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ROCKVILLE, Md.--(BUSINESS WIRE)--John C. Landon, Ph.D., founded BIOQUAL in 1982. He led BIOQUAL for more than 30 years as President and Chief Executive Officer and grew BIOQUAL to become a $20M+ life sciences corporation. He retired as Chief Executive Officer on June 13, 2013, and was succeeded by Dr. Mark G. Lewis, BIOQUAL’s President. Dr. Landon remained as Chairman of the Board of Directors. Effective April 19, 2017, Dr. Landon retired as Chairman of the Board of Directors and as a member of the Board of Directors. Dr. Lewis, was appointed to succeed Dr. Landon as Chairman of the Board. Also on April 19, 2017, the Board of Directors elected David B. Landon, Ph.D., to fill the vacancy on the Board of Directors resulting from the retirement of Dr. John C. Landon. Dr. Lewis joined BIOQUAL as Senior Scientist in August 2003. He became the Executive Vice President in October 2008, and served in that capacity until he became President in 2010. Dr. Lewis, 62, received his B.A. (1977) degree from Ohio Wesleyan University and his Masters (1980) and Ph.D. (1983) degrees from Ohio State University, Department of Veterinary Pathology. He performed his post-doctoral studies (1983-1984) in the OSU Department of Pharmacology, and continued at OSU as a Research Associate until 1988. From 1988-1991, he was a Staff Virologist at the Southern Research Institute, Frederick, Maryland. From 1991 to 1998, he was a Principal Scientist for the Henry M. Jackson Foundation, Rockville, Maryland. In 1999, Dr. Lewis rejoined the Southern Research Institute as a Staff Scientist, and in 2002 was appointed Acting Director, Senior Scientist. Since joining BIOQUAL in 2003, Dr. Lewis has been the primary driver of BIOQUAL’s growth in the area of viral infectious diseases and has attracted to BIOQUAL several new commercial and government clients. He led the Company in its acquisition of the in-vivo animal model services -related assets from, and entry into a Strategic Teaming Agreement with Advanced Bioscience Laboratories, Inc. (ABL) in 2014. Dr. David Landon was appointed in 2003 as the Associate Director of the Andrew Fiske Memorial Center for Archaeological Research and an Adjunct Associate Professor in the Department of Anthropology at University of Massachusetts Boston, having served as a Senior Scientist in the Fiske Center from 2000 to 2002. He received his Ph.D. in 1991 from Boston University, and his B.A. in Economics in 1985 from Wesleyan University. He was an Associate Professor, Department of Social Sciences, Michigan Technological University; a Postdoctoral Research Fellow, Department of Anthropology, Smithsonian Institution in 1997-98; and Assistant Professor, Department of Social Sciences, Michigan Technological University in 1991-97. He has published in more than a dozen journals and has received funding for projects supported by the National Science Foundation, National Endowment for the Humanities, USDA Forest Service, National Park Service, Smithsonian, and other government and private sources. In his capacity as the Associate Director of the Fiske Center for Archaeological Research Dr. David Landon has primary responsibility for financial oversight of the Center’s expenditures, including research project budgets and the disbursements from the Center’s endowment. Dr. David Landon is 54 years old, and is a son of BIOQUAL’s founder, John C. Landon. He will be compensated at the same rate that the other BIOQUAL directors are compensated, currently $4,500 per quarter and $1,500 per meeting. Statements herein that are not descriptions of historical facts are forward-looking and subject to risk and uncertainties. Actual results could differ materially from those currently anticipated due to a number of factors including risks relating to the ability to continue to extend current government contracts and obtain new contracts; the Company’s ability to obtain new commercial contracts; the performance of the business acquired in the ABL acquisition; the Company’s ability to perform under its contracts in accordance with the requirements of the contracts; the actual cost incurred in performing its contracts and the Company’s ability to manage its costs; dependence on third parties; future capital needs; the ability to fund its capital needs through the use of its cash on hand and line of credit; and the future availability and cost of financing/capital sources to the Company.


