Heinz Feldmann

National Institutes of Health, 베서스다, Maryland, United States

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Publications (327)2001.94 Total impact

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    ABSTRACT: The ongoing Ebola outbreak in West Africa has resulted in fast-track development of vaccine candidates. We tested a vesicular stomatitis virus vector expressing Ebola virus glycoprotein for safety in pigs. Inoculation did not cause disease and vaccine virus shedding was minimal, which indicated that the vaccine virus does not pose a risk of dissemination in pigs.
    Emerging infectious diseases 04/2015; 21(4). DOI:10.3201/eid2104.142012 · 7.33 Impact Factor
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    ABSTRACT: Fruit bats are suspected to be a natural reservoir of filoviruses, including Ebola and Marburg viruses. Using an enzyme-linked immunosorbent assay based on the viral glycoprotein antigens, we detected filovirus-specific immunoglobulin G antibodies in 71 of 748 serum samples collected from migratory fruit bats (Eidolon helvum) in Zambia during 2006-2013. Although antibodies to African filoviruses (eg, Zaire ebolavirus) were most prevalent, some serum samples showed distinct specificity for Reston ebolavirus, which that has thus far been found only in Asia. Interestingly, the transition of filovirus species causing outbreaks in Central and West Africa during 2005-2014 seemed to be synchronized with the change of the serologically dominant virus species in these bats. These data suggest the introduction of multiple species of filoviruses in the migratory bat population and point to the need for continued surveillance of filovirus infection of wild animals in sub-Saharan Africa, including hitherto nonendemic countries. © The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.
    The Journal of Infectious Diseases 03/2015; DOI:10.1093/infdis/jiv063 · 5.78 Impact Factor
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    ABSTRACT: Safe and effective vaccines and drugs are needed for the prevention and treatment of Ebola virus disease, including following a potentially high-risk exposure such as a needlestick. To assess response to postexposure vaccination in a health care worker who was exposed to the Ebola virus. Case report of a physician who experienced a needlestick while working in an Ebola treatment unit in Sierra Leone on September 26, 2014. Medical evacuation to the United States was rapidly initiated. Given the concern about potentially lethal Ebola virus disease, the patient was offered, and provided his consent for, postexposure vaccination with an experimental vaccine available through an emergency Investigational New Drug application. He was vaccinated on September 28, 2014. The vaccine used was VSVΔG-ZEBOV, a replicating, attenuated, recombinant vesicular stomatitis virus (serotype Indiana) whose surface glycoprotein gene was replaced by the Zaire Ebola virus glycoprotein gene. This vaccine has entered a clinical trial for the prevention of Ebola in West Africa. The vaccine was administered 43 hours after the needlestick occurred. Fever and moderate to severe symptoms developed 12 hours after vaccination and diminished over 3 to 4 days. The real-time reverse transcription polymerase chain reaction results were transiently positive for vesicular stomatitis virus nucleoprotein gene and Ebola virus glycoprotein gene (both included in the vaccine) but consistently negative for Ebola virus nucleoprotein gene (not in the vaccine). Early postvaccination cytokine secretion and T lymphocyte and plasmablast activation were detected. Subsequently, Ebola virus glycoprotein-specific antibodies and T cells became detectable, but antibodies against Ebola viral matrix protein 40 (not in the vaccine) were not detected. It is unknown if VSVΔG-ZEBOV is safe or effective for postexposure vaccination in humans who have experienced a high-risk occupational exposure to the Ebola virus, such as a needlestick. In this patient, postexposure vaccination with VSVΔG-ZEBOV induced a self-limited febrile syndrome that was associated with transient detection of the recombinant vesicular stomatitis vaccine virus in blood. Strong innate and Ebola-specific adaptive immune responses were detected after vaccination. The clinical syndrome and laboratory evidence were consistent with vaccination response, and no evidence of Ebola virus infection was detected.
