R C Gallo

University of Maryland, Baltimore, Baltimore, Maryland, United States

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Publications (936)10742.06 Total impact

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    ABSTRACT: Rhesus macaques were vaccinated with rhFLSC targeting HIV CD4i envelope epitopes.•Strong mucosal and systemic cellular and humoral immune responses were induced.•Protective neutralizing antibody levels did not prevent SHIVSF162P4 acquisition.•Memory T and B cells declined rapidly post-challenge with delayed anamnestic response.•Different vector/adjuvant pairing might foster persistent T- and B-cell immune memory.
    Virology. 12/2014; 471.
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    ABSTRACT: Background and aims: Hydrogen sulfide (H2S), together with nitric oxide (NO) and carbon monoxide (CO), belongs to a family of endogenous signaling mediators termed "gasotransmitters". Recent studies suggest that H2S modulates many cellular processes and it has been recognized to play a central role in inflammation, in the cardiovascular and nervous systems. By infecting monocytes/macrophages with Mycoplasma fermentans (M.F.), a well-known pro-inflammatory agent, we evaluated the effects of H2S.
    Journal of translational medicine. 05/2014; 12(1):145.
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    ABSTRACT: Shortly after the discovery of human herpesvirus 6 (HHV-6), two distinct variants, HHV-6A and HHV-6B, were identified. In 2012, the International Committee on Taxonomy of Viruses (ICTV) classified HHV-6A and HHV-6B as separate viruses. This review outlines several of the documented epidemiological, biological, and immunological distinctions between HHV-6A and HHV-6B, which support the ICTV classification. The utilization of virus-specific clinical and laboratory assays for distinguishing HHV-6A and HHV-6B is now required for further classification. For clarity in biological and clinical distinctions between HHV-6A and HHV-6B, scientists and physicians are herein urged, where possible, to differentiate carefully between HHV-6A and HHV-6B in all future publications.
    Archives of Virology 11/2013; · 2.28 Impact Factor
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    ABSTRACT: Human Immunodeficiency Virus Type I (HIV-1) infection is associated with a high incidence of B-cell lymphomas. The role of HIV in these lymphomas is unclear and currently there are no valid in vivo models for better understanding HIV-related lymphomagenesis. Transgenic (Tg) 26 mice have a 7.4-kb pNL4-3 HIV-1 provirus lacking a 3.1-kb sequence encompassing parts of the gag-pol region. Approximately 15% of these HIV Tg mice spontaneously develop lymphoma with hallmark pre-diagnostic markers including skin lesions, diffuse lymphadenopathy and an increase in pro-inflammatory serum cytokines. Here we describe the phenotypic and molecular characteristics of the B cell leukemia/lymphoma in the Tg mice. The transformed B cell population consists of CD19+pre-BCR+CD127+CD43+CD93+ precursor B cells. The tumor cells are clonal and characterized by an increased expression of several cellular oncogenes. Expression of B cell-stimulatory cytokines IL-1beta, IL-6, IL-10, IL-12p40, IL-13 and TNFalpha and HIV proteins p17, gp120 and nef were elevated in the Tg mice with lymphoma. Increased expression of HIV proteins and the B-cell stimulatory factors is consistent with the interpretation that one or more of these factors play a role in lymphoma development. The lymphomas share many similarities with those occurring in HIV/AIDS+ patients and may provide a valuable model for understanding AIDS-related lymphomagenesis and elucidating the role played by HIV-1.
    Retrovirology 08/2013; 10(1):92. · 5.66 Impact Factor
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    ABSTRACT: The HIV-1 envelope glycoprotein (Env) undergoes conformational transitions consequent to CD4 binding and coreceptor engagement during viral entry. The physical steps in this process are becoming defined, but less is known about their significance as targets of antibodies potentially protective against HIV-1 infection. Here we probe the functional significance of transitional epitope exposure by characterizing 41 human mAbs specific for epitopes exposed on trimeric Env after CD4 engagement. These mAbs recognize three epitope clusters: cluster A, the gp120 face occluded by gp41 in trimeric Env; cluster B, a region proximal to the coreceptor-binding site (CoRBS) and involving the V1/V2 domain; and cluster C, the coreceptor-binding site. The mAbs were evaluated functionally by antibody-dependent, cell-mediated cytotoxicity (ADCC) and for neutralization of Tiers 1 and 2 pseudoviruses. All three clusters included mAbs mediating ADCC. However, there was a strong potency bias for cluster A, which harbors at least three potent ADCC epitopes whose cognate mAbs have electropositive paratopes. Cluster A epitopes are functional ADCC targets during viral entry in an assay format using virion-sensitized target cells. In contrast, only cluster C contained epitopes that were recognized by neutralizing mAbs. There was significant diversity in breadth and potency that correlated with epitope fine specificity. In contrast, ADCC potency had no relationship with neutralization potency or breadth for any epitope cluster. Thus, Fc-mediated effector function and neutralization coselect with specificity in anti-Env antibody responses, but the nature of selection is distinct for these two antiviral activities.
