BIOQUAL Inc.

Rockville, MD, United States

BIOQUAL Inc.

Rockville, MD, United States
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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.


Moore A.C.,Uniformed Services University of the Health Sciences | Bixler S.L.,Uniformed Services University of the Health Sciences | Lewis M.G.,BIOQUAL Inc. | Verthelyi D.,CDER | Mattapallil J.J.,Uniformed Services University of the Health Sciences
Journal of Virology | Year: 2012

Massive infection of memory CD4 T cells is a hallmark of early simian immunodeficiency virus (SIV) infection, with viral infection peaking at day 10 postinfection (p.i.), when a majority of memory CD4 T cells in mucosal and peripheral tissues are infected. It is not clear if mononuclear cells from the monocyte and macrophage lineages are similarly infected during this early phase of explosive HIV and SIV infections. Here we show that, at day 10 p.i., Lin - HLA-DR + CD11c/123 - CD13 + CD14 - macrophages in the jejunal mucosa were infected, albeit at lower levels than CD4 memory T cells. Interestingly, Lin - HLA-DR + CD11c/123 - CD13 + CD14 - macrophages in peripheral blood, like their mucosal counterparts, were preferentially infected compared to Lin - HLA-DR + CD11c/123 - CD13 + CD14 - monocytes, suggesting that differentiated macrophages were selectively infected by SIV. CD13 + CD14 - macrophages expressed low levels of CD4 compared to CD4 T cells but expressed similar levels of CCR5 as lymphocytes. Interestingly, CD13 + CD14 - macrophages expressed Apobec3G at lower levels than CD13 + CD14 + monocytes, suggesting that intracellular restriction may contribute to the differential infection of mononuclear subsets. Taken together, our results suggest that CD13 + CD14 - macrophages in mucosal and peripheral tissues are preferentially infected very early during the course of SIV infection. © 2012, American Society for Microbiology.


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.


Bok K.,National Institute of Allergy and Infectious Diseases | Parra G.I.,National Institute of Allergy and Infectious Diseases | Mitra T.,National Institute of Allergy and Infectious Diseases | Abente E.,National Institute of Allergy and Infectious Diseases | And 8 more authors.
Proceedings of the National Academy of Sciences of the United States of America | Year: 2011

Noroviruses are global agents of acute gastroenteritis, but the development of control strategies has been hampered by the absence of a robust animal model. Studies in chimpanzees have played a key role in the characterization of several fastidious hepatitis viruses, and we investigated the feasibility of such studies for the noroviruses. Seronegative chimpanzees inoculated i.v. with the human norovirus strain Norwalk virus (NV) did not show clinical signs of gastroenteritis, but the onset and duration of virus shedding in stool and serum antibody responses were similar to that observed in humans. NV RNA was detected in intestinal and liver biopsies concurrent with the detection of viral shedding in stool, and NV antigen expression was observed in cells of the small intestinal lamina propria. Two infected chimpanzees rechallenged 4, 10, or 24 mo later with NV were resistant to reinfection, and the presence of NV-specific serum antibodies correlated with protection. We evaluated the immunogenicity and efficacy of virus-like particles (VLPs) derived from NV (genogroup I, GI) and MD145 (genogroup II, GII) noroviruses as vaccines. Chimpanzees vaccinated intramuscularly with GI VLPs were protected from NV infection when challenged 2 and 18 mo after vaccination, whereas chimpanzees that received GII VLPs vaccine or a placebo were not. This study establishes the chimpanzee as a viable animal model for the study of norovirus replication and immunity, and shows that NV VLP vaccines could induce protective homologous immunity even after extended periods of time.


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.


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.


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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