’Connor; Jens H. Kuhn. Characteristic and quantifiable COVID-19-like abnormalities in CT- and PET/CT-imaged lungs of SARS-CoV-2-infected crab-eating macaques (Macaca fascicularis). 2020, 1 .

AMA Style

Courtney L. Finch, Ian Crozier, Ji Hyun Lee, Russ Byrum, Timothy K. Cooper, Janie Liang, Kaleb Sharer, Jeffrey Solomon, Philip J. Sayre, Gregory Kocher, Christopher Bartos, Nina M. Aiosa, Marcelo Castro, Peter A. Larson, Ricky Adams, Brett Beitzel, Nicholas Di Paola, Jeffrey R. Kugelman, Jonathan R. Kurtz, Tracey Burdette, Martha C. Nason, Irwin M. Feuerstein, Gustavo Palacios, Marisa C. St. Claire, Matthew G. Lackemeyer, Reed F. Johnson, Katarina M. Braun, Mitchell D. Ramuta, Jiro Wada, Connie S. Schmaljohn, Thomas C. Friedrich, David H. O’Connor, Jens H. Kuhn. Characteristic and quantifiable COVID-19-like abnormalities in CT- and PET/CT-imaged lungs of SARS-CoV-2-infected crab-eating macaques (Macaca fascicularis). . 2020; ():1.

Chicago/Turabian Style

Courtney L. Finch; Ian Crozier; Ji Hyun Lee; Russ Byrum; Timothy K. Cooper; Janie Liang; Kaleb Sharer; Jeffrey Solomon; Philip J. Sayre; Gregory Kocher; Christopher Bartos; Nina M. Aiosa; Marcelo Castro; Peter A. Larson; Ricky Adams; Brett Beitzel; Nicholas Di Paola; Jeffrey R. Kugelman; Jonathan R. Kurtz; Tracey Burdette; Martha C. Nason; Irwin M. Feuerstein; Gustavo Palacios; Marisa C. St. Claire; Matthew G. Lackemeyer; Reed F. Johnson; Katarina M. Braun; Mitchell D. Ramuta; Jiro Wada; Connie S. Schmaljohn; Thomas C. Friedrich; David H. O’Connor; Jens H. Kuhn. 2020. "Characteristic and quantifiable COVID-19-like abnormalities in CT- and PET/CT-imaged lungs of SARS-CoV-2-infected crab-eating macaques (Macaca fascicularis)." , no. : 1.

Comparative study
Published: 15 January 2019 in Viruses
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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.

ACS Style

Joseph P. Cornish; Ian N. Moore; Donna L. Perry; Abigail Lara; Mahnaz Minai; Dominique Promeneur; Katie R. Hagen; Kimmo Virtaneva; Monica Paneru; Connor R. Buechler; David H. O’Connor; Adam L. Bailey; Kurt Cooper; Steven Mazur; John G. Bernbaum; James Pettitt; Peter B. Jahrling; Jens H. Kuhn; Reed F. Johnson. 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, 11, 67 .

AMA Style

Joseph P. Cornish, Ian N. Moore, Donna L. Perry, Abigail Lara, Mahnaz Minai, Dominique Promeneur, Katie R. Hagen, Kimmo Virtaneva, Monica Paneru, Connor R. Buechler, David H. O’Connor, Adam L. Bailey, Kurt Cooper, Steven Mazur, John G. Bernbaum, James Pettitt, Peter B. Jahrling, Jens H. Kuhn, Reed F. Johnson. 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; 11 (1):67.

Chicago/Turabian Style

Joseph P. Cornish; Ian N. Moore; Donna L. Perry; Abigail Lara; Mahnaz Minai; Dominique Promeneur; Katie R. Hagen; Kimmo Virtaneva; Monica Paneru; Connor R. Buechler; David H. O’Connor; Adam L. Bailey; Kurt Cooper; Steven Mazur; John G. Bernbaum; James Pettitt; Peter B. Jahrling; Jens H. Kuhn; Reed F. Johnson. 2019. "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 11, no. 1: 67.

Journal article
Published: 26 December 2018 in mSphere
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Advanced medical imaging such as single photon emission computed tomography with computed tomography (SPECT/CT) enhances fields such as oncology and cardiology. Application of SPECT/CT, magnetic resonance imaging, and positron emission tomography to infectious disease may enhance pathogenesis studies and provide alternate biomarkers of disease progression. The experiments described in this article focus on insertion of a SPECT/CT-compatible reporter gene into MERS-CoV to demonstrate that a functional SPECT/CT reporter gene can be inserted into a virus.

ACS Style

Svetlana Chefer; Jurgen Seidel; Adam S. Cockrell; Boyd Yount; Jeffrey Solomon; Katie R. Hagen; David X. Liu; Louis M. Huzella; Mia R. Kumar; Elena Postnikova; J. Kyle Bohannon; Matthew G. Lackemeyer; Kurt Cooper; Ariel Endlich-Frazier; Heema Sharma; David Thomasson; Christopher Bartos; Philip J. Sayre; Amy Sims; Julie Dyall; Michael R. Holbrook; Peter B. Jahrling; Ralph S. Baric; Reed F. Johnson. The Human Sodium Iodide Symporter as a Reporter Gene for Studying Middle East Respiratory Syndrome Coronavirus Pathogenesis. mSphere 2018, 3, e00540-18 .

