Thomas C. Merigan
Stanford University
515 Papers
14K Citations
Thomas C. Merigan is an academic researcher from Stanford University. The author has contributed to research in topics: Interferon & Virus. The author has an hindex of 98, co-authored 514 publications. Previous affiliations of Thomas C. Merigan include University of Arizona & Rockefeller Institute of Government.
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Papers
Association of a Novel Human Immunodeficiency Virus Type 1 Protease Substrate Cleft Mutation, L23I, with Protease Inhibitor Therapy and In Vitro Drug Resistance
Elizabeth Johnston,Mark A. Winters,Soo-Yon Rhee,Thomas C. Merigan,Celia A. Schiffer,Robert W. Shafer +5 more
TL;DR: A previously uncharacterized mutation in the protease substrate cleft, L23I, was observed in 31 of 4,303 persons undergoing human immunodeficiency virus type 1 genotypic resistance testing and was associated with a sevenfold reduction in nelfinavir susceptibility and a decrease in replication capacity.
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Synthesis of Viral-Specific Ribonucleic Acid in Rubella Virus-Infected Cells
TL;DR: Monolayers of BHK-21/W1-2 cells were pulsed with (3)H-uridine at different times after infection with rubella virus, and viral-specific cytoplasmic ribonucleic acid species were demonstrated.
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DNA of 21 clinical cytomegalovirus strains detected by hybridization to cloned DNA fragments of laboratory strain AD-169.
TL;DR: Nine distinct DNA probes prepared from cloned DNA fragments of the cytomegalovirus (CMV) strain AD‐169, each representing a relatively small portion of the total genome, were able to detect all 21 epidemiologically distinct clinical isolates of CMV that had been passaged in tissue culture.
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Lymph Node Human Immunodeficiency Virus RNA Levels and Resistance Mutations in Patients Receiving High-Dose Saquinavir
TL;DR: The development of resistance mutations and human immunodeficiency virus (HIV) RNA levels were compared in lymph nodes and plasma of patients receiving antiretroviral therapy and the presence or absence of a resistance mutation to saquinavir at codons 48 or 90 of the HIV-1 protease gene was identical in 13 of 14 biopsies, suggesting that resistance mutations appear within close temporal proximity in lymph node and plasma.
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Multiplicity-dependent Replication of Varicella-zoster Virus in Interferon-treated Cells
TL;DR: It is suggested that some herpesviruses may establish "reservoirs' of infectivity and thus provide a prolonged challenge to IF-treated cells which are not uniformly resistant to infection.
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