  • Darryl Falzarano, Heinz Feldmann
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    ABSTRACT: Laguna Negra virus (LNV) is a New World hantavirus associated with severe and often fatal cardiopulmonary disease in humans, known as hantavirus pulmonary syndrome (HPS). Five hamster species were evaluated for clinical and serologic responses following inoculation with 4 hantaviruses. Of the 5 hamster species, only Turkish hamsters infected with LNV demonstrated signs consistent with HPS and a fatality rate of 43%. Clinical manifestations in infected animals that succumbed to disease included severe and rapid onset of dyspnea, weight loss, leukopenia, and reduced thrombocyte numbers as compared to uninfected controls. Histopathologic examination revealed lung lesions that resemble the hallmarks of HPS in humans, including interstitial pneumonia and pulmonary edema, as well as generalized infection of endothelial cells and macrophages in major organ tissues. Histologic lesions corresponded to the presence of viral antigen in affected tissues. To date, there have been no small animal models available to study LNV infection and pathogenesis. The Turkish hamster model of LNV infection may be important in the study of LNV-induced HPS pathogenesis and development of disease treatment and prevention strategies. © The Author(s) 2015.
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    ABSTRACT: We demonstrated that previous vaccination with a vesicular stomatitis virus (VSV)-based Lassa virus vaccine does not alter protective efficacy of subsequent vaccination with a VSV-based Ebola virus vaccine. These findings demonstrate the utility of VSV-based vaccines against divergent viral pathogens, even when preexisting immunity to the vaccine vector is present.
    Emerging infectious diseases 02/2015; 21(2):305-7. DOI:10.3201/eid2102.141649 · 7.33 Impact Factor
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    ABSTRACT: Vesicular stomatitis virus expressing Zaire Ebola virus (EBOV) glycoprotein (VSVΔG/EBOVgp) could be used as a vaccine to meet the 2014 Ebola virus outbreak. To characterize host response to this vaccine, we used mRNA sequencing to analyze PBMC from cynomolgus macaques after VSVΔG/EBOVgp immunization and subsequent EBOV challenge. We found a controlled transcriptional response that transitioned to immune regulation as the EBOV was cleared. This observation supported the safety of the vaccine. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
    Clinical and vaccine Immunology: CVI 01/2015; DOI:10.1128/CVI.00733-14 · 2.37 Impact Factor
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    ABSTRACT: To identify host factors associated with arenavirus virulence, we used a cynomolgus macaque model to evaluate the pathogenesis of Lujo virus (LUJV), a recently emerged arenavirus that caused an outbreak of severe viral hemorrhagic fever in southern Africa. In contrast to human cases, LUJV caused mild, non-lethal illness in macaques. We then compared this to opposed clinical outcomes during arenavirus infection, specifically to samples obtained from macaques infected with three highly pathogenic lines of Lassa virus (LASV), the causative agent of Lassa fever (LF). We assessed gene expression in peripheral blood mononuclear cells (PBMC), and determined genes that significantly changed expression relative to uninfected animals over the course of infection. We detected a 72-hour delay in induction of host responses to infection during LUJV infection compared to the animals infected with LASV. This included genes associated with inflammatory and antiviral responses, and was particularly apparent among groups of genes promoting cell death. We also observed early differential expression of a subset of genes specific to LUJV infection that accounts for the delayed inflammatory response. Cell-type enrichment analysis suggested that host response induction delay and LUJV-specific profile may be due to a different proportion of natural killer cells responding in LUJV infection compared to the LASV-infected animals. Together, these data indicate that delayed pro-inflammatory and pro-apoptotic host responses to arenavirus infection could ameliorate disease severity. This conclusion provides insight into the cellular and molecular mechanisms of arenaviral hemorrhagic fever, as well as suggests potential strategies for therapeutic development. Old World arenaviruses are significant human pathogens that are often associated with high mortality. However, mechanisms underlying disease severity and virulence in arenavirus hemorrhagic fever are largely unknown, particularly regarding host responses that contribute to pathogenicity. This study describes a comparison between Lujo and Lassa virus infection in cynomolgus macaques. Lujo-infected macaques developed only mild illness, while Lassa-infected macaques developed severe illness consistent with Lassa fever. We determined that mild disease is associated with a delay in host expression of genes linked to virulence, such as those causing inflammation and cell death, and with distinct cell types that may mediate this delay. This is the first study to associate the timing and directionality of gene expression with arenaviral pathogenicity and disease outcome, and evokes new potential approaches for developing effective therapeutics for treating these deadly emerging pathogens. Copyright © 2014, American Society for Microbiology. All Rights Reserved.
