The pathogenicity mechanisms employed by the bovine pathogen Campylobacter fetus are poorly understood. Despite their close genetic relationship, the two subspecies C. fetus fetus and C. fetus venerealis exhibit distinct host and tissue preferences, rendering them an ideal model system to study the molecular basis of host adaption.The C. fetus venerealis-specific type 4 secretion system has previously been linked to virulence by demonstrating its involvement in invasion of a human cultured cell line. Furthermore, several lines of evidence have assigned effector functions to the Cfv proteins Fic1 and Fic2. This study thus aimed at characterizing these two putative effectors with respect to their translocation by bacterial type 4 secretion systems and their phenotype in eukaryotic cells. Transfer studies employing the CRAfT (Cre reporter assay for translocation) have remained negative concerning Fic transport and have thus highlighted the need for a test system more closely mimicking the natural conditions for Campylobacter protein translocation. Creation of an fic1fic2 knockout strain via homologous recombination has been hampered by the existence of a yet unidentified chromosomal site of suicide vector integration preferred to the fic locus. As an alternative to deletion of the genes, the effect of their overexpression on invasion of eukaryotic cells was studied. In first trials, however, the invasion phenotype of C. fetus venerealis remained unchanged despite Fic overexpression.Construction of Fic1 and Fic2 overexpression constructs has nevertheless paved the way for future experiments on cell invasion and cytotoxicity, employing different Cfv strain backgrounds and human cell lines. Studies of this kind will eventually provide insight into the function of the putative Campylobacter fetus venerealis effector proteins Fic1 and Fic2.