Barouch D.H.,Beth Israel Deaconess Medical Center | Barouch D.H.,Massachusetts Institute of Technology | Whitney J.B.,Beth Israel Deaconess Medical Center | Moldt B.,Scripps Research Institute | And 25 more authors.
Nature | Year: 2013

Human immunodeficiency virus type 1 (HIV-1)-specific monoclonal antibodies with extraordinary potency and breadth have recently been described. In humanized mice, combinations of monoclonal antibodies have been shown to suppress viraemia, but the therapeutic potential of these monoclonal antibodies has not yet been evaluated in primates with an intact immune system. Here we show that administration of a cocktail of HIV-1-specific monoclonal antibodies, as well as the single glycan-dependent monoclonal antibody PGT121, resulted in a rapid and precipitous decline of plasma viraemia to undetectable levels in rhesus monkeys chronically infected with the pathogenic simian-human immunodeficiency virus SHIV-SF162P3. A single monoclonal antibody infusion afforded up to a 3.1 log decline of plasma viral RNA in 7 days and also reduced proviral DNA in peripheral blood, gastrointestinal mucosa and lymph nodes without the development of viral resistance. Moreover, after monoclonal antibody administration, host Gag-specific T-lymphocyte responses showed improved functionality. Virus rebounded in most animals after a median of 56 days when serum monoclonal antibody titres had declined to undetectable levels, although, notably, a subset of animals maintained long-term virological control in the absence of further monoclonal antibody infusions. These data demonstrate a profound therapeutic effect of potent neutralizing HIV-1-specific monoclonal antibodies in SHIV-infected rhesus monkeys as well as an impact on host immune responses. Our findings strongly encourage the investigation of monoclonal antibody therapy for HIV-1 in humans. © 2013 Macmillan Publishers Limited. All rights reserved.


Purcell R.H.,U.S. National Institutes of Health | Engle R.E.,U.S. National Institutes of Health | Kabrane-Lazizi Y.,U.S. National Institutes of Health | Nguyen H.T.,U.S. National Institutes of Health | And 4 more authors.
Emerging Infectious Diseases | Year: 2011

The role of rats in human hepatitis E virus (HEV) infections remains controversial. A genetically distinct HEV was recently isolated from rats in Germany, and its genome was sequenced. We have isolated a genetically similar HEV from urban rats in Los Angeles, California, USA, and characterized its ability to infect laboratory rats and nonhuman primates. Two strains of HEV were isolated from serum samples of 134 wild rats that had a seroprevalence of antibodies against HEV of ≈80%. Virus was transmissible to seronegative Sprague-Dawley rats, but transmission was spotty and magnitude and duration of infection were not robust. Viremia was higher in nude rats. Serologic analysis and reverse transcription PCR were comparably sensitive in detecting infection. The sequence of the Los Angeles virus was virtually identical to that of isolates from Germany. Rat HEV was not transmissible to rhesus monkeys, suggesting that it is not a source of human infection.


Lugli E.,National Institute of Allergy and Infectious Diseases | Mueller Y.M.,Drexel University | Lewis M.G.,BIOQUAL Inc. | Villinger F.,Emory University | And 3 more authors.
Blood | Year: 2011

Human immunodeficiency virus (HIV) infection is characterized by a progressive loss of memory CD4+ T cells in multiple tissues, especially at mucosal surfaces where most of these cells reside. Although antiretroviral therapy (ART) suppresses viral replication and promotes the recovery of peripheral CD4+ T cells, HIV-infected patients fail to fully reconstitute the CD4+ T-cell pool at mucosal sites. IL-15 has been shown to preferentially expand memory-phenotype T cells and promote their migration to nonlymphoid tissues. Here we examined IL-15 treatment in combination with highly active ART in chronically SIV-infected rhesus macaques and found that IL-15 delayed viral suppression and failed to enhance ART-induced total and antigen-specific CD4+ T-cell reconstitution at mucosal and lymphoid sites. IL-15 was able to induce the transient proliferation of SIV-specific, CMV-specific, and total memory CD8+ T cells, but not of SIV-specific or total CD4+ T cells. Moreover, upon treatment interruption, macaques receiving combined IL-15+ART lost CD4+ T cells faster than those receiving ART alone. These results suggest that the combination of IL-15 with highly active ART is not more efficient than ART alone in promoting CD4+ T-cell recovery in HIV-infected individuals and may accelerate CD4+ T-cell loss after treatment interruption. © 2011 by The American Society of Hematology.


Rao S.S.,National Institute of Allergy and Infectious Diseases | Kong W.-P.,National Institute of Allergy and Infectious Diseases | Wei C.-J.,National Institute of Allergy and Infectious Diseases | Van Hoeven N.,Centers for Disease Control and Prevention | And 5 more authors.
PLoS ONE | Year: 2010