AMA Style

Svetlana Chefer, Jurgen Seidel, Adam S. Cockrell, Boyd Yount, Jeffrey Solomon, Katie R. Hagen, David X. Liu, Louis M. Huzella, Mia R. Kumar, Elena Postnikova, J. Kyle Bohannon, Matthew G. Lackemeyer, Kurt Cooper, Ariel Endlich-Frazier, Heema Sharma, David Thomasson, Christopher Bartos, Philip J. Sayre, Amy Sims, Julie Dyall, Michael R. Holbrook, Peter B. Jahrling, Ralph S. Baric, Reed F. Johnson. The Human Sodium Iodide Symporter as a Reporter Gene for Studying Middle East Respiratory Syndrome Coronavirus Pathogenesis. mSphere. 2018; 3 (6):e00540-18.

Chicago/Turabian Style

Svetlana Chefer; Jurgen Seidel; Adam S. Cockrell; Boyd Yount; Jeffrey Solomon; Katie R. Hagen; David X. Liu; Louis M. Huzella; Mia R. Kumar; Elena Postnikova; J. Kyle Bohannon; Matthew G. Lackemeyer; Kurt Cooper; Ariel Endlich-Frazier; Heema Sharma; David Thomasson; Christopher Bartos; Philip J. Sayre; Amy Sims; Julie Dyall; Michael R. Holbrook; Peter B. Jahrling; Ralph S. Baric; Reed F. Johnson. 2018. "The Human Sodium Iodide Symporter as a Reporter Gene for Studying Middle East Respiratory Syndrome Coronavirus Pathogenesis." mSphere 3, no. 6: e00540-18.

Journal article
Published: 10 December 2018 in Viruses
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Simarteriviruses (Arteriviridae: Simarterivirinae) are commonly found at high titers in the blood of African monkeys but do not cause overt disease in these hosts. In contrast, simarteriviruses cause severe disease in Asian macaques upon accidental or experimental transmission. Here, we sought to better understand the host-dependent drivers of simarterivirus pathogenesis by infecting olive baboons (n = 4) and rhesus monkeys (n = 4) with the simarterivirus Southwest baboon virus 1 (SWBV-1). Surprisingly, none of the animals in our study showed signs of disease following SWBV-1 inoculation. Three animals (two rhesus monkeys and one olive baboon) became infected and sustained high levels of SWBV-1 viremia for the duration of the study. The course of SWBV-1 infection was highly predictable: plasma viremia peaked between 1 × 107 and 1 × 108 vRNA copies/mL at 3–10 days post-inoculation, which was followed by a relative nadir and then establishment of a stable set-point between 1 × 106 and 1 × 107 vRNA copies/mL for the remainder of the study (56 days). We characterized cellular and antibody responses to SWBV-1 infection in these animals, demonstrating that macaques and baboons mount similar responses to SWBV-1 infection, yet these responses are ineffective at clearing SWBV-1 infection. SWBV-1 sequencing revealed the accumulation of non-synonymous mutations in a region of the genome that corresponds to an immunodominant epitope in the simarterivirus major envelope glycoprotein GP5, which likely contribute to viral persistence by enabling escape from host antibodies.

ACS Style

Connor R. Buechler; Matthew Semler; David A. Baker; Christina Newman; Joseph P. Cornish; Deborah Chavez; Bernadette Guerra; Robert Lanford; Kathy Brasky; Jens H. Kuhn; Reed F. Johnson; David H. O’Connor; Adam L. Bailey. Subclinical Infection of Macaques and Baboons with A Baboon Simarterivirus. Viruses 2018, 10, 701 .

AMA Style

Connor R. Buechler, Matthew Semler, David A. Baker, Christina Newman, Joseph P. Cornish, Deborah Chavez, Bernadette Guerra, Robert Lanford, Kathy Brasky, Jens H. Kuhn, Reed F. Johnson, David H. O’Connor, Adam L. Bailey. Subclinical Infection of Macaques and Baboons with A Baboon Simarterivirus. Viruses. 2018; 10 (12):701.

Chicago/Turabian Style

Connor R. Buechler; Matthew Semler; David A. Baker; Christina Newman; Joseph P. Cornish; Deborah Chavez; Bernadette Guerra; Robert Lanford; Kathy Brasky; Jens H. Kuhn; Reed F. Johnson; David H. O’Connor; Adam L. Bailey. 2018. "Subclinical Infection of Macaques and Baboons with A Baboon Simarterivirus." Viruses 10, no. 12: 701.

Journal article
Published: 05 December 2018 in Journal of Infectious Diseases
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Lassa fever (LF) survivors develop various clinical manifestations including polyserositis, myalgia, epididymitis, and hearing loss weeks to months after recovery from acute infection. We demonstrate a systemic lymphoplasmacytic and histiocytic arteritis and periarteritis in guinea pigs more than 2 months after recovery from acute Lassa virus (LASV) infection. LASV was detected in the arterial tunica media smooth muscle cells by immunohistochemistry, in situ hybridization, and transmission electron microscopy. Our results suggest that the sequelae of LASV infection may be due to virus persistence resulting in systemic vascular damage. These findings shed light on the pathogenesis of LASV sequelae in convalescent human survivors.

ACS Style

David X Liu; Donna L Perry; Lisa Evans Dewald; Yingyun Cai; Katie R Hagen; Timothy K Cooper; Louis M Huzella; Randy Hart; Amanda Bonilla; John G Bernbaum; Krisztina B Janosko; Ricky Adams; Reed F Johnson; Jens H Kuhn; Matthias Schnell; Ian Crozier; Peter B Jahrling; Juan C De La Torre. Persistence of Lassa Virus Associated With Severe Systemic Arteritis in Convalescing Guinea Pigs (Cavia porcellus). Journal of Infectious Diseases 2018, 219, 1818 -1822.

