The genus Roseburia consists of obligate Gram-positive anaerobic bacteria that are slightly curved, rod-shaped and motile by means of multiple subterminal flagella. It includes five species: Roseburia intestinalis, R. hominis, R. inulinivorans, R. faecis and R. cecicola. Gut Roseburia spp. metabolize dietary components that stimulate their proliferation and metabolic activities. They are part of commensal bacteria producing short-chain fatty acids, especially butyrate, affecting colonic motility, immunity maintenance and anti-inflammatory properties. Modification in Roseburia spp. representation may affect various metabolic pathways and is associated with several diseases (including irritable bowel syndrome, obesity, Type 2 diabetes, nervous system conditions and allergies). Roseburia spp. could also serve as biomarkers for symptomatic pathologies (e.g., gallstone formation) or as probiotics for restoration of beneficial flora.

The early steps of the intracellular trafficking of human papillomavirus type 16 (HPV-16), -31, and -58 pseudovirions were studied by investigating the effects of drugs acting at defined points of endocytosis pathways on virus-like particle-mediated pseudoinfection by overexpression of a dominant-negative form of the Eps15 protein to inhibit clathrin-mediated endocytosis and by electron microscopy. The results obtained suggested the involvement of clathrin-mediated endocytosis in HPV-16 and HPV-58 entry and caveola-mediated endocytosis in HPV-31 entry.As a consequence of interactions with their receptors, viruses can follow a variety of pathways for entry into cells. Among nonenveloped DNA viruses, adenovirus (16), adenoassociated virus (2), and human polyomavirus JC (23) enter cells by means of clathrin-coated endocytic vesicles whereas simian virus 40 (SV40) and mouse polyomavirus are taken up into cells via caveolae (1,21,22,24).Papillomaviruses are small nonenveloped tumorigenic DNA viruses that infect the basal cells of the epithelium. Papillomavirions contain two proteins, L1 and L2, which encapsidate a closed, circular, double-stranded DNA of about 8 kbp. The viral capsid of 50 to 55 nm contains 72 pentamers of L1, and expression of the major capsid protein L1 results in the selfassembly of virus-like particles (VLPs) which have similar characteristics to the virions. Attempts to efficiently grow human papillomaviruses (HPVs) in cell culture have to date been unsuccessful, and consequently, surrogate systems using HPV pseudovirions have been developed to test for viral infectivity (4,13,25,26,29,30).It has previously been reported that in order to infect target cells, papillomaviruses bind to specific cell surface receptors (19,31), penetrate the plasma membrane by an unknown mechanism, and target their genomes to the cell nucleus (18,20,33). There is a growing body of evidence that heparan sulfate proteoglycans act as primary receptors for papillomaviruses and mediate viral attachment (5, 10, 12). Heparan sulfate proteoglycans interact with the carboxyl terminus of the HPV L1 protein (12). Although heparan sulfate proteoglycans are widely distributed on the surfaces of many cell types, they may not be sufficient to allow efficient HPV entry. Evander et al. (9) and McMillan et al. (17) have already shown that alpha-6 integrin is used by HPV type 6 (HPV-6) as a receptor for HPV entry into host cells.Electron microscopy examination has shown that bovine papillomavirus type 1 (BPV-1) virions are seen in the lipid layer-surrounded vesicles (33), suggesting that caveolae are involved in BPV-1 internalization and that they are associated with microtubules in the cytoplasm (15). In addition, uptake of HPV-33 by small and smooth endocytic vesicles (27, 31) suggests that this virus is internalized by caveolae. However, it was reported recently that this virus entry is not inhibited by nystatin, suggesting that it does not require a caveola-dependent pathway (27). The papillomaviruses then penetrate the nuclear me...

Although human papillomavirus (HPV) DNA is detected in the majority of squamous intraepithelial lesions (SILs) and squamous cell carcinomas (SCCs) of the uterine cervix, the persistence and progression of cervical lesions suggest that viral antigens are not adequately presented to the immune system. This hypothesis is reinforced by the observation that most SILs show quantitative and functional alterations of Langerhans cells (LCs). The aim of this study was to determine whether modulation of E-cadherin-mediated homophilic and heterotypic interactions between keratinocytes and LCs is involved in these abnormalities of LCs in (pre)neoplastic cervical epithelium. Cell membrane expression of E-cadherin and the density of CD1a+ LCs were low in the epithelium of SILs and SCC biopsy specimens, compared with normal exocervical epithelium. Dendritic cells (DCs) and LCs generated in vitro were randomly distributed throughout the full thickness of organotypic cultures of E-cadherin- HPV-transformed cells. In contrast, these cells rapidly adhered to the keratinocyte cell layers when HPV-transformed cells transfected with E-cadherin were used. These data suggest that the E-cadherin-mediated contact between keratinocytes and LCs is potentially important for initiating or maintaining the immune response during chronic HPV infection.