Abstract

This proposal will examine some of the potential determinants of perinatal transmission of HIV. Recently it was shown that the susceptibility of CD4+ T cells to HIV infection is related to both the quantity of b chemokine (MIP-1a, MIP-1 b and RANTES) produced by their CD4+ T cells and to the expression of the b chemokine receptor 5 (CCR5). This receptor was recently identified as the co-receptor for monocytotropic (M-tropic) isolates of HIV, which are the viruses that are mainly transmitted heterosexually and perinatally. Individuals who have homozygous mutations of the CCR5 receptor are resistant to HIV infection with M-tropic isolates. We will examine whether there is a correlation between either CCR5 expression or chemokine production and perinatal HIV transmission. As these chemokines also mediate CD8+ T-cell-mediated HIV suppression, which we have identified as an important early protective immune response in HIV-infected infants, we will also measure CD8 viral suppressive activity (CD8-VSA) to try to assess whether it also plays a role in perinatal HIV transmission. The laboratory was used for oligonucleotide synthesis, and recombinant DNA techniques.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
General Clinical Research Centers Program (M01)
Project #
5M01RR000096-39
Application #
6305968
Study Section
Project Start
1999-12-01
Project End
2000-11-30
Budget Start
1998-10-01
Budget End
1999-09-30
Support Year
39
Fiscal Year
2000
Total Cost
$21,006
Indirect Cost

  Institution

Name
New York University
Department
Type
DUNS #
City
New York
State
NY
Country
United States
Zip Code
10016

  Publications

Jun, Gyungah R; Chung, Jaeyoon; Mez, Jesse et al. (2017) Transethnic genome-wide scan identifies novel Alzheimer's disease loci. Alzheimers Dement 13:727-738
Homann, O R; Misura, K; Lamas, E et al. (2016) Whole-genome sequencing in multiplex families with psychoses reveals mutations in the SHANK2 and SMARCA1 genes segregating with illness. Mol Psychiatry 21:1690-1695
Ridge, Perry G; Hoyt, Kaitlyn B; Boehme, Kevin et al. (2016) Assessment of the genetic variance of late-onset Alzheimer's disease. Neurobiol Aging 41:200.e13-200.e20
Hohman, Timothy J; Bush, William S; Jiang, Lan et al. (2016) Discovery of gene-gene interactions across multiple independent data sets of late onset Alzheimer disease from the Alzheimer Disease Genetics Consortium. Neurobiol Aging 38:141-150
Jun, G; Ibrahim-Verbaas, C A; Vronskaya, M et al. (2016) A novel Alzheimer disease locus located near the gene encoding tau protein. Mol Psychiatry 21:108-17
Ebbert, Mark T W; Boehme, Kevin L; Wadsworth, Mark E et al. (2016) Interaction between variants in CLU and MS4A4E modulates Alzheimer's disease risk. Alzheimers Dement 12:121-129
Hohman, Timothy J; Cooke-Bailey, Jessica N; Reitz, Christiane et al. (2016) Global and local ancestry in African-Americans: Implications for Alzheimer's disease risk. Alzheimers Dement 12:233-43
Li, Yi; Tsui, Wai; Rusinek, Henry et al. (2015) Cortical laminar binding of PET amyloid and tau tracers in Alzheimer disease. J Nucl Med 56:270-3
Ghani, Mahdi; Reitz, Christiane; Cheng, Rong et al. (2015) Association of Long Runs of Homozygosity With Alzheimer Disease Among African American Individuals. JAMA Neurol 72:1313-23
Beecham, Gary W; Dickson, Dennis W; Scott, William K et al. (2015) PARK10 is a major locus for sporadic neuropathologically confirmed Parkinson disease. Neurology 84:972-80

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