The present invention encompasses monoclonal and chimeric antibodies that bind to lipoteichoic acid of Gram positive bacteria. The antibodies also bind to whole bacteria and enhance phagocytosis and killing of the bacteria in vitro and enhance protection from lethal infection in vivo. The mouse mono
The present invention encompasses monoclonal and chimeric antibodies that bind to lipoteichoic acid of Gram positive bacteria. The antibodies also bind to whole bacteria and enhance phagocytosis and killing of the bacteria in vitro and enhance protection from lethal infection in vivo. The mouse monoclonal antibody has been humanized and the resulting chimeric antibody provides a previously unknown means to diagnose, prevent and/or treat infections caused by gram positive bacteria bearing lipoteichoic acid. This invention also encompasses a peptide mimic of the lipoteichoic acid epitope binding site defined by the monoclonal antibody. This epitope or epitope peptide mimic identifies other antibodies that may bind to the lipoteichoic acid epitope. Moreover, the epitope or epitope peptide mimic provides a valuable substrate for the generation of vaccines or other therapeutics.
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The present invention encompasses monoclonal and chimeric antibodies that bind to lipoteichoic acid of Gram positive bacteria. The antibodies also bind to whole bacteria and enhance phagocytosis and killing of the bacteria in vitro and enhance protection from lethal infection in vivo. The mouse mono
The present invention encompasses monoclonal and chimeric antibodies that bind to lipoteichoic acid of Gram positive bacteria. The antibodies also bind to whole bacteria and enhance phagocytosis and killing of the bacteria in vitro and enhance protection from lethal infection in vivo. The mouse monoclonal antibody has been humanized and the resulting chimeric antibody provides a previously unknown means to diagnose, prevent and/or treat infections caused by gram positive bacteria bearing lipoteichoic acid. This invention also encompasses a peptide mimic of the lipoteichoic acid epitope binding site defined by the monoclonal antibody. This epitope or epitope peptide mimic identifies other antibodies that may bind to the lipoteichoic acid epitope. Moreover, the epitope or epitope peptide mimic provides a valuable substrate for the generation of vaccines or other therapeutics. e-sensitive Mutant ts K," J. Gen Virol. 65:859-863 (1984). De Koninc et al., "Substance P-Mediated Slow Excitatory Postsynaptic Potential Elicited In Dorsal Horn Neurons In Vivo by Noxious Stimulation," PNAS USA 88:11344-11348 (1991). Dobson et al., "A Latent Nonpathogenic HSV-1-Derived Vector Stably Expresses β-Galactosidase In Mouse Neurons," Neuron 5:353-360 (1990). Dobson et al., "Identification of the Latency-Associated Promoter by Expression of Rabbit Beta-Globin mRNA In Mouse Sensory Nerve Ganglia Latently Infected with a Recombinant Herpes Simplex Virus," J. of Virology 63(9):3844-3851 (1989). Efstathiou et al., "The Role of Herpes Simplex Virus Type 1 Thymidine Kinase In Pathogenesis," J. Gen. Virol. 70:869-879 (1989). Efstathiou et al., "Detection of Herpes Simplex Virus-Specific DNA Sequences In Latently Infected Mice and In Humans, " J. of Virology 57(2):446-455 (1986). Fenwick, M.L., "The Effects of Herpesviruses On Cellular Macromolecular Synthesis," Compr. Virol. 19:359-390 (1984). Forss-Petter et al., "Transgenic Mice Expressing β-Galactosidase In Mature Neurons Under Neuron-Specific Enolase Promoter Control," Neuron 5:187-197 (1990). Friedmann, T., "Progress Toward Human Gene Therapy", Science 244:1275-1281 (1989). Geller et al., "Infection of Cultured Central Nervous System Neurous with a Defective Herpes Simplex Virus 1 Vector Results In Stable Expression of Escherichia coli β-Galactosidase," PNAS USA 87:1149-1153 (1990). Geller et al., "A Defective HSV-1 Vector Expresses Escherichia coli β-Galactosidase In Cultured Peripheral Neurons," Science 241:1667-1669 (1988). Heilbronn et al., "A Subset of Herpes Simplex Virus Replication Genes Induces DNA Amplification within the Host Cell Genome," J. of Virology 63 (9) :3683-3692 (1989). Ho et al., "β-Galactosidase as a Marker In the Peripheral and Neural Tissues of the Herpes Simplex Virus-Infected Mouse," Virology 167:279-283 (1988). Ho et al., "Herpes Simplex Virus Latent RNA (LAT) Is Not Required for Latent Infection In the Mouse," PNAS USA 86:7596-7600 (1989). Huang et al., "Introduction of a Foreign Gene (Escherichia coli lacZ) into Rat Neostriatal Neurons Using Herpes Simplex Virus Mutants: A Light and Electron Microscopic Study," Experimental Neurology 115:303-316 (1992). Javier et al., "Localization of a herpes Simplex Virus Neurovirulence Gene Dissociated from High-Titer Virus Replication In the Brain," J. of Virology 62 (4) :1381-1387 (1988). Javier et al., "A Herpes Simplex Virus Transcript Abundant In Latently Infected Neurons Is Dispensable for Establishment of the Latent State," Virology 166:254-257 (1988). Koprowski, H., "Possible Role of Herpes Virus In the Chronic CNS Diseases", in Persistent Viruses, F.G. Stevens (ed.), Academic Press, N.Y., pp. 691-699 (1978). Kosz-Vnenchak et al., "Restricted Expression of Herpes Simplex Virus Lytic Genes During Establishment of Latent Infection by Thymidine Kinase-Negative Mutant Viruses", J. of Virology 64 (11):5396-5402 (1990). Kuwayama et al., "A Quantitative Correlation of Substance P-, Calcitonin Gene-Related Peptide- and Cholecystokinin-LIke Immunoreactivity with Retrogradely Labeled Trigeminal Ganglion Cells Innervating the Eye," Brain Research 405:220-226 (1987). Kuypers et al., "Viruses as Transneuronal Tracers," TINS 13(2):71-75 (1990). Kwong et al., "The Herpes Simplex Virus Virion Host Shutoff Function," J. of Virology 63(11) :4834-4839 (1989). Leib et al., "A Deletion Mutant of the Latency-Associated Transcript of Herpes Simplex Virus Type 1 Reactivates from the Latent State with Reduced Frequency," J. of Virology 63 (7):2893-2900 (1989). Leib et al., "Immediate-Early Regulatory Gene Mutants Define Different Stages In the Establishment and Reactivation of Herpes Simplex Virus Latency," J. of Virology 63(2):759-768 (1989). Leist et al., "Latent Infections In Spinal Ganglia with Thymidine Kinase-Deficient Herpes Simplex Virus", J. of Virology 63(11) :4976-4978 (1989). Lo
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