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Michael S. Saag

Researcher at University of Alabama at Birmingham

Publications -  504
Citations -  65873

Michael S. Saag is an academic researcher from University of Alabama at Birmingham. The author has contributed to research in topics: Viral load & Acquired immunodeficiency syndrome (AIDS). The author has an hindex of 110, co-authored 480 publications receiving 62247 citations. Previous affiliations of Michael S. Saag include University of Oxford & ViiV Healthcare.

Papers
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Viral dynamics in human immunodeficiency virus type 1 infection

TL;DR: Almost complete replacement of wild-type virus in plasma by drug-resistant variants occurs after fourteen days, indicating that HIV-1 viraemia is sustained primarily by a dynamic process involving continuous rounds of de novo virus infection and replication and rapid cell turnover.
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Circulating microRNAs in sera correlate with soluble biomarkers of immune activation but do not predict mortality in ART treated individuals with HIV-1 infection : a case control study

Daniel D Murray, +1489 more
- 14 Oct 2015 - 
TL;DR: No associations with mortality were found with any circulating miRNAs studied and these results cast doubt onto the effectiveness of circulating miRNA as early predictors of mortality or the major underlying diseases that contribute to mortality in participants treated for HIV-1 infection.
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Antibody neutralization and escape by HIV-1

TL;DR: The detection of autologous Nab as early as 52 days after detection of HIV-specific antibodies is reported, indicating a new mechanism contributing to HIV-1 persistence in the face of an evolving antibody repertoire.
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Identification and characterization of transmitted and early founder virus envelopes in primary HIV-1 infection

TL;DR: A mathematical model of random viral evolution and phylogenetic tree construction is developed and used to analyze 3,449 complete env sequences derived by single genome amplification from 102 subjects with acute HIV-1 (clade B) infection, suggesting a finite window of potential vulnerability of HIV- 1 to vaccine-elicited immune responses, although phenotypic properties of transmitted Envs pose a formidable defense.