R
Rachel D. Schrier
Researcher at University of California, San Diego
Publications - 40
Citations - 2275
Rachel D. Schrier is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Retinitis & Immune system. The author has an hindex of 19, co-authored 37 publications receiving 2172 citations. Previous affiliations of Rachel D. Schrier include University of Southern California & Stanford University.
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Journal ArticleDOI
Cellular localization of human immunodeficiency virus infection within the brains of acquired immune deficiency syndrome patients
TL;DR: The brains of 12 AIDS patients were studied using in situ hybridization to identify human immunodeficiency virus nucleic acid sequences and immunocytochemistry to identify viral and cellular proteins, suggesting that CNS dysfunction is due to indirect effects rather than neuronal or glial infection.
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CMV retinitis recurs after stopping treatment in virological and immunological failures of potent antiretroviral therapy.
Francesca J. Torriani,William R. Freeman,J C MacDonald,Marietta P. Karavellas,D. M. Durand,D. D. Jeffrey,Pascal Meylan,Rachel D. Schrier +7 more
TL;DR: CMV disease recurs after virological and immunological failure of HAART if CD4 cell counts drop below 50, and anti-CMV agents should be resumed before clinical reactivation ensues, because of the risk of contralateral retinal involvement and systemic disease.
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Immune predispositions for cytomegalovirus retinitis in AIDS. The HNRC Group.
TL;DR: AIDS patients with immunogenetically related hyporesponsiveness to CMV antigens may be at increased risk of retinitis, as well as HIV infected, HLA typed, longitudinal study population.
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Cerebrospinal fluid (CSF) CD8+ T-cells that express interferon-gamma contribute to HIV associated neurocognitive disorders (HAND).
Rachel D. Schrier,Suzi Hong,Melanie Crescini,Ronald J. Ellis,Josué Pérez-Santiago,Celsa A. Spina,Scott Letendre +6 more
TL;DR: The presence of IFNγ expressing CD8+ T-cells, absence of cytolytic CD8+, high myeloid activation, and failure of ART to suppress HIV replication in CSF contribute to increased risk of HAND.
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T-cell-induced expression of human immunodeficiency virus in macrophages.
TL;DR: HIV-seronegative nonadherent cells were able to induce HIV expression in macrophages from HIV-seropositive donors, demonstrating that the virus originated in the monocytes and was reactivated in the context of a classic T-cell-mediated immune reaction.