    Journal of Virology 12/2014; 89(5). DOI:10.1128/JVI.02246-14 · 4.65 Impact Factor
  • David Safronetz, Heinz Feldmann, Emmie de Wit
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    ABSTRACT: Emerging infectious diseases of zoonotic origin are shaping today's infectious disease field more than ever. In this article, we introduce and review three emerging zoonotic viruses. Novel hantaviruses emerged in the Americas in the mid-1990s as the cause of severe respiratory infections, designated hantavirus pulmonary syndrome, with case fatality rates of around 40%. Nipah virus emerged a few years later, causing respiratory infections and encephalitis in Southeast Asia, with case fatality rates ranging from 40% to more than 90%, A new coronavirus emerged in 2012 on the Arabian Peninsula with a clinical syndrome of acute respiratory infections, later designated as Middle East respiratory syndrome (MERS), and an initial case fatality rate of more than 40%. Our current state of knowledge on the pathogenicity of these three severe, emerging viral infections is discussed. Expected final online publication date for the Annual Review of Pathology: Mechanisms of Disease Volume 10 is January 24, 2015. Please see http://www.annualreviews.org/catalog/pubdates.aspx for revised estimates.
    Annual Review of Pathology Mechanisms of Disease 11/2014; DOI:10.1146/annurev-pathol-012414-040501 · 22.13 Impact Factor
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    ABSTRACT: The Syrian hamster (golden hamster, Mesocricetus auratus) is gaining importance as a new experimental animal model for multiple pathogens, including emerging zoonotic diseases such as Ebola. Nevertheless there are currently no publicly available transcriptome reference sequences or genome for this species.
    PLoS ONE 11/2014; 9(11):e112617. DOI:10.1371/journal.pone.0112617 · 3.53 Impact Factor
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    ABSTRACT: Here, we report the complete genome sequences, including the genome termini, of three Ebola virus isolates (species Zaire ebolavirus) originating from Guinea that are now being widely used in laboratories in North America for research regarding West African Ebola viruses. Copyright © 2014 Hoenen et al.
    Genome Announcements 11/2014; 2(6). DOI:10.1128/genomeA.01331-14
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    ABSTRACT: Existing mouse models of lethal Ebola virus infection do not reproduce hallmark symptoms of Ebola hemorrhagic fever, neither delayed blood coagulation and disseminated intravascular coagulation, nor death from shock, thus restricting pathogenesis studies to non-human primates. Here we show that mice from the Collaborative Cross exhibit distinct disease phenotypes following mouse-adapted Ebola virus infection. Phenotypes range from complete resistance to lethal disease to severe hemorrhagic fever characterized by prolonged coagulation times and 100% mortality. Inflammatory signaling was associated with vascular permeability and endothelial activation, and resistance to lethal infection arose by induction of lymphocyte differentiation and cellular adhesion, likely mediated by the susceptibility allele Tek. These data indicate that genetic background determines susceptibility to Ebola hemorrhagic fever.
    Science 10/2014; 346(6212). DOI:10.1126/science.1259595 · 31.48 Impact Factor
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    ABSTRACT: Nipah virus is a paramyxovirus in the genus Henipavirus, which has caused outbreaks in humans in Malaysia, India, Singapore, and Bangladesh. Whereas the human cases in Malaysia were characterized mainly by neurological symptoms and a case fatality rate of ~40%, cases in Bangladesh also exhibited respiratory disease and had a case fatality rate of ~70%. Here, we compared the histopathologic changes in the respiratory tract of Syrian hamsters, a well-established small animal disease model for Nipah virus, inoculated oronasally with Nipah virus isolates from human cases in Malaysia and Bangladesh. The Nipah virus isolate from Bangladesh caused slightly more severe rhinitis and bronchointerstitial pneumonia 2 days after inoculation in Syrian hamsters. By day 4, differences in lesion severity could no longer be detected. Immunohistochemistry demonstrated Nipah virus antigen in the nasal cavity and pulmonary lesions; the amount of Nipah virus antigen present correlated with lesion severity. Immunohistochemistry indicated that both Nipah virus isolates exhibited endotheliotropism in small- and medium-caliber arteries and arterioles, but not in veins, in the lung. This correlated with the location of ephrin B2, the main receptor for Nipah virus, in the vasculature. In conclusion, Nipah virus isolates from outbreaks in Malaysia and Bangladesh caused a similar type and severity of respiratory tract lesions in Syrian hamsters, suggesting that the differences in human disease reported in the outbreaks in Malaysia and Bangladesh are unlikely to have been caused by intrinsic differences in these 2 virus isolates.