AMA Style

David X Liu, Donna L Perry, Lisa Evans Dewald, Yingyun Cai, Katie R Hagen, Timothy K Cooper, Louis M Huzella, Randy Hart, Amanda Bonilla, John G Bernbaum, Krisztina B Janosko, Ricky Adams, Reed F Johnson, Jens H Kuhn, Matthias Schnell, Ian Crozier, Peter B Jahrling, Juan C De La Torre. Persistence of Lassa Virus Associated With Severe Systemic Arteritis in Convalescing Guinea Pigs (Cavia porcellus). Journal of Infectious Diseases. 2018; 219 (11):1818-1822.

Chicago/Turabian Style

David X Liu; Donna L Perry; Lisa Evans Dewald; Yingyun Cai; Katie R Hagen; Timothy K Cooper; Louis M Huzella; Randy Hart; Amanda Bonilla; John G Bernbaum; Krisztina B Janosko; Ricky Adams; Reed F Johnson; Jens H Kuhn; Matthias Schnell; Ian Crozier; Peter B Jahrling; Juan C De La Torre. 2018. "Persistence of Lassa Virus Associated With Severe Systemic Arteritis in Convalescing Guinea Pigs (Cavia porcellus)." Journal of Infectious Diseases 219, no. 11: 1818-1822.

Preprint
Published: 31 October 2018
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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. 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.

ACS Style

Joseph P. Cornish; Ian N. Moore; Donna L. Perry; Abigail Lara; Mahnaz Minai; Dominique Promeneur; Katie R. Hagen; Kimmo Virtaneva; Monica Paneru; Connor Buechler; David H. O’Connor; Adam L. Bailey; Kurt Cooper; Steven Mazur; John G. Bernbaum; James Pettitt; Peter B. Jahrling; Jens H. Kuhn; Reed F. Johnson; Katie R Hagan. 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, 454462 .

AMA Style

Joseph P. Cornish, Ian N. Moore, Donna L. Perry, Abigail Lara, Mahnaz Minai, Dominique Promeneur, Katie R. Hagen, Kimmo Virtaneva, Monica Paneru, Connor Buechler, David H. O’Connor, Adam L. Bailey, Kurt Cooper, Steven Mazur, John G. Bernbaum, James Pettitt, Peter B. Jahrling, Jens H. Kuhn, Reed F. Johnson, Katie R Hagan. 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; ():454462.

Chicago/Turabian Style

Joseph P. Cornish; Ian N. Moore; Donna L. Perry; Abigail Lara; Mahnaz Minai; Dominique Promeneur; Katie R. Hagen; Kimmo Virtaneva; Monica Paneru; Connor Buechler; David H. O’Connor; Adam L. Bailey; Kurt Cooper; Steven Mazur; John G. Bernbaum; James Pettitt; Peter B. Jahrling; Jens H. Kuhn; Reed F. Johnson; Katie R Hagan. 2018. "Clinical Characterization of Host Response to Simian Hemorrhagic Fever Virus Infection in Permissive and Refractory Hosts: A Model for Determining Mechanisms of VHF Pathogenesis." , no. : 454462.

Journal article
Published: 04 July 2018 in The Journal of Infectious Diseases
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ACS Style

Lisa Evans Dewald; Julie Dyall; Jennifer M Sword; Lisa Torzewski; Huanying Zhou; Elena Postnikova; Erin Kollins; Isis Alexander; Robin Gross; Yu Cong; Dawn M Gerhardt; Reed F Johnson; Gene G Olinger; Michael R Holbrook; Lisa E Hensley; Peter B Jahrling. The Calcium Channel Blocker Bepridil Demonstrates Efficacy in the Murine Model of Marburg Virus Disease. The Journal of Infectious Diseases 2018, 218, S588 -S591.

AMA Style

Lisa Evans Dewald, Julie Dyall, Jennifer M Sword, Lisa Torzewski, Huanying Zhou, Elena Postnikova, Erin Kollins, Isis Alexander, Robin Gross, Yu Cong, Dawn M Gerhardt, Reed F Johnson, Gene G Olinger, Michael R Holbrook, Lisa E Hensley, Peter B Jahrling. The Calcium Channel Blocker Bepridil Demonstrates Efficacy in the Murine Model of Marburg Virus Disease. The Journal of Infectious Diseases. 2018; 218 (suppl_5):S588-S591.

Chicago/Turabian Style

Lisa Evans Dewald; Julie Dyall; Jennifer M Sword; Lisa Torzewski; Huanying Zhou; Elena Postnikova; Erin Kollins; Isis Alexander; Robin Gross; Yu Cong; Dawn M Gerhardt; Reed F Johnson; Gene G Olinger; Michael R Holbrook; Lisa E Hensley; Peter B Jahrling. 2018. "The Calcium Channel Blocker Bepridil Demonstrates Efficacy in the Murine Model of Marburg Virus Disease." The Journal of Infectious Diseases 218, no. suppl_5: S588-S591.

Journal article
Published: 08 February 2018 in The American Journal of Pathology
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Sexual transmission of Ebola virus (EBOV) has been demonstrated more than a year after recovery from the acute phase of Ebola virus disease (EVD). The mechanisms underlying EBOV persistence and sexual transmission are not currently understood. Using the acute macaque model of EVD, we hypothesized EBOV would infect the reproductive tissues and sought to localize the infection in these tissues using immunohistochemistry and transmission electron microscopy. In four female and eight male macaques that succumbed to EVD between 6 and 9 days after EBOV challenge, we demonstrate widespread EBOV infection of the interstitial tissues and endothelium in the ovary, uterus, testis, seminal vesicle, epididymis, and prostate gland, with minimal associated tissue immune response or organ pathology. Given the widespread involvement of EBOV in the reproductive tracts of both male and female macaques, it is reasonable to surmise that our understanding of the mechanisms underlying sexual transmission of EVD and persistence of EBOV in immune-privileged sites would be facilitated by the development of a nonhuman primate model in which the macaques survived past the acute stage into convalescence.