    Proceedings of the National Academy of Sciences 12/2012; · 9.81 Impact Factor
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    ABSTRACT: T-cell-derived soluble factors that inhibit both X4 and R5 HIV are recognized as important in controlling HIV. Whereas three β chemokines, regulated-on-activation normal T-cell expressed and secreted (RANTES), macrophage inflammatory protein (MIP)-1α, and MIP-1β, account for the suppression of R5 HIV by blockade of HIV entry, the major components responsible for the inhibition of X4 HIV strains have not been identified previously. We identify these factors primarily as a mixture of three β chemokines [macrophage-derived chemokine (MDC), thymus and activation-regulated chemokine (TARC), and I-309] and two RNases (angiogenin and RNase 4) of lesser potency and show that in a clade B population, some correlate with clinical status and are produced by both CD4(+) and CD8(+) T cells (chemokines, angiogenin) or only by CD8(+) T cells (RNase 4). The antiviral mechanisms of these HIV X4-suppressive factors differ from those of the previously described HIV R5-suppressive β chemokines.
    Proceedings of the National Academy of Sciences 03/2012; 109(14):5411-6. · 9.81 Impact Factor
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    ABSTRACT: Anticytokine (AC) immune therapies derived from vaccine procedures aim at enhancing natural immune defense mechanisms ineffective to contain abnormally produced cytokines and counteract their pathogenic effects. Given their short half-life, cytokines, the production of which by effector immune cells (T and B lymphocytes, antigen-presenting cells (APCs), natural killer (NK) and endothelial cells) is inducible and controlled by negative feedback regulation, (1) exert locally their signaling to paracrine/autocrine target responder cells carrying high-affinity membrane receptors and (2) are commonly present at minimal concentration in the body fluid (lymph, serum). Aberrant signaling triggered by cytokines, uncontrolly released by effector immune cells or produced by cancer and other pathologic cells, contribute to the pathogenesis of chronic diseases including cancer, viral infections, allergy, and autoimmunity. To block these ectopic cytokine signaling and prevent their pathogenic effects, AC Abs supplied either by injections (passive AC immune therapy) or elicited by immunization with cytokine-derived immunogenes called Kinoids (active AC immune therapy) proved to be experimentally effective and safe. In this review, we detailed the rationale and the requirements for the use of AC immunotherapies in humans, the proof of efficacy of these medications in animal disease models, and their current clinical development and outcome, including adverse side effects they may generate. We particularly show that, to date, the benefit:risk ratio of AC immune therapies is highly positive.
    Advances in Immunology 01/2012; 115:187-227. · 7.26 Impact Factor
  • Robert C Gallo
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    ABSTRACT: Human T-cell lymphoma virus (HTLV)-1 was the first human retrovirus to be discovered. It has been recognized as the cause of adult T-cell leukemia (ATL). In addition to giving a historical perspective on HTLV-1 and other retrovirus research, this paper discusses the origin of HTLV-1; the modes of transmission and global epidemiology of HTLV-1 infection; the genome of HTLV-1 and the mechanism of HTLV-1-induced leukemogenesis; the role of HTLV-1 in other diseases, and recent breakthroughs in ATL therapy.