    Veterinary Pathology 10/2014; 52(1). DOI:10.1177/0300985814556189 · 2.04 Impact Factor
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    ABSTRACT: Crimean-Congo hemorrhagic fever (CCHF) is an expanding tick-borne hemorrhagic disease with increasing human and animal health impact. Immense knowledge was gained over the past 10 years mainly due to advances in molecular biology, but also driven by an increased global interest in CCHFV as an emerging/re-emerging zoonotic pathogen. In the present article, we discuss the advances in research with focus on CCHF ecology, epidemiology, pathogenesis, diagnostics, prophylaxis and treatment. Despite tremendous achievements, future activities have to concentrate on the development of vaccines and antivirals/therapeutics to combat CCHF. Vector studies need to continue for better public and animal health preparedness and response. We conclude with a roadmap for future research priorities. Copyright © 2014 Elsevier B.V. All rights reserved.
    Journal of clinical virology: the official publication of the Pan American Society for Clinical Virology 10/2014; 64. DOI:10.1016/j.jcv.2014.08.029 · 3.47 Impact Factor
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    ABSTRACT: The emerging zoonotic pathogens Hendra virus (HeV) and Nipah virus (NiV) are in the genus Henipaviridae family Paramyxoviridae. HeV and NiV infections can be highly fatal to humans and livestock. The goal of this study was to develop candidate vaccines against henipaviruses utilizing two well-established rhabdoviral vaccine vector platforms: recombinant rabies virus (RABV) and recombinant vesicular stomatitis virus (VSV), expressing either the codon-optimized or the wild-type HeV glycoprotein (G). The RABV vector expressing the codon-optimized HeV G showed a 2 to 3-fold increase in incorporation compared to the RABV vector expressing wild-type (wt) HeV G. There was no significant difference in HeV G incorporation in the VSV vectors expressing either wt or codon-optimized HeV G. Mice inoculated intranasally with any of these live recombinant viruses showed no signs of disease, including weight loss, indicating that HeV G expression and incorporation did not increase the neurotropism of the vaccine vector. To test immunogenicity of the vaccine candidates, we immunized mice intramuscularly with either one dose of the live vaccines or 3 doses of 10μg chemically inactivated viral particles. Increased codon-optimized HeV G incorporation into RABV virions resulted in higher antibody titers against HeV G compared to inactivated RABV virions expressing wt HeV G. The live VSV vectors induced more HeV G-specific antibodies as well as higher levels of HeV neutralizing antibodies than the RABV vectors. In the case of killed particles, HeV neutralizing serum titers were very similar between the two platforms. These results indicated that killed RABV with codon-optimized HeV G should be the vector of choice as a dual vaccine in areas where rabies is endemic.
    Journal of Virology 10/2014; DOI:10.1128/JVI.02308-14 · 4.65 Impact Factor
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    Thomas Hoenen, Heinz Feldmann
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    ABSTRACT: Response to the current ebolavirus outbreak based on traditional control measures has so far been insufficient to prevent the virus from spreading rapidly. This has led to urgent discussions on the use of experimental therapies and vaccines untested in humans and existing in limited quantities, raising political, strategic, technical and ethical questions. Ebolavirus outbreaks and disease The ongoing outbreak in West Africa of ebolavirus hemorrhagic fever (EHF) [1], lately also referred to as Ebola virus disease (EVD), has led to a surge in public interest and concern regarding this virus, which was first discovered in 1976 during simultaneous outbreaks in Zaire (now the Democratic Republic of the Congo) and Sudan [2]. Humans initially contract the virus either through contact with the infected reservoir, which is thought to be fruit bats, or by hunting and butchering of infected wildlife, particularly great apes. Since their dis-covery, ebolaviruses have caused frequent outbreaks al-most exclusively in Central Africa. However, the recent emergence of Zaire ebolavirus in West Africa, resulting in what is the largest outbreak to date (Figure 1), with 4,390 cases and 2,226 deaths as of 7 September 2014, shows that ebolaviruses are more widely distributed than previously thought. While EHF is commonly associated with high case fatality rates (up to 90% for Zaire ebolavirus, approximately 50% for Sudan ebolavirus, and approximately 35% for Bundibugyo ebolavirus), the pathogenicity of Taï Forest ebolavirus, which was discov-ered in the mid-1990s in Ivory Coast, is unknown be-cause only a single case has been reported, and Reston ebolavirus, which is found in the Philippines, is consi-dered apathogenic for humans. Outbreaks are usually
    BMC Biology 09/2014; 12:80. DOI:10.1186/s12915-014-0080-6 · 7.43 Impact Factor
  • Thomas Hoenen, Heinz Feldmann
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    ABSTRACT: Filoviruses cause severe hemorrhagic fevers with case fatality rates of up to 90%, for which no antivirals are currently available. Their categorization as biosafety level 4 agents restricts work with infectious viruses to a few maximum containment laboratories worldwide, which constitutes a significant obstacle for the development of countermeasures. Reverse genetics facilitates the generation of recombinant filoviruses, including reporter-expressing viruses, which have been increasingly used for drug screening and development in recent years. Further, reverse-genetics based lifecycle modeling systems allow modeling of the filovirus lifecycle without the need for a maximum containment laboratory and have recently been optimized for use in high-throughput assays. The availability of these reverse genetics-based tools will significantly improve our ability to find novel antivirals against filoviruses.