ACS Style

Donna L. Perry; Louis M. Huzella; John G. Bernbaum; Michael R. Holbrook; Peter B. Jahrling; Katie R. Hagen; Matthias J. Schnell; Reed F. Johnson. Ebola Virus Localization in the Macaque Reproductive Tract during Acute Ebola Virus Disease. The American Journal of Pathology 2018, 188, 550 -558.

AMA Style

Donna L. Perry, Louis M. Huzella, John G. Bernbaum, Michael R. Holbrook, Peter B. Jahrling, Katie R. Hagen, Matthias J. Schnell, Reed F. Johnson. Ebola Virus Localization in the Macaque Reproductive Tract during Acute Ebola Virus Disease. The American Journal of Pathology. 2018; 188 (3):550-558.

Chicago/Turabian Style

Donna L. Perry; Louis M. Huzella; John G. Bernbaum; Michael R. Holbrook; Peter B. Jahrling; Katie R. Hagen; Matthias J. Schnell; Reed F. Johnson. 2018. "Ebola Virus Localization in the Macaque Reproductive Tract during Acute Ebola Virus Disease." The American Journal of Pathology 188, no. 3: 550-558.

Journal article
Published: 12 January 2017 in Genome Announcements
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Reston virus (RESTV) was discovered in 1989–1990 during three connected epizootics of highly lethal viral hemorrhagic fever among captive macaques in primate housing facilities in the United States and Philippines. Currently, only one RESTV isolate from that outbreak (named Pennsylvania) has been sequenced. Here, we report the sequence of a second isolate, Reston virus/M.fascicularis-tc/USA/1990/Philippines89-AZ1435.

ACS Style

Joseph P. Cornish; Larissa Diaz; Stacy M. Ricklefs; Kishore Kanakabandi; Jennifer Sword; Peter B. Jahrling; Jens H. Kuhn; Stephen F. Porcella; Reed F. Johnson. Sequence of Reston Virus Isolate AZ-1435, an Ebolavirus Isolate Obtained during the 1989–1990 Reston Virus Epizootic in the United States. Genome Announcements 2017, 5, e01448-16 .

AMA Style

Joseph P. Cornish, Larissa Diaz, Stacy M. Ricklefs, Kishore Kanakabandi, Jennifer Sword, Peter B. Jahrling, Jens H. Kuhn, Stephen F. Porcella, Reed F. Johnson. Sequence of Reston Virus Isolate AZ-1435, an Ebolavirus Isolate Obtained during the 1989–1990 Reston Virus Epizootic in the United States. Genome Announcements. 2017; 5 (2):e01448-16.

Chicago/Turabian Style

Joseph P. Cornish; Larissa Diaz; Stacy M. Ricklefs; Kishore Kanakabandi; Jennifer Sword; Peter B. Jahrling; Jens H. Kuhn; Stephen F. Porcella; Reed F. Johnson. 2017. "Sequence of Reston Virus Isolate AZ-1435, an Ebolavirus Isolate Obtained during the 1989–1990 Reston Virus Epizootic in the United States." Genome Announcements 5, no. 2: e01448-16.

Journal article
Published: 19 September 2016 in Nucleic Acids Research
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Ebola virus (EBOV) is a single-stranded negative-sense RNA virus belonging to the Filoviridae family. The leader and trailer non-coding regions of the EBOV genome likely regulate its transcription, replication, and progeny genome packaging. We investigated the cis-acting RNA signals involved in RNA–RNA and RNA–protein interactions that regulate replication of eGFP-encoding EBOV minigenomic RNA and identified heat shock cognate protein family A (HSC70) member 8 (HSPA8) as an EBOV trailer-interacting host protein. Mutational analysis of the trailer HSPA8 binding motif revealed that this interaction is essential for EBOV minigenome replication. Selective 2΄-hydroxyl acylation analyzed by primer extension analysis of the secondary structure of the EBOV minigenomic RNA indicates formation of a small stem-loop composed of the HSPA8 motif, a 3΄ stem-loop (nucleotides 1868–1890) that is similar to a previously identified structure in the replicative intermediate (RI) RNA and a panhandle domain involving a trailer-to-leader interaction. Results of minigenome assays and an EBOV reverse genetic system rescue support a role for both the panhandle domain and HSPA8 motif 1 in virus replication.

ACS Style

Joanna Sztuba-Solinska; Larissa Diaz; Mia R. Kumar; Gaëlle Kolb; Michael Wiley; Lucas Jozwick; Jens H. Kuhn; Gustavo Palacios; Sheli R. Radoshitzky; Stuart F. J. Le Grice; Reed F. Johnson. A small stem-loop structure of the Ebola virus trailer is essential for replication and interacts with heat-shock protein A8. Nucleic Acids Research 2016, 44, 9831 -9846.

AMA Style

Joanna Sztuba-Solinska, Larissa Diaz, Mia R. Kumar, Gaëlle Kolb, Michael Wiley, Lucas Jozwick, Jens H. Kuhn, Gustavo Palacios, Sheli R. Radoshitzky, Stuart F. J. Le Grice, Reed F. Johnson. A small stem-loop structure of the Ebola virus trailer is essential for replication and interacts with heat-shock protein A8. Nucleic Acids Research. 2016; 44 (20):9831-9846.

Chicago/Turabian Style

Joanna Sztuba-Solinska; Larissa Diaz; Mia R. Kumar; Gaëlle Kolb; Michael Wiley; Lucas Jozwick; Jens H. Kuhn; Gustavo Palacios; Sheli R. Radoshitzky; Stuart F. J. Le Grice; Reed F. Johnson. 2016. "A small stem-loop structure of the Ebola virus trailer is essential for replication and interacts with heat-shock protein A8." Nucleic Acids Research 44, no. 20: 9831-9846.