    Best practice & research. Clinical haematology 12/2011; 24(4):559-65. · 3.13 Impact Factor
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    ABSTRACT: Immune suppressive activities exerted by regulatory T-cell subsets have several specific functions, including self-tolerance and regulation of adaptive immune reactions, and their dysfunction can lead to autoimmune diseases and contribute to AIDS and cancer. Two functionally distinct regulatory T-cell subsets are currently identified in peripheral tissues: thymus-developed natural T regulatory cells (nTregs) controlling self-tolerance and antiinflammatory IL-10-secreting type 1 regulatory T cells (Tr1) derived from Ag-stimulated T cells, which regulate inflammation-dependent adaptive immunity and minimize immunopathology. We establish herein that cell contact-mediated nTreg regulatory function is inhibited by inflammation, especially in the presence of the complement C3b receptor (CD46). Instead, as with other T-cell subsets, the latter inflammatory conditions of stimulation skew nTreg differentiation to Tr1 cells secreting IL-10, an effect potentiated by IFN-α. The clinical relevance of these findings was verified in a study of 152 lupus patients, in which we showed that lupus nTreg dysfunction is not due to intrinsic defects but is rather induced by C3b stimulation of CD46 and IFN-α and that these immune components of inflammation are directly associated with active lupus. These results provide a rationale for using anti-IFN-α Ab immunotherapy in lupus patients.
    Proceedings of the National Academy of Sciences 11/2011; 108(47):18995-9000. · 9.81 Impact Factor
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    ABSTRACT: Maraviroc, the only CCR5 antagonist HIV inhibitor currently approved, has potent antiviral activity in treatment-experienced individuals infected with CCR5-using HIV-1 (R5 HIV-1). However, recent data from the MOTIVATE trials indicate that R5 HIV-1 can develop resistance to Maraviroc, underscoring the need for additional CCR5 antagonists. The CCR5 antagonist aplaviroc (APL) is active against Maraviroc-resistant viral strains but its clinical development has ended because of dose-related toxicity. Here we demonstrate that reduction of CCR5 density (receptors/cell) with the immunomodulatory drug rapamycin (RAPA) enhances the antiviral activity of APL, allowing lower, non-toxic effective doses. In the presence of RAPA, the concentration of APL required for 90% inhibition of R5 HIV-1 in primary CD4 lymphocytes was reduced by as much as 25-fold. We conclude that low doses of RAPA may reduce the anti-HIV effective dose of APL-derivatives currently in development and thus minimize their potential toxicity. Combinations of RAPA and CCR5 antagonists could provide an effective means to control drug-resistant R5 HIV in patients, most notably those infected with Maraviroc-resistant viruses.
    Antiviral research 08/2009; 83(1):86-9. · 3.61 Impact Factor
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    ABSTRACT: Progression to AIDS is often associated with the evolution of HIV-1 toward increased virulence and/or pathogenicity. Evidence suggests that a virulence factor for HIV-1 is resistance to CCR5-binding chemokines, most notably RANTES, which are believed to play a role in HIV-1 control in vivo. HIV-1 can achieve RANTES resistance either by phenotypic switching from an exclusive CCR5 usage to an expanded coreceptor specificity, or by the acquisition of alternative modalities of CCR5 usage. An infectious agent that might promote the evolution of HIV-1 toward RANTES resistance is human herpesvirus 6A (HHV-6A), which is frequently reactivated in HIV-1-infected patients and is a potent RANTES inducer in lymphoid tissue. SIV isolates obtained from pig-tailed macaques (M. nemestrina) after approximately one year of single infection with SIV(smE660) or dual infection with SIV(smE660) and HHV-6A(GS) were characterized for their growth capacity and sensitivity to HHV-6A- and RANTES-mediated inhibition in human or macaque lymphoid tissues ex vivo. Four out of 4 HHV-6A-coinfected macaques, all of which progressed to full-blown AIDS within 2 years of infection, were found to harbor SIV variants with a reduced sensitivity to both HHV-6A and RANTES, despite maintaining an exclusive CCR5 coreceptor specificity; viruses derived from two of these animals replicated even more vigorously in the presence of exogenous HHV-6A or RANTES. The SIV variants that emerged in HHV-6A-coinfected macaques showed an overall reduced ex vivo replication capacity that was partially reversed upon addition of exogenous RANTES, associated with suppressed IL-2 and enhanced IFN-gamma production. In contrast, SIV isolates obtained from two singly-infected macaques, none of which progressed to AIDS, maintained HHV-6A/RANTES sensitivity, whereas the only AIDS progressor among singly-infected macaques developed an SIV variant with partial HHV-6A/RANTES resistance and increased replication capacity, associated with expanded coreceptor usage. These results provide in vivo evidence of SIV evolution toward RANTES resistance in macaques rapidly progressing to AIDS. RANTES resistance may represent a common virulence factor allowing primate immunodeficiency retroviruses to evade a critical mechanism of host antiviral defense.
