Long non-coding RNAs (lncRNAs) are a class of cellular transcripts, which are involved in various biological processes. There is conflicting data regarding to the origin of these non-coding molecules and lncRNAs are thought to be the origin of viral genome. Here we sought to find the homology between human lncRNAs and viruses. For this purpose, the lncRNAdb database was searched for human lncRNAs. The lncRNAs' sequences were aligned with virus taxa using NCBI's BLAST tool. The phylogenic study was performed with maximum-likelihood based algorithm. The database contains 152 human lncRNAs. As a result, 63 (41.44%) of the lncRNAs have homologies with viruses. Of which, 50 (79.36%) have homology with Stealth virus. Other viruses with homology to lncRNAs were nuclear integrating DNA/RNA viruses. Moreover, 35 of 64 (23.03%) of cancer-associated lncRNAs have sequence homology with the same viruses. In phylogenetic analyses, lncRNAs with no homology to viruses were found to be the ancestor of those with homology to viruses and cancer-irrelevant lncRNAs were found to be the ancestor of cancer-related transcripts. In conclusion, lncRNAs could be the origin of nuclear integrating viruses and the nuclear integrating viruses may evolved from the non-coding regions. The results imply the role of lncRNAs with homology to viruses in human cancers.

Background and Aims: Human Cytomegalovirus (HCMV) is one of the life-threatening agents in immunosuppressed patients and congenitally infected neonates in the world. Mutations in UL27 were suggested to confer low-to high-grade Maribavir (MBV) resistance. As pUL27 R233S variation may involve in either MBV-resistance, we aimed to establish a method for identifying R233 coding sequence mutation. Materials and Methods: Eleven boiled-DNA extracts from 2000 congenitally CMV infected (cCMV) neonates urines were provided. Polymerase Chain Reaction (PCR) was performed to amplify R233 coding sequence. Restriction Fragment Length Polymorphism (RFLP), after selection of HhaI as a proper cutting enzyme at given site by NEBcutter server, was performed. PCR amplicons and digested samples were run on gel-electrophoresis for demonstration expected fragments. Results: Our result has proved that HhaI can cut UL27 containing wild type R233 coding sequence but not theR233 mutants. Among eleven clinical samples, one has shown R233 mutation, but other 10 samples had no variations by PCR-RFLP. Conclusions: It seems that HhaI can be employed for molecular examination of HCMV UL27 R233 variations and this is the first report demonstrating that PCR-RFLP can be used to recognize CMV-pUL27 R233 mutation. Therefore, this work can open a new window for HCMV UL27 polymorphism analysis in the future.

Aim: To investigate the epidemiology of human herpes virus type-6 (HHV-6) among hemodialysis (HD) patients. Materials & methods: DNA was extracted from plasma samples of 149 patients undergoing HD with no history of organ transplantation from 2011 to 2013. Presence of HHV-6 was investigated by using real-time PCR. Results: Diabetes (36.2%) and hypertension (28.8%) were two major factors for HD. The HHV-6 DNA was identified in eight patients (5.37%). Conclusion: This study is one of the few reports of HHV-6 infection among HD patients. In HD patient population, it is critical to improve standards of infection control in dialysis and expand treatment coverage. Furthermore, studies on clinical implications of HHV-6 infection in HD patients are crucial.

Background: The Ccr4-Not protein complex (CNOT complex) is a key regulator of gene expression in eukaryotic cells. Ccr4-Not Complex is composed of at least nine conserved subunits in mammalian cells with two main enzymatic activities. CNOT8 is a subunit of the complex with deadenylase activity that interacts transiently with the CNOT6 or CNOT6L subunits. Here, we focused on the role of the human CNOT8 subunit in the DNA damage response (DDR). Methods: Cell viability was assessed to measure ATP level using a Cell Titer-Glo Luminescence reagent up to 4 days' post CNOT8 siRNA transfection. In addition, expression level of phosphorylated proteins in signalling pathways were detected by western blotting and immunofluorescence microscopy. CNOT8depleted Hela cells post-3 Gy ionizing radiation (IR) treatment were considered as a control. Results: Our results from cell viability assays indicated a significant reduction at 72-hour post CNOT8 siRNA transfection (p= 0.04). Western blot analysis showed slightly alteration in the phosphorylation of DNA damage response (DDR) proteins in CNOT8-depleted HeLa cells following treatment with ionizing radiation (IR). Increased foci formation of H2AX, RPA, 53BP1, and RAD51 foci was observed after IR in CNOT8-depleted cells compared to the control cells. Conclusions: We conclude that CNOT8 deadenylase subunit is involved in the cellular response to DNA damage.