It is important to note that this array was developed to be adapted by any laboratory. Comparison of experimentally obtained Tm peaks to the range of expected specific Tm peaks allows rapid identification or exclusion of the viral pathogen in a sample. This is an initial study to examine the suitability of using PCR arrays for the detection of a group of target viruses. The current array was developed utilizing five previously published and Table 4 . Tm and C(t) values obtained with primer sets specific for HIV-1, HCV, or HBV in testing of 17 human clinical samples in the format of PCR array targeting eight different viruses. 19 originally designed primers sets. However, it can be expanded to a larger number of targets for the same virus. Targeting of several genome areas increases the detection sensitivity of the target virus and provides an intra-assay confirmation of positive signals. Additionally, any new virus of interest can be added to the list of targeted pathogens. Efforts are underway to test the utility of this real-time PCR array using samples with more diverse biological origin and pathogen content.  TcdC Does Not Significantly Repress Toxin Expression in Clostridium difficile 630ΔErm In the past decade, Clostridium difficile has emerged as an important gut pathogen. Symptoms of C. difficile infection range from mild diarrhea to pseudomembranous colitis, sometimes resulting in colectomy or death. The main virulence factors of C. difficile are toxin A and toxin B. Besides the genes encoding these toxins (tcdA and tcdB), the pathogenicity locus (PaLoc) also contains genes encoding a sigma factor (tcdR) and a putative anti-sigma factor (tcdC). The important role of TcdR as a sigma factor for toxin expression is undisputed, whereas the role of TcdC as an anti-sigma factor, inhibiting toxin expression, is currently the subject of debate. To clarify the role of TcdC in toxin expression, we generated an isogenic ClosTron-based mutant of tcdC in Clostridium difficile strain 630Δ Erm (CT::tcdC) and determined the transcription levels of the PaLoc genes and the expression levels of the toxins in the wild type strain and the tcdC mutant strain. We found only minor differences in transcription levels of the PaLoc genes between the wild type and CT::tcdC strains and total toxin levels did not significantly differ either. These results suggest that in C. difficile 630Δerm TcdC is not a major regulator of toxin expression under the conditions tested. Clostridium difficile is an anaerobic, Gram-positive, spore forming rod shaped bacterium that can cause disease with a wide variety of symptoms, ranging from mild diarrhea to severe forms of pseudomembranous colitis [1] [2] [3] . Since 2004, numerous countries have reported outbreaks in health-care facilities caused by hypervirulent C. difficile PCR Ribotype (Type) 027 [1] [2] [3] [4] [5] [6] . Clostridium difficile infection (CDI) caused by Type 027 is associated with a more severe course of the disease and a higher mortality rate than other ribotypes [1, 3, 6] . Recently, increasing numbers of the hypervirulent Type 078 are reported [7] . C. difficile Type 078 is more frequently associated with community acquired CDI and affects a younger population than Type 027 [6] [7] [8] [9] . Furthermore, CDI caused by Type 078 is associated with an increased morbidity compared to other ribotypes [8] .