Are you A Elbaggari?

Claim your profile

Publications (6)22.52 Total impact

  • [show abstract] [hide abstract]
    ABSTRACT: HIV integration within host cell genomic DNA is a requisite step of the viral infection cycle. Yet, characteristics of the sites of provirus integration within the host genome remain obscure. The authors present evidence that in diseased tissues showing a high level of HIV DNA and macrophage-associated HIV p24 antigen expression from end stage forms of HIV disease, HIV-1 integration sites were favored within genes and transcriptionally active host cell genomic loci. Using an inverse PCR (IPCR) technique that identified dominant integrated forms of HIV, clonal IPCR products were isolated from AIDS dementia, AIDS lymphoma, and angioimmunoblastic lymphadenopathy tissues. Thirty of 34 disease-associated HIV-1 insertions were identified within annotated and hypothetical genes, an unexpected but highly nonrandom genetic coding region association (p <.026). The 1% sensitivity thresholds used for HIV IPCR suggested some form of selective expansion of cells containing these HIV proviruses. Consistent with this interpretation were the HIV-1 insertion sites identified within introns of genes that encoded for factors associated with signal transduction, apoptosis, and transcription regulation. In addition, HIV-1 proviruses were frequently found proximal to genes that encoded for receptor-associated, signal transduction-associated, transcription-associated, and translation-associated proteins. HIV-1 integration within host cell genomic DNA potentially represents a significant insertional mutagenic event. In certain cases, provirus insertions may mediate the dysregulation of specific gene expression events, providing mechanisms contributing to the pathogenesis associated with certain AIDS-related diseases.
    JAIDS Journal of Acquired Immune Deficiency Syndromes 08/2003; 33(3):308-20. · 4.65 Impact Factor
  • Source
    [show abstract] [hide abstract]
    ABSTRACT: The pathogenesis of immunodeficiency-associated lymphoma is poorly understood. During the past several years, numerous lines of evidence implicating a multistep process of malignant transformation, also known as sequential pathogenesis, have emerged. Tumor-associated macrophage production of specific lymphostimulatory products has been demonstrated and hypothesized to be central to this process. While attempting to establish primary effusion lymphoma in severe combined immunodeficient (SCID) mice, we discovered a potential model of murine lymphomagenesis consistent with the sequential pathogenesis model. This pathogenesis-based model of lymphoma could significantly impact the current thinking about posttransplantation and other immunodeficiency-related lymphoproliferative disorders. Human primary effusion lymphoma-derived CD14+ cell-injected SCID mice developed aggressive murine large cell lymphomas. Tumor cell preparations containing CD14 cells or isolated CD14 cells induced lymphoma/lymphoproliferative diseases in 74% (20 of 27) of injected SCID mice. No tumors were induced by tumor-associated CD3 cells (0 of 4), normal human macrophages (0 of 13), or a murine macrophage cell line (0 of 10). Human macrophages were detected in tumor-bearing animals up to 6 months postinjection in association with the murine T-cell tumors but were not detected in controls or unaffected animals. These observations are consistent with the macrophage-initiated sequential pathogenesis model of disease (M. S. McGrath et al., Acquir. Immune Defic. Syndr., 8: 379-385, 1995; M. S. McGrath et al., Infectious Causes of Cancer: Targets for Intervention, pp. 231-242, Totowa, NJ: Humana Press, 2000).
    Cancer Research 11/2002; 62(19):5536-42. · 8.65 Impact Factor
  • JAIDS Journal of Acquired Immune Deficiency Syndromes 03/1997; 14(4):A44. · 4.65 Impact Factor
  • Source
    [show abstract] [hide abstract]
    ABSTRACT: In vitro susceptibility testing of herpes simplex virus (HSV) isolates will play an increasingly important role in guiding the clinical management of immunocompromised hosts who have lesions that are poorly responsive to therapy with standard antiviral agents. We assessed the correlation between the in vitro susceptibility result using a plaque reduction assay in Vero cells and the response to antiviral therapy with acyclovir or foscarnet for 243 clinical isolates of HSV collected from 115 human immunodeficiency virus-infected patients. The in vitro results and clinical responses were highly associated for both acyclovir and foscarnet (P < 0.001 and P < 0.001, respectively). The predictive values of a susceptible result (50% effective concentrations, < 2 micrograms/ml for acyclovir and < 100 micrograms/ml for foscarnet) for complete healing of lesions were 62% for acyclovir and 82% for foscarnet; the predictive values of a resistant result for failure to heal were 95% for acyclovir and 88% for foscarnet. Thus, in vitro testing has clinical utility in guiding therapy, although the 1 to 2 weeks required to derive a definitive result by the plaque reduction assay is a major limitation.
    Antimicrobial Agents and Chemotherapy 06/1994; 38(6):1246-50. · 4.57 Impact Factor
  • Source
    [show abstract] [hide abstract]
    ABSTRACT: hosts whohavelesions thatarepoorly responsive totherapy withstandard antiviral agents. Weassessed thecorrelation between theinvitro susceptibility result using aplaque reduction assay inVerocells andtheresponse toantiviral therapy withacyclovir orfoscarnet for243clinical isolates ofHSVcollected from115humanimmunodeficiency virus-infected patients. Thein vitro results andclinical responses werehighly associated forbothacyclovir andfoscarnet (P< 0.001 andP < 0.001, respectively). Thepredictive values ofasusceptible result (50%elfective concentrations,
  • Ahmed. Elbaggari
    [show abstract] [hide abstract]
    ABSTRACT: SPEC. COLL. HAS ARCHIVAL COPY; MICRO. ROOM HAS MICROFICHE COPY (2 SHEETS). Thesis (M.A.)--U. of Calif., Davis. Typescript. Degree granted in Microbiology.