Alan S. Perelson

TL;DR: Treatment of infected patients with ABT-538 causes plasma HIV-1 levels to decrease exponentially and CD4 lymphocyte counts to rise substantially, indicating that replication of HIV- 1 in vivo is continuous and highly productive, driving the rapid turnover ofCD4 lymphocytes.

TL;DR: A new mathematical model was used to analyze a detailed set of human immunodeficiency virus-type 1 (HIV-1) viral load data collected from five infected individuals after the administration of a potent inhibitor of HIV-1 protease, providing not only a kinetic picture ofAIDS pathogenesis, but also theoretical principles to guide the development of treatment strategies.

TL;DR: Findings show that infection with hepatitis C virus is highly dynamic and that early monitoring of viral load can help guide therapy, with blocking efficacies of 81, 95, and 96% for daily doses of 5, 10, and 15 million international units, respectively.

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.

TL;DR: It is estimated that 2.3–3.1 years of a completely inhibitory treatment would be required to eliminate HIV-1 from these compartments, and even longer treatment may be needed because of the possible existence of undetected viral compartments or sanctuary sites.