Samuel K Campos, PhD

Associate Professor, Immunobiology

skcampos@arizona.edu

Links

Department Profile

NCBI Bibliography

Sam earned his Ph.D. from Rice University in 2005, studying the biology of adenoviral gene therapy vectors and vector targeting in the laboratory of Michael Barry now at Mayo Clinic in Rochester, MN. He then trained as a postdoc from 2005-2008 with Michelle Ozbun at the University of New Mexico, focusing on human papillomavirus (HPV) infection. Sam came to The University of Arizona in 2008 as an assistant research professor in the BIO5 Institute and joined the Department of Immunobiology as an assistant professor in 2011. Sam was promoted to Associate Professor with tenure in Spring 2017.

Cancer Focus

Persistent infections by the high-risk human papillomaviruses (HPVs) cause 5% of total cancers worldwide, including essentially all of the cervical cancers in women. The overall goal of our research is to understand the molecular mechanisms through which HPVs infect and attain persistence in host epithelium. Knowledge of these mechanisms will broaden our understanding of viral-host interactions, may unveil new aspects of cell biology, and could identify potential targets for therapeutic or prophylactic intervention to prevent HPV infections and their associated cancers.

Research Program Role

Cancer Biology Program

Display Name
Samuel K Campos, PhD

Publications

Vesicular trafficking permits evasion of cGAS/STING surveillance during initial human papillomavirus infection.

Uhlorn BL, Jackson R, Li S, Bratton SM, Van Doorslaer K, Campos SK. 2020. Vesicular trafficking permits evasion of cGAS/STING surveillance during initial human papillomavirus infection. PLoS Pathog. 16:e1009028. doi:10.1371/journal.ppat.1009028.

A central region in the minor capsid protein of papillomaviruses facilitates viral genome tethering and membrane penetration for mitotic nuclear entry.

Aydin I, Villalonga-Planells R, Greune L, Bronnimann MP, Calton CM, Becker M, Lai K-Y, Campos SK, Schmidt MA, Schelhaas M. 2017. A central region in the minor capsid protein of papillomaviruses facilitates viral genome tethering and membrane penetration for mitotic nuclear entry. PLoS Pathog. 13:e1006308. doi:10.1371/journal.ppat.1006308.

Translocation of the papillomavirus L2/vDNA complex across the limiting membrane requires the onset of mitosis.

Calton CM, Bronnimann MP, Manson AR, Li S, Chapman JA, Suarez-Berumen M, Williamson TR, Molugu SK, Bernal RA, Campos SK. 2017. Translocation of the papillomavirus L2/vDNA complex across the limiting membrane requires the onset of mitosis. PLoS Pathog. 13:e1006200. doi:10.1371/journal.ppat.1006200.

Subcellular Trafficking of the Papillomavirus Genome during Initial Infection: The Remarkable Abilities of Minor Capsid Protein L2.

Campos SK. 2017. Subcellular Trafficking of the Papillomavirus Genome during Initial Infection: The Remarkable Abilities of Minor Capsid Protein L2. Viruses. 9. doi:10.3390/v9120370.

Furin Cleavage of L2 during Papillomavirus Infection: Minimal Dependence on Cyclophilins.

Bronnimann MP, Calton CM, Chiquette SF, Li S, Lu M, Chapman JA, Bratton KN, Schlegel AM, Campos SK. 2016. Furin Cleavage of L2 during Papillomavirus Infection: Minimal Dependence on Cyclophilins. J Virol. 90:6224–6234. doi:10.1128/JVI.00038-16.

A transmembrane domain and GxxxG motifs within L2 are essential for papillomavirus infection.

Bronnimann MP, Chapman JA, Park CK, Campos SK. 2013. A transmembrane domain and GxxxG motifs within L2 are essential for papillomavirus infection. J Virol. 87:464–73. doi:10.1128/JVI.01539-12.