New York University

Aaron Diamond Aids Research Center

Other

Nathaniel R Landau

Rong Liu

Dan R Littman

Hongkui Deng

Wilfried Ellmeier

Thomas D Norton

William Paxton

Takuya Tada

Nicole Sunseri

Richard A Koup

Provided are polypeptides comprising an enzymatically inactive angiotensin-converting enzyme 2 (ACE2) ectodomain, a segment of an immunoglobulin Fc and optionally a purification tag. A cDNA or an expression vector encoding the polypeptide along with a method of culturing cells comprising the expression vector is also provided. The disclosure also provides a method for prophylaxis or therapy for a Coronavirus infection by administering the polypeptide to an individual in need thereof.

Angiotensin-converting enzyme 2 (ACE2) immunoadhesin microbody

The compositions and methods described herein relate to lentiviral vectors that can be used to generate virions/viruses that exhibit enhanced infectivity with respect to monocyte-derived macrophages (MDM) and dendritic cells (MDDC). Such compositions and methods further relate to production of virions/viruses that can be used as components of vaccines that effectively stimulate innate immune responses. In a particular embodiment, compositions and methods described herein relate to production of virions/viruses that can be used as components of human immunodeficiency-1 (HIV-1) vaccines administered to stimulate innate immune responses to HIV-1.

Chimeric human immunodeficiency virus type 1 (HIV-1) with enhanced dendritic cell and macrophage tropism comprising the simian immunodeficiency virus (SIV) minimal Vpx packaging domain

Entry of HIV-1 into target cells requires cell surface CD4 as well as additional host cell cofactors. A cofactor required for infection with virus adapted for growth in transformed T cell lines was recently identified and named fusin. Fusin, however, does not promote entry of macrophage-tropic viruses that are believed to be the key pathogenic strains in vivo. It has now been determined that the principal cofactor for entry mediated by the envelope glycoproteins of primary macrophage-tropic strains of HIV-1 is CC-CKR5, a receptor for the &#x3b2;-chemokines RANTES, MIP-1&#x3b1;, and MIP-1&#x3b2;.

Methods of identifying g-couple receptors associated with macrophage-trophic HIV, and diagnostic and therapeutic uses thereof

Entry of HIV-1 into target cells requires cell surface CD4 as well as additional host cell cofactors. A cofactor required for infection with virus adapted for growth in transformed T cell lines was recently identified and named fusin. Fusin, however, does not promote entry of macrophage-tropic viruses that are believed to be the key pathogenic strains in vivo. It has now been determined that the principal cofactor for entry mediated by the envelope glycoproteins of primary macrophage-tropic strains of HIV-1 is CC-CKR5, a receptor for the &bgr;-chemokines RANTES, MIP-1&agr;, and MIP-1&bgr;.

Methods of identifying g-coupled receptors associated with macrophage-trophic HIV, and diagnostic and therapeutic uses thereof

Entry of HIV-1 into target cells requires cell surface CD4 as well as additional host cell cofactors. A cofactor required for infection with virus adapted for growth in transformed T cell lines was recently identified and named fusin. Fusin, however, does not promote entry of macrophage-tropic viruses that are believed to be the key pathogenic strains in vivo. It has now been determined that the principal cofactor for entry mediated by the envelope glycoproteins of primary macrophage-tropic strains of HIV-1 is CC-CKR5, a receptor for the .beta.-chemokines RANTES, MIP-1.alpha., and MIP-1.beta.. It has also been found that individuals who are homozygous for a mutation of the CKR-5 receptor are resistent to HIV infection; in vitro infection requires a 1000-fold higher dose of HIV than normal cells. The mutation results in complete suppression of CKR-5 expression.

HIV coreceptor mutants

Entry of HIV-1 into target cells requires cell surface CD4 as well as additional host cell cofactors. A cofactor required for infection with virus adapted for growth in transformed T cell lines was recently identified and named fusin. Fusin, however, does not promote entry of macrophage-tropic viruses that are believed to be the key pathogenic strains in vivo. It has now been determined that the principal cofactor for entry mediated by the envelope glycoproteins of primary macrophage-tropic strains of HIV-1 is CC-CKR5, a receptor for the .beta.-chemokines RANTES, MIP-1.alpha., and MIP-1.beta..

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New York, NY, United States of America

Nathaniel R Landau