Abstract: Method of inhibiting human rhinovirus (HRV) Infection by contacting said HRV with a polypeptide comprising a fragment of human rhinovirus major receptor (HRR), said fragment comprising the HRV binding site and being selected from a specific group consisting of HRR domains.

Abstract: The invention is directed to a polypeptide comprising a human IL-2 mutein numbered in accordance with wild-type IL-2 wherein said human IL-2 is substituted at at least one of positions 20, 88 or 126, whereby said mutein preferentially activates T cells over NK cells. D20H and I, N88G, I, and R, in particular have a relative T cell-differential activity much greater than native IL-2, with predicted associated reduced in vivo toxicity. The invention also includes polynucleotides coding for the muteins of the invention, vectors containing the polynucleotides, transformed host cells, pharmaceutical compositions comprising the muteins, and therapeutic methods of treatment.

Abstract: The invention is directed to a polypeptide comprising a human IL-2 mutein numbered in accordance with wild-type IL-2 wherein said human IL-2 is substituted at at least one of positions 20, 88 or 126, whereby said mutein preferentially activates T cells over NK cells. D20H and I, N88G, I, and R, in particular have a relative T cell-differential activity much greater than native IL-2, with predicted associated reduced in vivo toxicity. The invention also includes polynucleotides coding for the muteins of the invention, vectors containing the polynucleotides, transformed host cells, pharmaceutical compositions comprising the muteins, and therapeutic methods of treatment.

Abstract: The invention is directed to a polypeptide comprising a human IL-2 mutein numbered in accordance with wild-type IL-2 wherein said human IL-2 is substituted at at least one of positions 20, 88 or 126, whereby said mutein preferentially activates T cells over NK cells. D20H and I, N88G, I, and R, in particular have a relative T cell-differential activity much greater than native IL-2, with predicted associated reduced in vivo toxicity. The invention also includes polynucleotides coding for the muteins of the invention, vectors containing the polynucleotides, transformed host cells, pharmaceutical compositions comprising the muteins, and therapeutic methods of treatment.

Abstract: The present invention relates to novel forms and configurations of intercellular adhesion molecule (ICAM) including multimeric configurations that effectively bind to human rhinovirus and can effectively reduce HRV infectivity. When in a multimeric configuration, preferably as dimers, these proteins display enhanced binding of HRV and are able to reduce HRV infectivity as well as the infectivity of other viruses known to bind to the “major” group human rhinovirus receptor (HRR). The multimerized proteins may also be used to block tICAM interaction with lymphocyte function-associated antigen-1 (LFA-1).

Abstract: A method for substantially inhibiting initiation or spread of infection by rhinovirus or Coxsackie A virus of host cells expressing the major human rhinovirus receptor (ICAM-1), comprising the step of contacting the virus with a soluble polypeptide comprising the HRV binding site in domains I and II of ICAM-1; which polypeptide is capable of binding to the virus and reducing infectivity thereof; the contact being under conditions which permit the virus to bind to the polypeptide.

Abstract: This invention realizes a less toxic IL-4 mutant that allows greater therapeutic use of interleukin 4. Further, the invention is directed to IL-4 muteins having single and double mutations represented by the designators R121E and T13D/R121E, numbered in accordance with wild type IL-4 (His=1). The invention also includes polynucleotides coding for the muteins of the invention, vectors containing the polynucleotides, transformed host cells, pharmaceutical compositions comprising the muteins, and therapeutic methods of treatment.

Abstract: Antiviral methods comprising contacting human rhinovirus with tICAM(453).

Abstract: A recombinant human IL-4 mutein numbered in accordance with wild-type IL-4 wherein the mutein comprises at least one amino acid substitution in the binding surface of either the A- or C-alpha helices of the wild-type IL-4 whereby the mutein binds to the IL-4R&agr; receptor with at least greater affinity than native IL-4. The substitution is more preferably selected from the group of positions consisting of, in the A-helix, positions 13 and 16, and in the C-helix, positions 81 and 89. A most preferred embodiment is the recombinant human IL-4 mutein wherein the substitution at position 13 is Thr to Asp. Pharmaceutical compositions, amino acid and polynucleotide sequences encoding the muteins, transformed host cells, antibodies to the muteins, and methods of treatment are also described.

Abstract: Novel analogs of ICAM-1 and methods of using same for reducing human rhinovirus infection.

Abstract: Methods for inhibiting infectivity and reducing infection by human rhinovirus (HRV) of host cells susceptible to infection by HRV and methods of inhibiting initiation and spread of the common cold, said methods comprising contacting HRV under conditions favorable for binding with a multimeric antiviral agent comprising two or more units wherein said units may be the same or different and are each independently selected from the group consisting of transmembrane intercellular adhesion molecule-1 (tmICAM-1) and truncated forms of intercellular adhesion molecule-1 (tICAMs), each of said units containing at least one unpaired cysteine residue at a position selected from the group consisting of 307 and 309, wherein each of said units is linked to at least one other of said units via a disulfide bridge, and wherein said multimeric antiviral agent binds to HRV and reduces infectivity thereof.