    Expert Review of Anti-infective Therapy 08/2014; DOI:10.1586/14787210.2014.948848 · 2.28 Impact Factor
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    ABSTRACT: The availability of a robust disease model is essential for the development of countermeasures for Middle East respiratory syndrome coronavirus (MERS-CoV). While a rhesus macaque model of MERS-CoV has been established, the lack of uniform, severe disease in this model complicates the analysis of countermeasure studies. Modeling of the interaction between the MERS-CoV spike glycoprotein and its receptor dipeptidyl peptidase 4 predicted comparable interaction energies in common marmosets and humans. The suitability of the marmoset as a MERS-CoV model was tested by inoculation via combined intratracheal, intranasal, oral and ocular routes. Most of the marmosets developed a progressive severe pneumonia leading to euthanasia of some animals. Extensive lesions were evident in the lungs of all animals necropsied at different time points post inoculation. Some animals were also viremic; high viral loads were detected in the lungs of all infected animals, and total RNAseq demonstrated the induction of immune and inflammatory pathways. This is the first description of a severe, partially lethal, disease model of MERS-CoV, and as such will have a major impact on the ability to assess the efficacy of vaccines and treatment strategies as well as allowing more detailed pathogenesis studies.
    PLoS Pathogens 08/2014; 10(8):e1004250. DOI:10.1371/journal.ppat.1004250 · 8.14 Impact Factor
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    ABSTRACT: In March 2013, three fatal human cases of infection with influenza A virus (H7N9) were reported in China. Since then, human cases have been accumulating. Given the public health importance of this virus, we performed a pathogenicity study of the H7N9 virus in the cynomolgus macaque model, focusing on clinical aspects of disease, radiographic, histological, and gene expression profile changes in the upper and lower respiratory tracts, and changes in systemic cytokine and chemokine profiles during infection. Cynomolgus macaques developed transient, mild to severe disease with radiographic evidence of pulmonary infiltration. Virus replicated in the upper as well as lower respiratory tract, with sustained replication in the upper respiratory tract until the end of the experiment at 6 days after inoculation. Virus shedding occurred mainly via the throat. Histopathological changes in the lungs were similar to those observed in humans, albeit less severe, with diffuse alveolar damage, infiltration of polymorphonuclear cells, formation of hyaline membranes, pneumocyte hyperplasia, and fibroproliferative changes. Analysis of gene expression profiles in lung lesions identified pathways involved in tissue damage during H7N9 infection as well as leads for development of therapeutics targeting host responses rather than virus replication. Overall, H7N9 infection was not as severe in cynomolgus macaques as in humans, supporting the possible role of underlying medical complications in disease severity as discussed for human H7N9 infection (H. N. Gao et al., N. Engl. J. Med. 368:2277-2285, 2013, doi:10.1056/NEJMoa1305584).
