Abstract: Coxsackievirus B3 (CVB3) is the most common agent known to cause viral myocarditis. The viral genome encodes a single polyprotein that is cleaved to produce several proteins by virally encoded proteases. Most of this proteolytic processing is catalyzed by a cysteine protease called 3C. The 3C protease plays major role in viral replication and cellular damage. To understand the mechanism of 3C function in virus infected cells and also development of antiviral agants against the virus, a 3C expressing plasmid was constructed. The cDNA of 3C protease was synthesized using CVB3 infected cells through reverse transcription process and was cloned in pcDNA3.1- . The constructed plasmid was confirmed by sequencing and restriction enzyme analysis. By transfection of the constructed plasmid into HeLa and MCF-7 cells, we showed that 3C protease induced cell death through multiple converging pathways, such as down regulation of cellular factors and decreasing of mRNA transcripts. This affect on HeLa cells as stronger than MCF-7 cells. 

Background and Aims: It has been documented that in addition to the genetic susceptibility, environmental factors particularly viruses can also play an important role in the initiation or development of the pathogenesis of type 1 diabetes (T1D). However, findings from several epidemiological studies have shown conflicting results regarding the role of enteroviruses infections in this field of research. The purpose of the current study was to investigate a link between coxsackieviruses B3 and B4 infection and the development of T1D in children.
Materials and Methods: In this case-control study, 80 pediatric patients under 14 year of age with T1D and 80 non-diabetic children controls were enrolled between October 2017 to March 2018 from the Children's Medical Center in Tehran. Then, anti-GAD65 and anti-IA-2 autoantibodies were assessed in two groups using commercially available Enzyme linked immunosorbent assay (ELISA) kits. IgG antibodies of both Coxsackieviruses B3 and B4 were also measured by direct ELISA kits.
Results: The mean anti-GAD65 antibody titer in CV B3+  samples was 4.26 ± 2.46 IU/mL,
and was slightly higher than that found in the CV B3-  samples with a mean titer of 3.62 ± 2.08 IU/mL (p = 0.22; 95% CI: -1.69 to 0.4). Also, the mean anti-IA-2 ELISA OD450 values in CV B3+ samples (0.260 ± 0.155) was similar with that of the CV B3- samples (0.260 ± 0.160) (p = 0.98; 95% CI: -0.079 to 0.077).
Conclusion: This study showed that the titer of autoantibodies in CVB3+ or CVB4+ samples were not significantly different compared to CVB- samples. The results of this study suggest that there is still a need for further investigations to prove the association of coxsackieviruses and diabetes.