Journal article
Published: 01 August 2016 in Journal of General Virology
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We previously demonstrated that small-particle (0.5-3.0 µm) aerosol infection of rhesus monkeys (Macaca mulatta) with cowpox virus (CPXV)-Brighton Red (BR) results in fulminant respiratory tract disease characterized by severe lung parenchymal pathology but only limited systemic virus dissemination and limited classic epidermal pox-like lesion development (Johnson et al., 2015). Based on these results, and to further develop CPXV as an improved model of human smallpox, we evaluated a novel large-particle aerosol (7.0-9.0 µm) exposure of rhesus monkeys to CPXV-BR and monitored for respiratory tract disease by serial computed tomography (CT). As expected, the upper respiratory tract and large airways were the major sites of virus-induced pathology following large-particle aerosol exposure. Large-particle aerosol CPXV exposure of rhesus macaques resulted in severe upper airway and large airway pathology with limited systemic dissemination.

ACS Style

Reed F. Johnson; Dima A. Hammoud; Donna L. Perry; Jeffrey Solomon; Ian N. Moore; Matthew G. Lackemeyer; Jordan K. Bohannon; Philip J. Sayre; Mahnaz Minai; Amy B. Papaneri; Katie R. Hagen; Krisztina B. Janosko; Catherine Jett; Kurt Cooper; Joseph E. Blaney; Peter B. Jahrling. Exposure of rhesus monkeys to cowpox virus Brighton Red by large-particle aerosol droplets results in an upper respiratory tract disease. Journal of General Virology 2016, 97, 1942 -1954.

AMA Style

Reed F. Johnson, Dima A. Hammoud, Donna L. Perry, Jeffrey Solomon, Ian N. Moore, Matthew G. Lackemeyer, Jordan K. Bohannon, Philip J. Sayre, Mahnaz Minai, Amy B. Papaneri, Katie R. Hagen, Krisztina B. Janosko, Catherine Jett, Kurt Cooper, Joseph E. Blaney, Peter B. Jahrling. Exposure of rhesus monkeys to cowpox virus Brighton Red by large-particle aerosol droplets results in an upper respiratory tract disease. Journal of General Virology. 2016; 97 (8):1942-1954.

Chicago/Turabian Style

Reed F. Johnson; Dima A. Hammoud; Donna L. Perry; Jeffrey Solomon; Ian N. Moore; Matthew G. Lackemeyer; Jordan K. Bohannon; Philip J. Sayre; Mahnaz Minai; Amy B. Papaneri; Katie R. Hagen; Krisztina B. Janosko; Catherine Jett; Kurt Cooper; Joseph E. Blaney; Peter B. Jahrling. 2016. "Exposure of rhesus monkeys to cowpox virus Brighton Red by large-particle aerosol droplets results in an upper respiratory tract disease." Journal of General Virology 97, no. 8: 1942-1954.

Journal article
Published: 02 March 2016 in mBio
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Simian hemorrhagic fever (SHF) is a highly lethal disease in captive macaques. Three distinct arteriviruses are known etiological agents of past SHF epizootics, but only one, simian hemorrhagic fever virus (SHFV), has been isolated in cell culture. The natural reservoir(s) of the three viruses have yet to be identified, but African nonhuman primates are suspected. Eleven additional divergent simian arteriviruses have been detected recently in diverse and apparently healthy African cercopithecid monkeys. Here, we report the successful isolation in MARC-145 cell culture of one of these viruses, Kibale red colobus virus 1 (KRCV-1), from serum of a naturally infected red colobus ( Procolobus [ Piliocolobus ] rufomitratus tephrosceles ) sampled in Kibale National Park, Uganda. Intramuscular (i.m.) injection of KRCV-1 into four cynomolgus macaques ( Macaca fascicularis ) resulted in a self-limiting nonlethal disease characterized by depressive behavioral changes, disturbance in coagulation parameters, and liver enzyme elevations. In contrast, i.m. injection of SHFV resulted in typical lethal SHF characterized by mild fever, lethargy, lymphoid depletion, lymphoid and hepatocellular necrosis, low platelet counts, increased liver enzyme concentrations, coagulation abnormalities, and increasing viral loads. As hypothesized based on the genetic and presumed antigenic distance between KRCV-1 and SHFV, all four macaques that had survived KRCV-1 injection died of SHF after subsequent SHFV injection, indicating a lack of protective heterotypic immunity. Our data indicate that SHF is a disease of macaques that in all likelihood can be caused by a number of distinct simian arteriviruses, although with different severity depending on the specific arterivirus involved. Consequently, we recommend that current screening procedures for SHFV in primate-holding facilities be modified to detect all known simian arteriviruses. IMPORTANCE Outbreaks of simian hemorrhagic fever (SHF) have devastated captive Asian macaque colonies in the past. SHF is caused by at least three viruses of the family Arteriviridae : simian hemorrhagic fever virus (SHFV), simian hemorrhagic encephalitis virus (SHEV), and Pebjah virus (PBJV). Nine additional distant relatives of these three viruses were recently discovered in apparently healthy African nonhuman primates. We hypothesized that all simian arteriviruses are potential causes of SHF. To test this hypothesis, we inoculated cynomolgus macaques with a highly divergent simian arterivirus (Kibale red colobus virus 1 [KRCV-1]) from a wild Ugandan red colobus. Despite being only distantly related to red colobuses, all of the macaques developed disease. In contrast to SHFV-infected animals, KRCV-1-infected animals survived after a mild disease presentation. Our study advances the understanding of an important primate disease. Furthermore, our data indicate a need to include the full diversity of simian arteriviruses in nonhuman primate SHF screening assays.