Efforts to develop a broadly protective vaccine against the highly pathogenic avian influenza A (HPAI) H5N1 virus have focused on highly conserved influenza gene products. The viral nucleoprotein (NP) and ion channel matrix protein (M2) are highly conserved among different strains and various influenza A subtypes. Here, we investigate the relative efficacy of NP and M2 compared to HA in protecting against HPAI H5N1 virus. In mice, previous studies have shown that vaccination with NP and M2 in recombinant DNA and/or adenovirus vectors or with adjuvants confers protection against lethal challenge in the absence of HA. However, we find that the protective efficacy of NP and M2 diminishes as the virulence and dose of the challenge virus are increased. To explore this question in a model relevant to human disease, ferrets were immunized with DNA/rAd5 vaccines encoding NP, M2, HA, NP+M2 or HA+NP+M2. Only HA or HA+NP+M2 vaccination conferred protection against a stringent virus challenge. Therefore, while gene-based vaccination with NP and M2 may provide moderate levels of protection against low challenge doses, it is insufficient to confer protective immunity against high challenge doses of H5N1 in ferrets. These immunogens may require combinatorial vaccination with HA, which confers protection even against very high doses of lethal viral challenge.


Fraietta J.A.,Drexel University | Mueller Y.M.,Drexel University | Yang G.,Drexel University | Boesteanu A.C.,Drexel University | And 9 more authors.
PLoS Pathogens | Year: 2013

The role of Type I interferon (IFN) during pathogenic HIV and SIV infections remains unclear, with conflicting observations suggesting protective versus immunopathological effects. We therefore examined the effect of IFNα/β on T cell death and viremia in HIV infection. Ex vivo analysis of eight pro- and anti-apoptotic molecules in chronic HIV-1 infection revealed that pro-apoptotic Bak was increased in CD4+ T cells and correlated directly with sensitivity to CD95/Fas-mediated apoptosis and inversely with CD4+ T cell counts. Apoptosis sensitivity and Bak expression were primarily increased in effector memory T cells. Knockdown of Bak by RNA interference inhibited CD95/Fas-induced death of T cells from HIV-1-infected individuals. In HIV-1-infected patients, IFNα-stimulated gene expression correlated positively with ex vivo T cell Bak levels, CD95/Fas-mediated apoptosis and viremia and negatively with CD4+ T cell counts. In vitro IFNα/β stimulation enhanced Bak expression, CD95/Fas expression and CD95/Fas-mediated apoptosis in healthy donor T cells and induced death of HIV-specific CD8+ T cells from HIV-1-infected patients. HIV-1 in vitro sensitized T cells to CD95/Fas-induced apoptosis and this was Toll-like receptor (TLR)7/9- and Type I IFN-dependent. This sensitization by HIV-1 was due to an indirect effect on T cells, as it occurred in peripheral blood mononuclear cell cultures but not purified CD4+ T cells. Finally, peak IFNα levels and viral loads correlated negatively during acute SIV infection suggesting a potential antiviral effect, but positively during chronic SIV infection indicating that either the virus drives IFNα production or IFNα may facilitate loss of viral control. The above findings indicate stage-specific opposing effects of Type I IFNs during HIV-1 infection and suggest a novel mechanism by which these cytokines contribute to T cell depletion, dysregulation of cellular immunity and disease progression. © 2013 Fraietta et al.


Tebas P.,University of Pennsylvania | Frank I.,University of Pennsylvania | Lewis M.,BIOQUAL Inc. | Quinn J.,University of Pennsylvania | And 7 more authors.
AIDS | Year: 2010

Objective: To evaluate the safety and immunogenicity of the H1N1 2009 vaccine in HIV-positive individuals. Design: A single-arm study. Setting: Clinic at the Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA. Participants: HIV-infected adults with an indication for H1N1 vaccination. Intervention: Single intramuscular 15 μg dose of the monovalent, unadjuvanted, inactivated, split virus H1N1 vaccine. Main outcomes: Immunogenicity, safety and tolerability. Results: A total of 120 participants were enrolled, 71% men, 68% African-American, with median age of 46 years. All of them but one were on antiretroviral treatment, with a median current CD4 cell counts of 502 cells/μl, and a nadir CD4 cell counts of 132 cells/μl. The HIV RNA level was below 400 copies/ml in 92% of participants. All participants completed the 3 weeks of follow-up. Thirty of the 120 (25%) participants had antibody hemagglutination-inhibition assay titers equal or greater than 1: 40 at baseline. Among participants without evidence of previous exposure, only 61% develop protective titers by week 3 of the study. Nonresponders had lower current and nadir CD4 cell counts than responders. Only four of nine participants with detectable HIV viral load at baseline developed protective antibody titers. Age and race were not predictors of the response to the vaccine. The vaccine was well tolerated. Conclusion: These results suggest that only 60% of well controlled HIV-infected individuals without preexisting immunity to H1N1 develop protective antibody titers after immunization. Alternative vaccines, dosing, adjuvants or schedule strategies are needed to achieve effective immunization of this vulnerable population. © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins.


