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Background: Herpes simplex virus (HSV) infections are prevalent worldwide, posing challenges due to asymptomatic carriage and recurrent outbreaks. Conventional treatments, including antiviral medications, are limited by drug resistance. Photodynamic therapy (PDT) offers a promising alternative, leveraging photosensitizers to induce viral inactivation via reactive oxygen species (ROS) generation upon light activation., Methods: This study investigates the efficacy of 5-aminolevulinic acid (5-ALA) as a photosensitizer in antiviral PDT against HSV-1. HSV-1 was treated with varying concentrations of 5-ALA and subjected to light irradiation at a 630 nm wavelength. Virus titers were assessed using the 50 % Tissue Culture Infectious dose (TCID50) assay. Six experimental groups were used: [1] Control (no 5-ALA or light), HSV-1 with 0.05 g/ml 5-ALA and 630 nm light, [2] HSV-1 with 0.05 g/ml 5-ALA (no light), [3] HSV-1 with 0.1 g/ml 5-ALA and light, [4] HSV-1 with 0.1 g/ml 5-ALA (no light), and [5] HSV-1 with light (no 5-ALA)., Results: Virus treatment with 0.1 g/ml 5-ALA combined with light irradiation significantly reduced HSV-1 titer compared to control groups (p < 0.05). Specifically, the virus titer decreased from 10 6.3 TCID50/ml in the control group to 10 4.5 TCID50/ml in the treated group. However, lower concentrations of 5-ALA or light irradiation alone did not yield significant reductions in HSV-1 titer (p > 0.05). Group 4, receiving 0.1 g/ml 5-ALA with light irradiation, exhibited a significantly greater reduction in virus titer than group 2, receiving 0.05 g/ml 5-ALA with light irradiation (p < 0.05)., Conclusions: 5-ALA-mediated PDT demonstrates selective antiviral efficacy against HSV-1, particularly at higher concentrations coupled with light irradiation. These findings underscore the potential of 5-ALA-based PDT as a promising approach for HSV-1 treatment, especially in cases of drug-resistant strains and immunocompromised individuals. Optimization of dosage and treatment protocols is essential for maximizing effectiveness in clinical applications, highlighting the need for further research in this area., Competing Interests: Declaration of competing interest None., (Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.)

Centromeres are critical structures involved in chromosome segregation, maintaining genomic stability, and facilitating the accurate transmission of genetic information. They are key in coordinating the assembly and help keep the correct structure, location, and function of the kinetochore, a proteinaceous structure vital for ensuring proper chromosome segregation during cell division. Abnormalities in centromere structure can lead to aneuploidy or chromosomal instability, which have been implicated in various diseases, including cancer. Accordingly, abnormalities in centromeres, such as structural rearrangements and dysregulation of centromere-associated proteins, disrupt gene function, leading to uncontrolled cell growth and tumor progression. For instance, altered expression of CENP-A, CENP-E, and others such as BUB1, BUBR1, MAD1, and INCENP, have been shown to ascribe to centromere over-amplification, chromosome missegregation, aneuploidy, and chromosomal instability; this, in turn, can culminate in tumor progression. These centromere abnormalities also promoted tumor heterogeneity by generating genetically diverse cell populations within tumors. Advanced techniques like fluorescence in situ hybridization (FISH) and chromosomal microarray analysis are crucial for detecting centromere abnormalities, enabling accurate cancer classification and tailored treatment strategies. Researchers are exploring strategies to disrupt centromere-associated proteins for targeted cancer therapies. Thus, this review explores centromere abnormalities in cancer, their molecular mechanisms, diagnostic implications, and therapeutic targeting. It aims to advance our understanding of centromeres' role in cancer and develop advanced diagnostic tools and targeted therapies for improved cancer management and treatment., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Background and Objectives: Host genetic changes like single nucleotide polymorphisms (SNPs) are one of the main factors influencing susceptibility to viral infectious diseases. This study aimed to investigate the association between the host SNP of Toll-Like Receptor3 (TLR3) and Toll-Like Receptor7 (TLR7) genes involved in the immune system and susceptibility to COVID-19 in a sample of the Iranian population., Materials and Methods: This retrospective case-control study evaluated 244 hospitalized COVID-19 patients as the case group and 156 suspected COVID-19 patients with mild signs as the control group. The genomic DNA of patients was genotyped for TLR7 (rs179008 and rs179009) and TLR3 (rs3775291 and rs3775296) SNPs using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method., Results: A significant association between rs179008 SNP in the TLR7 gene and the susceptibility of COVID-19 was found between case and control groups. The AT genotype (Heterozygous) of TLR7 rs179008 A>T polymorphism showed a significant association with a 2.261-fold increased odds of COVID-19 (P=0.003; adjusted OR: 2.261; 99% CI: 1.117-4.575). In addition, a significant association between TC genotype of TLR7 rs179009 T>C polymorphism and increased odds of COVID-19 (P<0.0001; adjusted OR: 6.818; 99% CI: 3.149-14.134) were determined. The polymorphism frequency of TLR3 rs3775291 and rs3775296 genotypes were not significantly different between the case and control groups (P> 0.004167)., Conclusion: SNPs in TLR7 rs179008 and rs179009 genotypes are considered host genetic factors that could be influenced individual susceptibility to COVID-19. The SNPs in TLR3 (rs3775296 and rs3775291) showed no significant association with COVID-19 in Iranian population., (Copyright© 2024 The Authors. Published by Tehran University of Medical Sciences.)

Coronavirus disease 2019 (COVID-19) is an infectious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), but the pathogenesis is unclear. Host genetic background is one of the main factors influencing the patients' susceptibility to several viral infectious diseases. This study aimed to investigate the association between host genetic polymorphisms of two genes, including vitamin D receptor (VDR) and vitamin D binding protein (DBP), and susceptibility to COVID-19 in a sample of the Iranian population. This case-control study enrolled 188 hospitalized COVID-19 patients as the case group and 218 suspected COVID-19 patients with mild signs as the control group. The VDR (rs7975232, rs731236 and rs2228570) and DBP (rs7041) gene single nucleotide polymorphisms (SNPs) were genotyped by Polymerase Chain Reaction Restriction - Fragment Length Polymorphism (PCR-RFLP) method. A significant association between rs2228570 SNP in the VDR gene and the susceptibility of COVID-19 was found between case and control groups. The CT genotype (Heterozygous) of rs2228570 C > T polymorphism showed significant association with a 3.088 fold increased odds of COVID-19 (p < .0001; adjusted OR: 3.088; 95% CI: 1.902-5.012). In addition, a significant association between CC genotype of rs2228570 CT polymorphism and increased odds of COVID-19 in male and female groups (p = .001; adjusted OR: 3.125; 95% CI: 1.630-5.991 and p = .002; adjusted OR: 3.071; 95% CI: 1.485-6.354 respectively) were determined. Our results revealed no significant differences in the frequency of genotype and allele of VDR (rs7975232 and rs731236) and DBP (rs7041) between SARS-CoV-2-infected patients and controls (p > .05). Our results showed that polymorphism of VDR (rs2228570) probably could influence individual susceptibility to COVID-19. The polymorphisms of VDR (rs7975232 and rs731236) and DBP (rs7041) were not associated with SARS-CoV-2 infection susceptibility., (© 2022 John Wiley & Sons Ltd.)