John S. Albin

Year Entered: 2005

Degrees Received:
B.A., Microbiology and Spanish, University of Kansas, 2005

Honors and Awards:
Honors, Years 1 and 2, Medical School
Warwick Scholarship, 2008-2009

Thesis Advisor: Reuben Harris, Ph.D., MICaB Graduate Program

Current Research:

My work in the Harris lab focuses on the human DNA cytosine deaminases APOBEC3F and APOBEC3G. Both of these proteins are able to block infection by human immunodeficiency virus type 1 (HIV-1) in the absence of the viral accessory protein virion infectivity factor (Vif). This restrictive activity does not typically manifest in vivo, however, because wild-type Vif-proficient viruses target APOBEC3F and APOBEC3G for degradation.

I am interested in the mechanisms by which APOBEC3F and APOBEC3G may block HIV-1 infection when no longer targeted by Vif. This work anticipates a future in which new classes of antiretroviral drugs will block the interaction of Vif with APOBEC3 proteins. In addition to this developing therapeutic scenario, I am also interested in the implications of APOBEC3 mutational activity for the efficacy of current antiretroviral therapies.

Publications:

Haché G, Shindo K, Albin JS, Harris RS. Evolution of HIV-1 isolates that use a novel Vif-independent  mechanism to resist restriction by human APOBEC3G. Curr Biol. 2008;18:819-824.

Sundaram P, Han W, Cohen N, Echalier B, Albin J, Timmons L. Caenorhabditis elegans ABC_RNAi transporters interact genetically with rde-2 and mut-7. Genetics 2008;178:801-814.