    Retrovirology 08/2009; 6:61. · 5.66 Impact Factor
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    ABSTRACT: A major involvement of IFNalpha in the etiopathogenesis of systemic lupus erythematosus has been suggested by clinical observations, including the increase of serum levels of this cytokine in patients with active disease. Supporting this hypothesis, we have shown that expression of IFNalpha from a recombinant adenovirus (IFNalpha Adv) precipitates lupus manifestations in genetically susceptible New Zealand Black (NZB) x New Zealand White (NZW)F(1) mice (NZB/W) but not in BALB/c mice. In the present investigation, we have prepared an IFNalpha immunogen, termed IFNalpha kinoid, which, appropriately adjuvanted, induces transient neutralizing antibodies (Abs) but no cellular immune response to the cytokine and without apparent side effects. Using this preparation, we also showed that, in kinoid-vaccinated NZB/W mice, lupus manifestations, including proteinuria, histological renal lesions, and death triggered by IFNalpha Adv challenge were delayed/prevented as long as an effective threshold of anti-IFNalpha inhibitory capacity was present in the serum.
    Proceedings of the National Academy of Sciences 04/2009; 106(13):5294-9. · 9.81 Impact Factor
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    ABSTRACT: Long-lived memory B cells (B(Mem)) provide an archive of historic Ab responses. By contrast, circulating Abs typically decline once the immunogen is cleared. Consequently, circulating Abs can underestimate the nature of cognate humoral immunity. On the other hand, the B(Mem) pool should provide a comprehensive picture of Ab specificities that arise over the entire course of infection. To test this hypothesis, we compared circulating Ab and B(Mem) from natural virus suppressors who control HIV-1 without therapy and maintain a relatively intact immune system. We found high frequencies of B(Mem) specific for the conserved neutralizing CD4 induced or CD4 binding site epitopes of gp120, whereas low Ab titers to these determinants were detected in contemporaneous plasma. These data suggest that plasma Ab repertoires can underestimate the breadth of humoral immunity, and analyses of B(Mem) should be included in studies correlating Ab specificity with protective immunity to HIV-1.
    Proceedings of the National Academy of Sciences 03/2009; 106(10):3952-7. · 9.81 Impact Factor
  • JAIDS Journal of Acquired Immune Deficiency Syndromes 01/2009; 51. · 4.65 Impact Factor
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    ABSTRACT: Vicriviroc (VCV) is a chemokine (C-C motif) receptor 5 (CCR5) antagonist with potent anti-HIV activity that currently is being evaluated in phase III clinical trials. In the present study, donor CCR5 density (CCR5 receptors/CD4 lymphocytes) inversely correlated with VCV antiviral activity (Spearman's correlation test; r = 0.746, P = 0.0034). Low doses of the transplant drug rapamycin (RAPA) reduced CCR5 density and enhanced VCV antiviral activity. In drug interaction studies, the RAPA/VCV combination had considerable antiviral synergy (combination indexes of 0.1-0.04) in both multicycle and single-cycle infection of lymphocytes. The synergy between RAPA and VCV translated into dose reduction indexes of 8- to 41-fold reductions for RAPA and 19- to 658-fold reductions for VCV. RAPA enhanced VCV antiviral activity against both B and non-B clade isolates, potently suppressing clade G viruses with reported reduced sensitivities to VCV and to the licensed CCR5 antagonist maraviroc. Importantly, RAPA reduction of CCR5 density in lymphocytes sensitized VCV-resistant strains to VCV, inhibiting virus production by approximately 90%. We further demonstrated the role of CCR5 density on VCV activity against resistant virus in donor lymphocytes and in cell lines expressing varying CCR5 densities. Together, these results suggest that low doses of RAPA may increase the durability of VCV-containing regimens in patients by enhancing VCV viral suppression, by allowing the use of lower doses of VCV with reduced potential for toxicity, and by controlling emerging VCV-resistant variants.