ACS Style

Victoria Wahl-Jensen; Joshua C. Johnson; Michael Lauck; Jason T. Weinfurter; Louise H. Moncla; Andrea M. Weiler; Olivia Charlier; Oscar Rojas; Russell Byrum; Dan R. Ragland; Louis Huzella; Erika Zommer; Melanie Cohen; John G. Bernbaum; Yíngyún Caì; Hannah B. Sanford; Steven Mazur; Reed F. Johnson; Jing Qin; Gustavo F. Palacios; Adam L. Bailey; Peter B. Jahrling; Tony L. Goldberg; David H. O’Connor; Thomas C. Friedrich; Jens H. Kuhn. Divergent Simian Arteriviruses Cause Simian Hemorrhagic Fever of Differing Severities in Macaques. mBio 2016, 7, e02009-15 -15.

AMA Style

Victoria Wahl-Jensen, Joshua C. Johnson, Michael Lauck, Jason T. Weinfurter, Louise H. Moncla, Andrea M. Weiler, Olivia Charlier, Oscar Rojas, Russell Byrum, Dan R. Ragland, Louis Huzella, Erika Zommer, Melanie Cohen, John G. Bernbaum, Yíngyún Caì, Hannah B. Sanford, Steven Mazur, Reed F. Johnson, Jing Qin, Gustavo F. Palacios, Adam L. Bailey, Peter B. Jahrling, Tony L. Goldberg, David H. O’Connor, Thomas C. Friedrich, Jens H. Kuhn. Divergent Simian Arteriviruses Cause Simian Hemorrhagic Fever of Differing Severities in Macaques. mBio. 2016; 7 (1):e02009-15-15.

Chicago/Turabian Style

Victoria Wahl-Jensen; Joshua C. Johnson; Michael Lauck; Jason T. Weinfurter; Louise H. Moncla; Andrea M. Weiler; Olivia Charlier; Oscar Rojas; Russell Byrum; Dan R. Ragland; Louis Huzella; Erika Zommer; Melanie Cohen; John G. Bernbaum; Yíngyún Caì; Hannah B. Sanford; Steven Mazur; Reed F. Johnson; Jing Qin; Gustavo F. Palacios; Adam L. Bailey; Peter B. Jahrling; Tony L. Goldberg; David H. O’Connor; Thomas C. Friedrich; Jens H. Kuhn. 2016. "Divergent Simian Arteriviruses Cause Simian Hemorrhagic Fever of Differing Severities in Macaques." mBio 7, no. 1: e02009-15-15.

Research article
Published: 31 March 2015 in Inhalation Toxicology
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Aerosol droplets or particles produced from infected respiratory secretions have the potential to infect another host through inhalation. These respiratory particles can be polydisperse and range from 0.05 to 500 µm in diameter. Animal models of infection are generally established to facilitate the potential licensure of candidate prophylactics and/or therapeutics. Consequently, aerosol-based animal infection models are needed to properly study and counter airborne infections. Ideally, experimental aerosol exposure should reliably result in animal disease that faithfully reproduces the modeled human disease. Few studies have been performed to explore the relationship between exposure particle size and induced disease course for infectious aerosol particles. The center flow tangential aerosol generator (CenTAG™) produces large-particle aerosols capable of safely delivering a variety of infectious aerosols to non-human primates (NHPs) within a Class III Biological Safety Cabinet (BSC) for establishment or refinement of NHP infectious disease models. Here, we report the adaptation of this technology to the Animal Biosafety Level 4 (ABSL-4) environment for the future study of high-consequence viral pathogens and the characterization of CenTAG™-created sham (no animal, no virus) aerosols using a variety of viral growth media and media supplements.

ACS Style

J. Kyle Bohannon; Matthew Lackemeyer; Jens H. Kuhn; Jiro Wada; Laura Bollinger; Peter B. Jahrling; Reed F. Johnson. Generation and characterization of large-particle aerosols using a center flow tangential aerosol generator with a non-human-primate, head-only aerosol chamber. Inhalation Toxicology 2015, 27, 247 -253.

AMA Style

J. Kyle Bohannon, Matthew Lackemeyer, Jens H. Kuhn, Jiro Wada, Laura Bollinger, Peter B. Jahrling, Reed F. Johnson. Generation and characterization of large-particle aerosols using a center flow tangential aerosol generator with a non-human-primate, head-only aerosol chamber. Inhalation Toxicology. 2015; 27 (5):247-253.

Chicago/Turabian Style

J. Kyle Bohannon; Matthew Lackemeyer; Jens H. Kuhn; Jiro Wada; Laura Bollinger; Peter B. Jahrling; Reed F. Johnson. 2015. "Generation and characterization of large-particle aerosols using a center flow tangential aerosol generator with a non-human-primate, head-only aerosol chamber." Inhalation Toxicology 27, no. 5: 247-253.

Short communication
Published: 04 December 2014 in Virus Research
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Using a recombinant rabies (RABV) vaccine platform, we have developed several safe and effective vaccines. Most recently, we have developed a RABV-based ebolavirus (EBOV) vaccine that is efficacious in nonhuman primates. One safety feature of this vaccine is the utilization of a live but replication-deficient RABV construct. In this construct, the RABV glycoprotein (G) has been deleted from the genome, requiring G trans complementation in order for new infectious viruses to be released from the initial infected cell. Here we analyze this safety feature of the bivalent RABV-based EBOV vaccine comprised of the G-deleted RABV backbone expressing EBOV glycoprotein (GP). We found that, while the level of RABV genome in infected cells is equivalent regardless of G supplementation, the production of infectious virus is indeed restricted by the lack of G, and most importantly, that the presence of EBOV GP does not substitute for G. These findings further support the safety profile of this replication-deficient RABV-EBOV bivalent vaccine.