Abstract: Multimers comprising two or more monomers, wherein said monomers may be the same or different and are each independently selected from the group consisting of transmembrane intercellular adhesion molecule-1 (tmICAM-1) and fragments thereof, with the proviso that said monomers must comprise domains I and II of ICAM-1 and with the proviso that when said multimer is a dimer, the monomers cannot both be tmICAM-1, wherein said multimer binds to a ligand that binds to the human rhinovirus (HRV) binding site on ICAM-1, and wherein at least two of said monomers are oriented so that relative to each other they mimic the multimeric configuration of native tmICAM-1, such that said multimer exhibits enhanced binding to said ligand relative to at least one of its constituent monomers, and methods of use.

Abstract: Multimeric antiviral agents comprising two or more monomers selected from the group consisting of monomers of transmembrane intracellular adhesion molecule-1 (tmICAM-1) and truncated intercellular adhesion molecule-1 (tICAMs), with the proviso that when said multimer is a dimer said monomers cannot both be tmICAM-1, wherein each of said monomers comprises the human rhinovirus (HRV) binding site and retains the ability to bind to HRV and reduce infectivity thereof, and wherein said multimeric antiviral agent mimics the multimeric configuration of tmICAM-1 and exhibits enhanced binding to said HRV relative to at least one of the constituent monomers.

Abstract: Methods for reducing the infection by human rhinovirus (HRV) of host cells susceptible to infection by HRV, comprising contacting the virus under conditions favorable for binding with an antiviral agent comprising a fragment of human rhinovirus major receptor protein (HRR) in a form that exhibits the ability to bind to HRV capsids and reduce infectivity of the virus, and an intranasal spray comprising HRR or a fragment thereof suitable for use in said method. Human rhinovirus receptor has subsequently been discovered by Greve et al. to be intercellular adhesion molecule-1.

Abstract: This invention is directed to recombinant human IL-4 muteins numbered in accordance with wild-type IL-4 wherein the muteins comprise at least one amino acid substitution selected from the group consisting of substitutions at positions 13, 16, 81 and 89 of the wild-type IL-4, whereby the mutein binds to the IL-4R.alpha. receptor with at least greater affinity than native IL-4. The invention is further directed to recombinant human IL-4 antagonist muteins numbered in accordance with wild-type IL-4 wherein the muteins comprise substitutions R121D and Y124D in the D-helix of said wild-type IL-4; and at least one amino acid substitution selected from the group consisting of substitutions at positions 13, 16, 81 and 89 of said wild-type IL-4, whereby the mutein binds to the IL-4R.alpha. receptor with at least greater affinity than native IL-4. The invention is also directed to pharmaceutical compositions comprising individual muteins in combination with pharmaceutically acceptable carriers.

Abstract: The present invention relates to novel forms and configurations of intercellular adhesion molecule (ICAM) including multimeric configurations that effectively bind to human rhinovirus and can effectively reduce HRV infectivity. When in a multimeric configuration, preferably as dimers, these proteins display enhanced binding of HRV and are able to reduce HRV infectivity as well as the infectivity of other viruses known to bind to the "major" group human rhinovirus receptor (HRR). The multimerized proteins may also be used to block tICAM interaction with lymphocyte function-associated antigen-1 (LFA-1).

Abstract: The present invention relates to a soluble form of-intercellular adhesion molecule (sICAM-1) and purified and isolated human sICAM-1. This invention also relates to a purified and isolated DNA sequence encoding sICAM-1. The extracellular domain of sICAM-1 and insoluble ICAM-1 are substantially the same. ICAM-1 is involved in the process through which lymphocytes attach to cellular substrates during inflammation and serves as the major human rhinovirus receptor (HRR). sICAM-1 therefore has both the property of reducing immune inflammation and inhibiting infection of rhinovirus and Coxsackie A virus.

Abstract: The present invention relates to a soluble form of intercellular adhesion molecule (sICAM-1) and purified and isolated human sICAM-1. This invention also relates to a purified and isolated DNA sequence encoding sICAM-1. The extracellular domain of sICAM-1 and insoluble ICAM-1 are substantially the same. ICAM-1 is involved in the process through which lymphocytes attach to cellular substrates during inflammation and serves as the major human rhinovirus receptor (HRR). sICAM-1 therefore has both the property of reducing immune inflammation and inhibiting infection of rhinovirus and Coxsackie A virus.

Abstract: The present invention relates to a soluble form of intercellular adhesion molecule (sICAM-1) and purified and isolated human sICAM-1, and antibodies thereto. This invention also relates to a purified and isolated DNA sequence encoding sICAM-1. The extracellular domain of sICAM-1 and insoluble ICAM-1 are substantially the same. ICAM-1 is involved in the process through which lymphocytes attach to cellular substrates during inflammation and serves as the major human rhinovirus receptor (HRR). sICAM-1 therefore has both the property of reducing immune inflammation and inhibiting infection of rhinovirus and Coxsackie A virus.

Abstract: The present invention relates to novel forms and configurations of intercellular adhesion molecule (ICAM) including multimeric configurations that effectively bind to human rhinovirus and can effectively reduce HRV infectivity. When in a multimeric configuration, preferably as dimers, these proteins display enhanced binding of HRV and are able to reduce HRV infectivity as well as the infectivity of other viruses known to bind to the "major" group human rhinovirus receptor (HRR). The multimerized proteins may also be used to block tICAM interaction with lymphocyte function-associated antigen-1 (LFA-1).