T
Thomas C. Merigan
Researcher at Stanford University
Publications - 515
Citations - 34283
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 receiving 33941 citations. Previous affiliations of Thomas C. Merigan include University of Arizona & Rockefeller Institute of Government.
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Journal ArticleDOI
HIV type 1 genotypic resistance in a clinical database correlates with antiretroviral utilization.
TL;DR: The increased number of strains that were genotypically sensitive to all classes of ARV probably indicates an increase in genotypic assay use in ARV-naive individuals, however, the trends and correlations in this data set were similar when evaluated after removal of genotypesically sensitive strains.
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Human leukocyte interferon treatment of two children with insulin dependent diabetes.
K. H. Rand,Arlan L. Rosenbloom,N. K. Maclaren,Janet H. Silverstein,W. J. Riley,B. E. Butterworth,J. W. Yoon,Arthur H. Rubenstein,Thomas C. Merigan +8 more
TL;DR: Two patients with newly diagnosed insulin dependent diabetes mellitus were treated with human leukocyte interferon based on the hypothesis that the diabetes was induced by an active viral infection in the pancreatic islets and could be arrested and there was no sustained therapeutic benefit.
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Peripheral blood mononuclear cell human immunodeficiency virus type 1 proviral DNA quantification by polymerase chain reaction : relationship to immunodeficiency and drug effect
TL;DR: PBMC proviral DNA quantification by a nonisotopic polymerase chain reaction assay correlates with HIV-1 disease progression and could be used to monitor the effect of antiretroviral therapy.
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Human Immunodeficiency Virus Reverse Transcriptase Codon 215 Mutations Diminish Virologic Response to Didanosine-Zidovudine Therapy in Subjects with Non-Syncytium-Inducing Phenotype
TL;DR: Sustained 10-fold decreases in plasma RNA levels were seen only in subjects who initially had 215 wild type RNA, despite the development of a T215Y/F mutation during combination therapy.
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Transfusion-acquired cytomegalovirus infection in cardiac surgery patients.
TL;DR: Serological methods used, the age of the transfused blood, the immune status of the transplant recipient, and the administration of passive antibody in fresh frozen plasma are factors that may be responsible for the low incidence observed.