Anil C. Asrani

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Oral keratinocytes on the mucosal surface are frequently exposed to HIV-1 through contact with infected sexual partners or nursing mothers. To determine the plausibility that oral keratinocytes are primary targets of HIV-1, we tested the hypothesis that HIV-1 infects oral keratinocytes in a restricted manner. To study the fate of HIV-1, immortalized oral(More)
Porphyromonas gingivalis activates protease-activated receptors (PARs) on oral keratinocytes, resulting in downstream signalling for an innate immune response. Activation depends on P. gingivalis gingipains, but could be confounded by lipopolysaccharide signalling through Toll-like receptors. We therefore hypothesized that P. gingivalis cleaves oral(More)
BACKGROUND/OBJECTIVE HIV-1 infection is complicated by high rates of opportunistic infections against which specific antibodies contribute to immune defense. Antibody function depends on somatic hypermutation (SHM) of variable regions of immunoglobulin heavy chain genes (VH-D-J). We characterized the frequency of SHM in expressed IgG mRNA immunoglobulin(More)
Complex virus particles progress through a series of maturation intermediates between initial assembly and formation of the infectious virion. The process is required to accommodate the weak, equilibrium interactions between subunits that minimize errors in assembly and the need for a robust particle that will tolerate the hostile environment outside of the(More)
Systemic infection with HIV occurs infrequently through the oral route. The frequency of occurrence may be increased by concomitant bacterial infection of the oral tissues, since co-infection and inflammation of some cell types increases HIV-1 replication. A putative periodontal pathogen, Porphyromonas gingivalis selectively up-regulates expression of the(More)
Objective. Low gene expression in rare cell subpopulations can make it difficult to identify transcripts using real time quantitative RT-PCR (qRT-PCR). Transcript number can be increased using linear amplification, but this technique amplifies the 3’ end of mRNA, imposing severe limitations on qRT-PCR primer design. Artifacts such as primer-dimers,(More)
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