Virology News

Recombinant human papillomavirus (HPV) virus-like particle (VLP) vaccines based on the L1 capsid protein have been shown to be efficient prophylactic vaccines, albeit type-specific. As a first step to investigate the feasibility of extending protection against non-vaccine types, HPV-16 L1 chimaeras were generated. The region downstream of L1 amino acid (aa) 413 was replaced with selected cross-neutralising epitopes (aa 108-120; 56-81 and 17-36) derived from the HPV-16 L2 protein, generating proteins designated SAF, L2.56 and L2.17, respectively. The chimaera L1BPV containing BPV-1 L2 peptide aa 1-88 was similarly constructed. The chimaeras were evaluated for expression in insect cells; their ability to form particles was studied by electron microscopy, and their immunogenicity was evaluated in mice. SAF, L2.56 and L2.17 proteins were expressed to high concentrations in insect cells and elicited HPV-16 pseudovirus-neutralising anti-L1 antibodies. L2.56 and L2.17 also elicited anti-L2 antibodies. L1BPV was a poor vaccine candidate due to low levels of expression with concomitant lack of immunogenicity. All chimaeras assembled into tertiary structures. The results indicate that chimaeric L1 vaccines incorporating cross-neutralising L2 peptides could be promising second-generation prophylactic HPV vaccine candidates.

There are over 100 different types of human papilloma virus (HPV). Cervical cancer is known to be caused by infection with approximately 14 so-called "high-risk" types of this virus.  

Researchers from Manchester looked at the different types of HPV found in cervical smears and invasive cervical cancers from HIV positive and HIV negative women in Kenya. They found high numbers of a specific type of HPV (type 53) in normal cervical smears from HIV positive women, but this was rarely found in HIV negative women. This sub-type was also never found in cervical cancers from either HIV positive or negative women.

Dr Ian Hampson, a Senior Lecturer in Viral Oncology from The University of Manchester who lead the study, said: "It is well known that HIV increases the number of different types of HPV found in any one patient which implies that HIV opens the door for infection with multiple types of HPV. If only high-risk types are present these will undoubtedly accelerate progression to cancer whereas if other types (eg type 53) are also present they may actually compete with the high-risk types to inhibit progression to cervical cancer."