The Vector Labs are structured and organized under a new paradigm for Vector Core operations that is designed to provide investigators with a single source that can supply their vector needs throughout the development of the research programs. The labs utilize an integrated systems approach to speed the flow of vector technologies and information. These systems are designed to provide comprehensive resources to investigators so they can avoid many of the common pitfalls and delays that occur during the translational research period. These pitfalls and delays are caused when a specific vector-disease approach must transition from a basic research environment into the highly regulated and controlled processes of final preclinical safety testing and human clinical trials. The UNC Vector Labs will support MTCC investigators by providing expertise with vector design, construction, and development as well as by providing investigators with the viral vector reagents themselves. Investigators will be able to select the optimal type of viral platform (adenoviral, AAV, lentiviral, retroviral, PIV, cell-based, or plasmid) for the specific research in which they are involved. Investigators can also select from a range of standard quality grades (research, preclinical, or clinical), or can custom design intermediate grades as necessary. The combined staff at the Vector Labs and the Gene Therapy Center have prior experience in bringing to clinical trials virtually all the major viral platforms. Investigators will be able to utilize this experience to aid in creating drug development templates as their research progresses into the clinical arena.

Public Health Relevance

The Vector Core will provide a broad range of services that will benefit public health. Its foremost mission is to provide gene transfer vectors that will treat people with genetic diseases. An important parallel mission is to develop gene transfer vectors that may aid in immunization of the general population to a variety of communicable diseases.

National Institute of Health (NIH)
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Center Core Grants (P30)
Project #
Application #
Study Section
Special Emphasis Panel (ZDK1-GRB-1)
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
University of North Carolina Chapel Hill
Chapel Hill
United States
Zip Code
Panganiban, Ronald A; Sun, Maoyun; Dahlin, Amber et al. (2018) A functional splice variant associated with decreased asthma risk abolishes the ability of gasdermin B to induce epithelial cell pyroptosis. J Allergy Clin Immunol 142:1469-1478.e2
Muhlebach, Marianne S; Hatch, Joseph E; Einarsson, Gisli G et al. (2018) Anaerobic bacteria cultured from cystic fibrosis airways correlate to milder disease: a multisite study. Eur Respir J 52:
Ghaedi, Mahboobe; Le, Andrew V; Hatachi, Go et al. (2018) Bioengineered lungs generated from human iPSCs-derived epithelial cells on native extracellular matrix. J Tissue Eng Regen Med 12:e1623-e1635
Livraghi-Butrico, Alessandra; Wilkinson, Kristen J; Volmer, Allison S et al. (2018) Lung disease phenotypes caused by overexpression of combinations of ?-, ?-, and ?-subunits of the epithelial sodium channel in mouse airways. Am J Physiol Lung Cell Mol Physiol 314:L318-L331
Chen, Gang; Volmer, Allison S; Wilkinson, Kristen J et al. (2018) Role of Spdef in the Regulation of Muc5b Expression in the Airways of Naive and Mucoobstructed Mice. Am J Respir Cell Mol Biol 59:383-396
Goralski, Jennifer L; Wu, Dan; Thelin, William R et al. (2018) The in vitro effect of nebulised hypertonic saline on human bronchial epithelium. Eur Respir J 51:
Hussain, Shah S; George, Shebin; Singh, Shashi et al. (2018) A Small Molecule BH3-mimetic Suppresses Cigarette Smoke-Induced Mucous Expression in Airway Epithelial Cells. Sci Rep 8:13796
Agostini, Maria L; Andres, Erica L; Sims, Amy C et al. (2018) Coronavirus Susceptibility to the Antiviral Remdesivir (GS-5734) Is Mediated by the Viral Polymerase and the Proofreading Exoribonuclease. MBio 9:
Tomati, Valeria; Caci, Emanuela; Ferrera, Loretta et al. (2018) Thymosin ?-1 does not correct F508del-CFTR in cystic fibrosis airway epithelia. JCI Insight 3:
Kim, Christine Seulki; Ahmad, Saira; Wu, Tongde et al. (2018) SPLUNC1 is an allosteric modulator of the epithelial sodium channel. FASEB J 32:2478-2491

Showing the most recent 10 out of 133 publications