Sarah Van Cor-Hosmer



Photo of Sarah Van Cor-HosmerSarah Van Cor-Hosmer received a Bachelors degree in Biotechnolgoy from Rochester Institute of Technology, Rochester NY. During her undergraduate career she worked in the lab of Dr. Jeffery Lodge on the bioremediation of crude oil and spent her summers monitoring water quality for the New Hampshire Green Mountain Conservation Group. After graduating, Sarah worked in the Lab of Dr. Mingtao Zeng at the University of Rochester researching anthrax edema toxin. She was accepted into the IMV Program as a Masters student at the University of Rochester in 2006 and then into the PhD program in 2007. In late 2007 she began her research on reverse transcriptase during the early stages of HIV-1 infection under the guidance of Dr. Baek Kim. In 2009, she presented her work on the role of the central polypurine tract of HIV-1 during the reverse transcription at The 11th Annual Symposium on Antiviral Drug Resistance. This work was published in late 2010 in Virology. In 2011, she was invited to give a talk on the function of the A114 residue in reverse transcriptase of HIV-1 at the Cold Spring Harbor Retrovirology Meeting.

Research Description

The majority of clinically approved HIV-1 anti-retrovirals target the early steps of infection. Therefore it is important to understand the biochemistry of these early stages, which include entry, reverse transcription, and integration. After HIV-1 binds and enters the cell, its single stranded RNA genome is converted into double stranded DNA through the action of a virally encoded reveres transcriptase. The pro-viral double stranded genome is then transported into the nucleus of the cell where it is integrated into the host chromosome by a viral integrase. Sarah’s research focuses on the biochemistry of reverse transcription, specifically reverse transcriptase and its interactions with natural substrate and the nucleoside reverse transcriptase inhibitors (NRTIs) AZT and 3TC. This research is also coupled with understanding a unique priming site of HIV-1 and other lentiviruses that generated during reverse transcription called the central polypurine tract, which can enhance reverse transcription and alter the sensitivity of reverse transcriptase to NRTIs. She also works on understanding the integration of proviral DNA, specifically the cellular machinery involved in repair.

Articles Published

  1. Van Cor-Hosmer et al. Mechanistic interplay among the M184I HIV-1 reverse transcriptase mutant, the central polypurine tract, cellular dNTP concentrations and drug sensitivity. Virology (2010) vol. 406 (2) pp. 253-60
  2. Van Cor-Hosmer et al. The impact of molecular manipulation in residue 114 of Human Immunodeficiency Virus Type-1 reverse transcriptase on dNTP substrate binding and viral replication (under review)

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