ABSTRACT
In this review, the authors survey the large number of antibacterial and antiviral proteins present in human saliva. Of interest, most of these antibacterial proteins display antiviral activity, typically against specific viral pathogens. The review focuses on one protein that interacts with both bacteria and viruses-gp340, originally referred to as salivary agglutinin. In the oral cavity, soluble gp340 binds to and aggregates a variety of bacteria, and this is thought to increase bacterial clearance from the mouth. However, when bound to the tooth surface, gp340 promotes bacterial adherence. In the oral cavity, most gp340 is found soluble in saliva and can function as a specific inhibitor of infectivity of HIV-1 and influenza A. In contrast, in the female reproductive track, most gp340 is bound to the cell surface, where it can promote HIV-1 infection.
Subject(s)
Antimicrobial Cationic Peptides/physiology , Antiviral Agents , HIV Infections/metabolism , Receptors, Cell Surface/physiology , Salivary Proteins and Peptides/physiology , Antiviral Agents/metabolism , Bacterial Adhesion , Calcium-Binding Proteins , DNA-Binding Proteins , HIV-1/metabolism , Humans , Influenza A virus/metabolism , Models, Molecular , Orthomyxoviridae , Protein Binding , Protein Conformation , Receptors, Cell Surface/chemistry , Tumor Suppressor ProteinsABSTRACT
The expression of the oncogenes E6 and E7 of the cervical cancer associated human papillomavirus type 18 was shown to be directed from the promoter in position 105 (P105), which is reportedly the only early promoter located within the long control region (LCR). However, in C33A cells transiently transfected with a reporter construct containing the LCR of HPV18 in front of the luciferase gene a transcript initiating at position 56 was present in addition to those initiating from the P105. A perfect TATA Box consensus sequence 30 bp further upstream, which is highly conserved among HPVs associated with cervical cancer, was required for the activity of this novel promoter, denoted here as P56. The P56 specific transcript obviously depends on promoter downstream sequences, since transcripts initiating from the P56 were not present when the CAT gene was cloned downstream of the LCR. We detected transcripts initiating from both the P105 and the P56 in primary keratinocytes harboring episomal HPV18 as well as in the HPV 18 positive cervical carcinoma cell lines HeLa, C4-1 and SW756. Our data suggest that in HPV18, the expression of the early viral proteins including the oncogenes might be directed from a second promoter, located within the LCR.