    mBio 07/2014; 5(4). DOI:10.1128/mBio.01331-14 · 6.88 Impact Factor
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    ABSTRACT: Work with infectious Ebola viruses is restricted to biosafety level (BSL) 4 laboratories, presenting a significant barrier for studying these viruses. Lifecycle modeling systems, including minigenome systems and transcription and replication-competent virus-like particle (trVLP) systems, allow modeling of the virus lifecycle under BSL2 conditions; however, all current systems model only certain aspects of the virus lifecycle, rely on plasmid-based viral protein expression, and have only been used to model single infectious cycles. We have developed a novel lifecycle modeling system allowing continuous passaging of infectious trVLPs containing a tetracistronic minigenome that encodes a reporter and the viral proteins VP40, VP24, and GP1,2. This system is ideally suited for studying morphogenesis, budding and entry, in addition to genome replication and transcription. Importantly, the specific infectivity of trVLPs in this system was ∼500 fold higher than in previous systems. Using this system for functional studies of VP24 we showed that, contrary to previous reports, VP24 only very modestly inhibits genome replication and transcription when expressed in a regulated fashion, which we confirmed using infectious Ebola viruses. Interestingly, we also discovered a genome length-dependent effect of VP24 on particle infectivity, which was previously undetected due to the short length of monocistronic minigenomes, and which is due at least partially to a previously unknown function of VP24 in RNA packaging. Based on our findings we propose a model for the function of VP24 that reconciles all currently available data regarding the role of VP24 in nucleocapsid assembly as well as genome replication and transcription.
    Journal of Virology 06/2014; 88(18). DOI:10.1128/JVI.01272-14 · 4.65 Impact Factor

Publication Stats

12k Citations
2,001.94 Total Impact Points


  • 2010–2015
    • National Institutes of Health
      • Laboratory of Virology (LV)
      베서스다, Maryland, United States
    • National Institute of Infectious Diseases, Tokyo
      Edo, Tōkyō, Japan
  • 2003–2015
    • National Institute of Allergy and Infectious Diseases
      • Laboratory of Immunoregulation
      베서스다, Maryland, United States
  • 2014
    • University of Washington Seattle
      • Department of Microbiology
      Seattle, Washington, United States
  • 2003–2014
    • University of Manitoba
      • • Department of Medical Microbiology and Infectious Diseases
      • • Department of Immunology
      Winnipeg, Manitoba, Canada
  • 2012–2013
    • Erasmus MC
      • Department of Virology
      Rotterdam, South Holland, Netherlands
  • 2010–2013
    • National Institute of Allergy and Infectious Disease
      Hamilton, Ohio, United States
  • 2002–2013
    • National Microbiology Laboratory, Canada
      Winnipeg, Manitoba, Canada
  • 2007–2012
    • Public Health Agency of Canada
      • Special Pathogens Program
      Ottawa, Ontario, Canada
    • The University of Tokyo
      • • Department of Microbiology and Immunology
      • • Institute of Medical Science
      • • International Research Center for Infectious Diseases
      Edo, Tōkyō, Japan
    • Columbia University
      • Center for Infection and Immunity
      New York City, NY, United States
    • The Academy of Sciences of Islamic Republic of Iran
      Teheran, Tehrān, Iran
  • 1991–2012
    • Philipps-Universität Marburg
      • Institut für Virologie
      Marburg, Hesse, Germany
  • 2011
    • University of Münster
      Muenster, North Rhine-Westphalia, Germany
    • Benaroya Research Institute
      Seattle, Washington, United States
  • 2003–2011
    • Technische Universität Dresden
      • Institut für Physiologie
      Dresden, Saxony, Germany
  • 2002–2011
    • University of Wisconsin, Madison
      • Department of Pathobiological Sciences
      Mississippi, United States
  • 2001–2010
    • Robert Koch Institut
      Berlín, Berlin, Germany
    • Carl Gustav Carus-Institut
      Pforzheim, Baden-Württemberg, Germany
  • 2006
    • U.S. Army Medical Research Institute of Infectious Diseases
      Maryland, United States
    • The University of Winnipeg
      Winnipeg, Manitoba, Canada
  • 2002–2006
    • Health Sciences Centre Winnipeg
      Winnipeg, Manitoba, Canada
  • 2005
    • Claude Bernard University Lyon 1
      Villeurbanne, Rhône-Alpes, France
  • 2004
    • Ludwig Institute for Cancer Research Sweden
      Uppsala, Uppsala, Sweden
    • Southern Research Institute
      Birmingham, Alabama, United States
  • 1993
    • Centers for Disease Control and Prevention
      • National Center for Emerging and Zoonotic Infectious Diseases
      Druid Hills, GA, United States
  • 1992
    • Georgia State University
      • Department of Biology
      Atlanta, GA, United States
  • 1988
    • Justus-Liebig-Universität Gießen
      • Institut für Virologie
      Gieben, Hesse, Germany