Mullins Molecular Retrovirology Lab

The Mullins laboratory is located in the Rosen Building on the South Lake Union campus of the University of Washington School of Medicine. Our lab uses molecular, computational, and virus biology techniques to provide insights into the relationship between HIV and its human hosts in an effort to fight the AIDS pandemic. We use a variety of methods to document and understand the implications of HIV's extraordinary genetic diversity on the immunopathogenesis of AIDS, with a particular emphasis on acute/early infection and superinfection. We then apply this information to develop more effective vaccines and therapies in collaboration with other investigators. Our research work focuses on the acquisition and computational characterization of HIV nucleotide sequences, the development of web tools for related computational studies, in vitro studies of the growth properties of viral isolates, host genetic polymorphism analysis, and high-throughput analysis of cellular transcription.

Lab News

New research featured in Science

"Cancer Genes Help HIV Persist, Complicating Cure Efforts."Science News & Analysis, 14 March 2014

RV144 Analysis Featured by Nature

"Vaccine trial reveals chinks in HIV's armour."Nature | News, 10 September 2012

Step Trial Analysis Featured in UW Today

"For first time, scientists show an HIV vaccine impacts the genetic makeup of the virus." UW Today, 1 March 2011

Recent Publications

Stekler JD, Milne R, Payant R, Beck I, Herbeck J, Maust B, Deng W, Tapia K, Holte S, Maenza J, Stevens CE, Mullins JI, Collier AC, Frenkel LM 2018 Transmission of HIV-1 drug resistance mutations within partner-pairs: A cross-sectional study of a primary HIV infection cohort. PLoS medicine153e1002537 pubmed

Mackelprang RD, Bamshad MJ, Chong JX, Hou X, Buckingham KJ, Shively K, deBruyn G, Mugo NR, Mullins JI, McElrath MJ, Baeten JM, Celum C, Emond MJ, Lingappa JR, 2017 Whole genome sequencing of extreme phenotypes identifies variants in CD101 and UBE2V1 associated with increased risk of sexually acquired HIV-1. PLoS pathogens1311e1006703 pubmed

deCamp AC, Rolland M, Edlefsen PT, Sanders-Buell E, Hall B, Magaret CA, Fiore-Gartland AJ, Juraska M, Carpp LN, Karuna ST, Bose M, LePore S, Miller S, O'Sullivan A, Poltavee K, Bai H, Dommaraju K, Zhao H, Wong K, Chen L, Ahmed H, Goodman D, Tay MZ, Gottardo R, Koup RA, Bailer R, Mascola JR, Graham BS, Roederer M, O'Connell RJ, Michael NL, Robb ML, Adams E, D'Souza P, Kublin J, Corey L, Geraghty DE, Frahm N, Tomaras GD, McElrath MJ, Frenkel L, Styrchak S, Tovanabutra S, Sobieszczyk ME, Hammer SM, Kim JH, Mullins JI, Gilbert PB 2017 Sieve analysis of breakthrough HIV-1 sequences in HVTN 505 identifies vaccine pressure targeting the CD4 binding site of Env-gp120. PloS one1211e0185959 pubmed

Herbeck JT, Peebles K, Edlefsen PT, Rolland M, Murphy JT, Gottlieb GS, Abernethy N, Mullins JI, Mittler JE, Goodreau SM 2018 HIV population-level adaptation can rapidly diminish the impact of a partially effective vaccine. Vaccine364514-520 pubmed

Dapp MJ, Kober KM, Chen L, Westfall DH, Wong K, Zhao H, Hall BM, Deng W, Sibley T, Ghorai S, Kim K, Chen N, McHugh S, Au L, Cohen M, Anastos K, Mullins JI 2017 Patterns and rates of viral evolution in HIV-1 subtype B infected females and males. PloS one1210e0182443 pubmed