Shytaj I.L.,Instituto Superiore Of Sanita | Norelli S.,Instituto Superiore Of Sanita | Chirullo B.,Instituto Superiore Of Sanita | Della Corte A.,Instituto Superiore Of Sanita | And 8 more authors.
PLoS Pathogens | Year: 2012

Stably suppressed viremia during ART is essential for establishing reliable simian models for HIV/AIDS. We tested the efficacy of a multidrug ART (highly intensified ART) in a wide range of viremic conditions (103-107 viral RNA copies/mL) in SIVmac251-infected rhesus macaques, and its impact on the viral reservoir. Eleven macaques in the pre-AIDS stage of the disease were treated with a multidrug combination (highly intensified ART) consisting of two nucleosidic/nucleotidic reverse transcriptase inhibitors (emtricitabine and tenofovir), an integrase inhibitor (raltegravir), a protease inhibitor (ritonavir-boosted darunavir) and the CCR5 blocker maraviroc. All animals stably displayed viral loads below the limit of detection of the assay (i.e. <40 RNA copies/mL) after starting highly intensified ART. By increasing the sensitivity of the assay to 3 RNA copies/mL, viral load was still below the limit of detection in all subjects tested. Importantly, viral DNA resulted below the assay detection limit (<2 copies of DNA/5*105 cells) in PBMCs and rectal biopsies of all animals at the end of the follow-up, and in lymph node biopsies from the majority of the study subjects. Moreover, highly intensified ART decreased central/transitional memory, effector memory and activated (HLA-DR+) effector memory CD4+ T-cells in vivo, in line with the role of these subsets as the main cell subpopulations harbouring the virus. Finally, treatment with highly intensified ART at viral load rebound following suspension of a previous anti-reservoir therapy eventually improved the spontaneous containment of viral load following suspension of the second therapeutic cycle, thus leading to a persistent suppression of viremia in the absence of ART. In conclusion, we show, for the first time, complete suppression of viral load by highly intensified ART and a likely associated restriction of the viral reservoir in the macaque AIDS model, making it a useful platform for testing potential cures for AIDS. © 2012 Shytaj et al.


Akahata W.,U.S. National Institutes of Health | Yang Z.-Y.,U.S. National Institutes of Health | Andersen H.,BIOQUAL Inc. | Sun S.,Purdue University | And 7 more authors.
Nature Medicine | Year: 2010

Chikungunya virus (CHIKV) has infected millions of people in Africa, Europe and Asia since this alphavirus reemerged from Kenya in 2004. The severity of the disease and the spread of this epidemic virus present a serious public health threat in the absence of vaccines or antiviral therapies. Here, we describe a new vaccine that protects against CHIKV infection of nonhuman primates. We show that selective expression of viral structural proteins gives rise to virus-like particles (VLPs) in vitro that resemble replication-competent alphaviruses. Immunization with these VLPs elicited neutralizing antibodies against envelope proteins from alternative CHIKV strains. Monkeys immunized with VLPs produced high-titer neutralizing antibodies that protected against viremia after high-dose challenge. We transferred these antibodies into immunodeficient mice, where they protected against subsequent lethal CHIKV challenge, indicating a humoral mechanism of protection. Immunization with alphavirus VLP vaccines represents a strategy to contain the spread of CHIKV and related pathogenic viruses in humans. © 2010 Nature America, Inc. All rights reserved.


Male hormonal contraceptive regimens are generally combinations of an androgen and a progestin which suppress gonadotropin secretion and, consequently, spermatogenesis. The activities of four synthetic progestins, levonorgestrel (LNG), norethindrone acetate (NETA), cyproterone acetate (CPA), and nestorone (NES), used in combination with testosterone for male hormonal contraception were compared in vitro and in vivo. In vitro assays (steroid hormone receptor binding and transactivation) focused on their relative androgenic vs progestational potencies. The relative androgenic potencies were LNG ≈ NETA > CPA > NES. Their order of potency as progestins was NES. > LNG > CPA ≈ NETA. A bioassay was developed using the castrate adult male rat to assess the activity of these progestins in vivo. Rats were treated with several doses (0.1-3.2. mg/kg/day) of LNG, NETA, CPA, or NES for 21 days, and blood was collected at various times for measurement of LH levels in serum. LH was suppressed to baseline by LNG at 0.8 and 1.6. mg/kg/day; NETA was effective at 3.2. mg/kg/day; and NES and CPA showed no or minimal LH suppression at doses up to 3.2. mg/kg/day. We concluded, therefore, that suppression of LH is correlated with androgenic, rather than progestational, potency of the synthetic progestins. © 2010 Elsevier Ireland Ltd.

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