Research in The Tumban Lab focuses on augmenting immune (B- and T-cells) responses against human papillomavirus (HPV) infections. HPV infections are associated with a number of malignancies including cervical cancer, genital warts, as well as oropharyngeal cancers. There are currently three FDA approved prophylactic vaccines to protect against HPV infection. The vaccines are composed of virus-like particles (VLPs) derived from the major capsid protein, L1; the L1 protein, also known as the major capsid protein, is one of the two capsid proteins (L1 and L2) that make up the icosahedaral capsid. These HPV vaccines elicit high titer antibody responses against HPV infection. However, they provide protection mostly against the HPV types included in the vaccines; i.e. against HPV types associated with 70-90% of cervical cancer. The L1 protein is not conserved among HPV types. The other capsid protein (minor capsid protein, L2), especially the N-terminus is conserved among HPV types. A number of studies within the last one or two decades have shown that immune responses directed towards L2 can cross-neutralize heterologous HPV types, albeit at low magnitudes. Recent work from our group within the last few years indicates that the display of L2 epitopes on a highly immunogenic platform such as bacteriophage VLPs can enhance the immunogenicity of L2 as well as the magnitudes of cross-protection against heterologous HPV types. Our Lab continues to explore strategies to enhance and refine B cell responses against infection with multiple HPV types; we are particularly interested in developing and testing novel recombinant antigens against HPV infections.
In addition to enhancing B cells responses against HPV, our Lab is also interested in exploring strategies to boost cell-mediated (T-cell) immune responses against HPV infections, especially HPV-associated neoplastic cells. We are interested in: 1) boosting T-cell responses against HPV viral oncogenes. 2) identifying novel ligands that can be used for targeted delivery of cargos to HPV-associated cancer cells.