ACS Style

Amy B. Papaneri; John G. Bernbaum; Joseph E. Blaney; Peter B. Jahrling; Matthias J. Schnell; Reed F. Johnson. Controlled viral glycoprotein expression as a safety feature in a bivalent rabies-ebola vaccine. Virus Research 2014, 197, 54 -8.

AMA Style

Amy B. Papaneri, John G. Bernbaum, Joseph E. Blaney, Peter B. Jahrling, Matthias J. Schnell, Reed F. Johnson. Controlled viral glycoprotein expression as a safety feature in a bivalent rabies-ebola vaccine. Virus Research. 2014; 197 ():54-8.

Chicago/Turabian Style

Amy B. Papaneri; John G. Bernbaum; Joseph E. Blaney; Peter B. Jahrling; Matthias J. Schnell; Reed F. Johnson. 2014. "Controlled viral glycoprotein expression as a safety feature in a bivalent rabies-ebola vaccine." Virus Research 197, no. : 54-8.

Preliminary research
Published: 16 September 2014 in EJNMMI Research
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2-deoxy-2-[18F]fluoro-D-glucose-positron emission tomography (18F-FDG-PET) is applied in the clinic for infection assessment and is under consideration for investigating the inflammatory/immune response in lymphoid tissue in animal models of viral infection. Assessing changes in 18F-FDG uptake of lymph nodes (LNs), primary lymphoid tissues targeted during viral infection, requires suitable methods for image analysis. Similar to tumor evaluation, reliable quantitation of the LN function via multiple 18F-FDG-PET sessions will depend how the volume of interest is defined. Volume of interest definition has a direct effect on statistical outcome. The current study objective is to compare for the first time agreement between conventional and modified VOI metrics to determine which method(s) provide(s) reproducible standardized uptake values (SUVs) for 18F-FDG uptake in the LN of rhesus macaques. Multiple 18F-FDG-PET images of LNs in macaques were acquired prior to and after monkeypox virus intravenous inoculation. We compared five image analysis approaches, SUVmax, SUVmean, SUVthreshold, modified SUVthreshold, and SUVfixed volume, to investigate the impact of these approaches on quantification of the changes in LN metabolic activity denoting the immune response during viral infection progression. The lowest data repeatability was observed with SUVmax. The best correspondence was between SUVfixed volume and conventional and modified SUVthreshold. A statistically significant difference in the LN 18F-FDG uptake between surviving and moribund animals was shown using modified SUVthreshold and SUVfixed volume (adjusted p = 0.0037 and p = 0.0001, respectively). Quantification of the LN 18F-FDG uptake is highly sensitive to the method applied for PET image analysis. SUVfixed volume and modified SUVthreshold demonstrate better reproducibility for SUV estimates than SUVmax, SUVmean, and SUVthreshold. SUVfixed volume and modified SUVthreshold are capable of distinguishing between groups with different disease outcomes. Therefore, these methods are the preferred approaches for evaluating the LN function during viral infection by 18F-FDG-PET. Validation of multiple approaches is necessary to choose a suitable method to monitor changes in LN metabolic activity during progression of viral infection.

ACS Style

Svetlana Chefer; Richard C Reba; Christopher Z Leyson; Jurgen Seidel; Reed F Johnson; Joseph E Blaney; Peter B Jahrling; Julie Dyall. The effect of volume of interest definition on quantification of lymph node immune response to a monkeypox virus infection assessed by 18F-FDG-PET. EJNMMI Research 2014, 4, 49 .

AMA Style

Svetlana Chefer, Richard C Reba, Christopher Z Leyson, Jurgen Seidel, Reed F Johnson, Joseph E Blaney, Peter B Jahrling, Julie Dyall. The effect of volume of interest definition on quantification of lymph node immune response to a monkeypox virus infection assessed by 18F-FDG-PET. EJNMMI Research. 2014; 4 (1):49.

Chicago/Turabian Style

Svetlana Chefer; Richard C Reba; Christopher Z Leyson; Jurgen Seidel; Reed F Johnson; Joseph E Blaney; Peter B Jahrling; Julie Dyall. 2014. "The effect of volume of interest definition on quantification of lymph node immune response to a monkeypox virus infection assessed by 18F-FDG-PET." EJNMMI Research 4, no. 1: 49.

Proceedings article
Published: 29 March 2013 in SPIE Medical Imaging
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Monkeypox virus is an emerging zoonotic pathogen that results in up to 10% mortality in humans. Knowledge of clinical manifestations and temporal progression of monkeypox disease is limited to data collected from rare outbreaks in remote regions of Central and West Africa. Clinical observations show that monkeypox infection resembles variola infection. Given the limited capability to study monkeypox disease in humans, characterization of the disease in animal models is required. A previous work focused on the identification of inflammatory patterns using PET/CT image modality in two non-human primates previously inoculated with the virus. In this work we extended techniques used in computer-aided detection of lung tumors to identify inflammatory lesions from monkeypox virus infection and their progression using CT images. Accurate estimation of partial volumes of lung lesions via segmentation is difficult because of poor discrimination between blood vessels, diseased regions, and outer structures. We used hard C-means algorithm in conjunction with landmark based registration to estimate the extent of monkeypox virus induced disease before inoculation and after disease progression. Automated estimation is in close agreement with manual segmentation.