    Proceedings of the National Academy of Sciences 01/2009; 105(51):20476-81. · 9.81 Impact Factor
  • JAIDS Journal of Acquired Immune Deficiency Syndromes 01/2009; 51. · 4.65 Impact Factor
  • JAIDS Journal of Acquired Immune Deficiency Syndromes 01/2009; 51. · 4.65 Impact Factor
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    ABSTRACT: We have recently shown that human immunodeficiency virus type 1 (HIV-1) Pr55(gag) virus-like particles (HIV-VLPs), produced in a baculovirus expression system and presenting a gp120 molecule from a Ugandan HIV-1 isolate of clade A, induce maturation and activation of monocyte-derived dendritic cells (MDDCs) with a production of Th1- and Th2-specific cytokines. Furthermore, HIV-VLP-loaded MDDCs are able to induce a primary and secondary response in autologous human CD4(+) T cells in an ex vivo immunization assay. In the present study, we show that similar data can be obtained directly with fresh peripheral blood mononuclear cells (PBMCs), and the HIV-1 seropositivity status, with either low or high viremia, does not significantly impair the immune activation status and the responsiveness of circulating monocyte CD14(+) cell populations to an immunogenic stimulus. Some HIV-1-seropositive subjects, however, show a complete lack of maturation induced by HIV-VLPs in CD14(+) circulating cells, which does not consistently correlate with an advanced status of HIV-1 infection. The established Th2 polarization in both HIV-seropositive groups is efficiently boosted by HIV-VLP induction and does not switch into a Th1 pattern, strongly suggesting that specific Th1 adjuvants would be required for therapeutic effectiveness in HIV-1-infected subjects. These results indicate the possibility of screening PBMCs for donor susceptibility to an immunogen treatment, which would greatly simplify the identification of "responsive" vaccinees as well as the understanding of eventual failures in individuals enrolled in clinical trials.
    Journal of Virology 11/2008; 83(1):304-13. · 5.08 Impact Factor
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    A. M. Wu, R. C. Gallo, J. Schlom
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    ABSTRACT: Abstract Recognition of RNA tumor viruses as causative agents of malignant disease started with the observation (by Ellerman and Bang in 1908) that a filterable agent transmitted avian leukemia1 and the subsequent isolation of chicken sarcoma virus by Rous in 1911.2 These findings were followed by an intense and continuous search for new isolates, the establishment of inbred strains of mice, and the development of tissue culture techniques. In the early 1960s, the significance of RNA tumor viruses was generally accepted, especially in avian and murine systems, but with some skepticism, probably because its role in natural disease was not yet evident. Moreover, the mode of replication of the RNA tumor viruses was still not understood. In recent years, the study of these viruses markedly intensified, principally because of a discovery which filled a major gap in the understanding of their replication. This is the independent discovery of the viral RNA-dependent DNA polymerase (reverse transcriptase) by Temin and Mizutani3 and by Baltimore4 in 1970. This discovery also extended our understanding of the mode of genetic information transfer, and it paved the way for the finding of viral-related components, reverse transcriptase5-11 and type-C viral related nucleic acids in human leukemic cells by Gallo, Spiegelman, and their co-workers (see later section10,12-17).
    09/2008; 3(3):289-347.
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    ABSTRACT: The role of plasmacytoid dendritic cells (pDC) and interferon alpha (IFN alpha) in HIV-1 infection is still unclear. On one hand, HIV-1 disease is associated with a progressive decline of pDC, which displays reduced ability to produce IFN alpha after in vitro challenge. On the other hand, high IFN alpha serum levels in HIV-1-infected individuals have been proposed to promote immune hyper-activation and disease progression. We sought to determine whether disappearance of pDC in HIV-1 disease is due to homing in lymphoid tissues. We also studied IFN alpha and myxovirus resistance protein A (MxA) expression in unstimulated pDC and correlated these results with selected clinical and laboratory parameters. We found that pDC decline markedly in peripheral blood of patients progressing to disease but at the same time express much higher levels of IFN alpha and MxA compared to control individuals. On the other hand, we observed steady pDC counts in lymph nodes of HIV-1 patients. The frequency of circulating pDC correlated directly with CD4 cell counts and inversely with viral load. However, we found no correlation between IFN alpha and MxA expression levels, CD4 counts, and viral load. Circulating pDC decline sharply in the course of HIV-1 disease, but express high levels of IFN alpha, which may represent a hallmark of systemic immune dysfunction.
