HIV is the etiological agent of AIDS and predisposes the host to oral infections such as HIV gingivitis, periodontitis, candidiasis and viral infections. Periodontal diseases represent a significant chronic bacterial challenge to the oral tissues and are likely to alter or be altered by the function of resident immunocompetent cells during retroviral infection. Macrophages are the major host cell of HIV infection in tissues. This proposal will test the hypothesis that the pathogenesis of oral lesions following infection, during the latent period and in AIDS, is founded in part on HIV infection and/or alteration of macrophages in the gingival mucosa. To that end, the following specific aims will be investigated. l.To verify the presence of infection and cellular localization of HIV in isolated gingival macrophages from tissue samples collected from HIV infected patients by determining the viral titer of gingival tissue explant cultures and using immunological and molecular probes for HIV and antigen presenting cells (APC). 2.To determine in each periodontal disease group (HIV infected and non- infected patients) the expression of macrophage cell surface membrane receptors and differentiation antigens related to stages of HIV infection. 3.To determine in macrophages explanted from HIV infected patients the ability to produce extra and intracellular cytokines such as IL-1 alpha, beta, and TNF-alpha as they relate to HIV infection of these cells. 4.To correlate these macrophage characteristics during various stages of HIV infection to the pathogenesis of oral HIV gingivitis and periodontitis through correlation of the results of accomplishing AIMS 1-3 and the clinical periodontal characterization of the patients. These studies should assist in defining appropriate assays to measure cellular immune function related to retroviral associated oral diseases. These studies should also result in a greater understanding of the pathogenesis of retroviral infections in humans. Appropriate correlates to other HIV related oral diseases in humans might result, eventually leading to improved strategies of therapeutic intervention.
| Baqui, A A; Jabra-Rizk, M A; Kelley, J I et al. (2000) Enhanced interleukin-1beta, interleukin-6 and tumor necrosis factor-alpha production by LPS stimulated human monocytes isolated from HIV+ patients. Immunopharmacol Immunotoxicol 22:401-21 |
| Baqui, A A; Meiller, T F; Zhang, M et al. (1999) The effects of HIV viral load on the phagocytic activity of monocytes activated with lipopolysaccharide from oral microorganisms. Immunopharmacol Immunotoxicol 21:421-38 |
| Baqui, A A; Meiller, T F; Turng, B F et al. (1998) Functional changes in THP-1 human monocytic cells after stimulation with lipopolysaccharide of oral microorganisms and granulocyte macrophage colony stimulating factor. Immunopharmacol Immunotoxicol 20:493-518 |