ACS Style

Marcelo A. Castro; David Thomasson; Nilo A. Avila; Jennifer Hufton; Justin Senseney; Reed F. Johnson; Julie Dyall. Optimization of automated segmentation of monkeypox virus-induced lung lesions from normal lung CT images using hard C-means algorithm. SPIE Medical Imaging 2013, 8672, 867222 .

AMA Style

Marcelo A. Castro, David Thomasson, Nilo A. Avila, Jennifer Hufton, Justin Senseney, Reed F. Johnson, Julie Dyall. Optimization of automated segmentation of monkeypox virus-induced lung lesions from normal lung CT images using hard C-means algorithm. SPIE Medical Imaging. 2013; 8672 ():867222.

Chicago/Turabian Style

Marcelo A. Castro; David Thomasson; Nilo A. Avila; Jennifer Hufton; Justin Senseney; Reed F. Johnson; Julie Dyall. 2013. "Optimization of automated segmentation of monkeypox virus-induced lung lesions from normal lung CT images using hard C-means algorithm." SPIE Medical Imaging 8672, no. : 867222.

Journal article
Published: 01 January 2012 in Journal of General Virology
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The public health threat of orthopoxviruses from bioterrorist attacks has prompted researchers to develop suitable animal models for increasing our understanding of viral pathogenesis and evaluation of medical countermeasures (MCMs) in compliance with the FDA Animal Efficacy Rule. We present an accessible intrabronchial cowpox virus (CPXV) model that can be evaluated under biosafety level-2 laboratory conditions. In this dose-ranging study, utilizing cynomolgus macaques, signs of typical orthopoxvirus disease were observed with the lymphoid organs, liver, skin (generally mild) and respiratory tract as target tissues. Clinical and histopathological evaluation suggests that intrabronchial CPXV recapitulated many of the features of monkeypox and variola virus, the causative agent of smallpox, infections in cynomolgus macaque models. These similarities suggest that CPXV infection in non-human primates should be pursued further as an alternative model of smallpox. Further development of the CPXV primate model, unimpeded by select agent and biocontainment restrictions, should facilitate the development of MCMs for smallpox.

ACS Style

Alvin L. Smith; Marisa St Claire; Srikanth Yellayi; Laura Bollinger; Peter B. Jahrling; Jason Paragas; Joseph E. Blaney; Reed F. Johnson. Intrabronchial inoculation of cynomolgus macaques with cowpox virus. Journal of General Virology 2012, 93, 159 -164.

AMA Style

Alvin L. Smith, Marisa St Claire, Srikanth Yellayi, Laura Bollinger, Peter B. Jahrling, Jason Paragas, Joseph E. Blaney, Reed F. Johnson. Intrabronchial inoculation of cynomolgus macaques with cowpox virus. Journal of General Virology. 2012; 93 (1):159-164.

Chicago/Turabian Style

Alvin L. Smith; Marisa St Claire; Srikanth Yellayi; Laura Bollinger; Peter B. Jahrling; Jason Paragas; Joseph E. Blaney; Reed F. Johnson. 2012. "Intrabronchial inoculation of cynomolgus macaques with cowpox virus." Journal of General Virology 93, no. 1: 159-164.

Journal article
Published: 20 December 2011 in Virology
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Simian Hemorrhagic Fever Virus (SHFV) has caused sporadic outbreaks of hemorrhagic fevers in macaques at primate research facilities. SHFV is a BSL-2 pathogen that has not been linked to human disease; as such, investigation of SHFV pathogenesis in non-human primates (NHPs) could serve as a model for hemorrhagic fever viruses such as Ebola, Marburg, and Lassa viruses. Here we describe the pathogenesis of SHFV in rhesus macaques inoculated with doses ranging from 50 PFU to 500,000 PFU. Disease severity was independent of dose with an overall mortality rate of 64% with signs of hemorrhagic fever and multiple organ system involvement. Analyses comparing survivors and non-survivors were performed to identify factors associated with survival revealing differences in the kinetics of viremia, immunosuppression, and regulation of hemostasis. Notable similarities between the pathogenesis of SHFV in NHPs and hemorrhagic fever viruses in humans suggest that SHFV may serve as a suitable model of BSL-4 pathogens.

ACS Style

Reed F. Johnson; Lori E. Dodd; Srikanth Yellayi; Wenjuan Gu; Jennifer A. Cann; Catherine Jett; John G. Bernbaum; Dan R. Ragland; Marisa St. Claire; Russell Byrum; Jason Paragas; Joseph E. Blaney; Peter B. Jahrling. Simian hemorrhagic fever virus infection of rhesus macaques as a model of viral hemorrhagic fever: Clinical characterization and risk factors for severe disease. Virology 2011, 421, 129 -140.

AMA Style

Reed F. Johnson, Lori E. Dodd, Srikanth Yellayi, Wenjuan Gu, Jennifer A. Cann, Catherine Jett, John G. Bernbaum, Dan R. Ragland, Marisa St. Claire, Russell Byrum, Jason Paragas, Joseph E. Blaney, Peter B. Jahrling. Simian hemorrhagic fever virus infection of rhesus macaques as a model of viral hemorrhagic fever: Clinical characterization and risk factors for severe disease. Virology. 2011; 421 (2):129-140.

Chicago/Turabian Style

Reed F. Johnson; Lori E. Dodd; Srikanth Yellayi; Wenjuan Gu; Jennifer A. Cann; Catherine Jett; John G. Bernbaum; Dan R. Ragland; Marisa St. Claire; Russell Byrum; Jason Paragas; Joseph E. Blaney; Peter B. Jahrling. 2011. "Simian hemorrhagic fever virus infection of rhesus macaques as a model of viral hemorrhagic fever: Clinical characterization and risk factors for severe disease." Virology 421, no. 2: 129-140.