    JAIDS Journal of Acquired Immune Deficiency Syndromes 08/2008; 48(5):522-30. · 4.65 Impact Factor

Publication Stats

58k Citations
10,742.06 Total Impact Points


  • 1996–2014
    • University of Maryland, Baltimore
      • Institute of Human Virology
      Baltimore, Maryland, United States
  • 2012
    • Institute of Human Virology
      Suleija, Niger, Nigeria
  • 2008–2011
    • French Institute of Health and Medical Research
      Lutetia Parisorum, Île-de-France, France
  • 2000–2009
    • University of Maryland Medical Center
      • Institute for Human Virology
      Baltimore, Maryland, United States
    • University of Wisconsin, Madison
      • Department of Pathology and Laboratory Medicine
      Madison, MS, United States
    • Johns Hopkins Medicine
      • Department of Neurology
      Baltimore, Maryland, United States
  • 2006–2008
    • Istituto Nazionale Tumori "Fondazione Pascale"
      Napoli, Campania, Italy
  • 1967–2008
    • National Institutes of Health
      • • Center for Clinical Research
      • • Laboratory of Cell Biology
      • • Basic Research Laboratory
      • • Critical Care Medicine Department
      Maryland, United States
  • 2007
    • San Raffaele Scientific Institute
      Milano, Lombardy, Italy
  • 2005–2006
    • University of Maryland, College Park
      • Department of Microbiology and Immunology
      Maryland, United States
    • Bernhard Nocht Institute for Tropical Medicine
      Hamburg, Hamburg, Germany
    • University Hospital Frankfurt
      Frankfurt, Hesse, Germany
  • 1969–2006
    • National Cancer Institute (USA)
      • • Laboratory of Cell Biology
      • • Basic Research Laboratory
      • • Developmental Therapeutics Program
      Maryland, United States
  • 1999–2005
    • Institute of Human Virology
      Maryland City, Maryland, United States
    • Istituto Superiore di Sanità
      • Laboratory of Virology
      Roma, Latium, Italy
  • 1987–2004
    • Pierre and Marie Curie University - Paris 6
      • Unité de recherche : Physiologie, Physiopathologie et. Vieillissement (UMR 7079)
      Lutetia Parisorum, Île-de-France, France
    • Duke University Medical Center
      • Department of Surgery
      Durham, NC, United States
    • Washington University in St. Louis
      • Division of Hematology and oncology
      Saint Louis, MO, United States
  • 2002
    • University of Baltimore
      Baltimore, Maryland, United States
  • 1996–2001
    • Loyola University Maryland
      Baltimore, Maryland, United States
  • 1998–1999
    • CILEA Interuniversity Consortium
      Segrate, Lombardy, Italy
    • Lund University
      Lund, Skåne, Sweden
    • Laval University
      Québec, Quebec, Canada
    • New York University
      New York City, New York, United States
    • Sapienza University of Rome
      Roma, Latium, Italy
    • AIDS Community Research Initiative of America
      New York City, New York, United States
  • 1997–1999
    • Universita degli studi di Ferrara
      • Department of Morphology, Surgery and Experimental Medicine
      Ferrara, Emilia-Romagna, Italy
  • 1992–1998
    • University of Southern California
      Los Angeles, California, United States
  • 1985–1996
    • National Eye Institute
      Maryland, United States
    • Dana-Farber Cancer Institute
      Boston, Massachusetts, United States
    • Vrije Universiteit Brussel
      Bruxelles, Brussels Capital Region, Belgium
    • University of Helsinki
      Helsinki, Southern Finland Province, Finland
    • Kyoto University
      • Institute for Virus Research
      Kioto, Kyōto, Japan
    • Massachusetts Department of Public Health
      Boston, Massachusetts, United States
  • 1995
    • National Heart, Lung, and Blood Institute
      • Hematology Branch
      Bethesda, MD, United States
  • 1993
    • University College Hospital Ibadan
      Ibadan, Oyo, Nigeria
  • 1991–1993
    • Advanced BioScience Laboratories Inc.
      Maryland, United States
    • National Institute of Allergy and Infectious Diseases
      • Laboratory of Immunoregulation
      Maryland, United States
  • 1990
    • Institut Jean-Godinot
      Rheims, Champagne-Ardenne, France
  • 1988–1990
    • Leidos Biomedical Research
      Maryland, United States
    • Walter Reed Army Institute of Research
      Silver Spring, Maryland, United States
    • Karolinska Institutet
      Solna, Stockholm, Sweden
  • 1989
    • University of Tampere
      • Institute of Biomedical Sciences
      Tampere, Western Finland, Finland
  • 1988–1989
    • NCI-Frederick
      Maryland, United States
  • 1979
    • Memorial Sloan-Kettering Cancer Center
      New York City, New York, United States