ABSTRACT
In recent years, there has been an increase in deaths due to infectious diseases, most notably in the context of viral respiratory pathogens. Consequently, the focus has shifted in the search for new therapies, with attention being drawn to the use of nanoparticles in mRNA vaccines for targeted delivery to improve the efficacy of these vaccines. Notably, mRNA vaccine technologies denote as a new era in vaccination due to their rapid, potentially inexpensive, and scalable development. Although they do not pose a risk of integration into the genome and are not produced from infectious elements, they do pose challenges, including exposing naked mRNAs to extracellular endonucleases. Therefore, with the development of nanotechnology, we can further improve their efficacy. Nanoparticles, with their nanometer dimensions, move more freely in the body and, due to their small size, have unique physical and chemical properties. The best candidates for vaccine mRNA transfer are lipid nanoparticles (LNPs), which are stable and biocompatible and contain four components: cationic lipids, ionizable lipids, polyethylene glycols (PEGs), and cholesterol, which are used to facilitate cytoplasmic mRNA delivery. In this article, the components and delivery system of mRNA-LNP vaccines against viral lung infections such as influenza, coronavirus, and respiratory syncytial virus are reviewed. Moreover, we provide a succinct overview of current challenges and potential future directions in the field.
ABSTRACT
BACKGROUND: Lung cancer is a leading cause of cancer morbidity and mortality worldwide. Several studies have suggested that Human papillomavirus (HPV) infection is an important risk factor in the development of lung cancer. In this study, we aim to address the role of HPV in the development of lung cancer mechanistically by examining the induction of inflammation and epithelial-mesenchymal transition (EMT) by this virus. METHODS: In this case-control study, tissue samples were collected from 102 cases with lung cancer and 48 controls. We examined the presence of HPV DNA and also the viral genotype in positive samples. We also examined the expression of viral genes (E2, E6 and E7), anti-carcinogenic genes (p53, retinoblastoma (RB)), and inflammatory cytokines in HPV positive cases. RESULTS: HPV DNA was detected in 52.9% (54/102) of the case samples and in 25% (12/48) of controls. A significant association was observed between a HPV positive status and lung cancer (OR = 3.37, 95% C.I = 1.58-7.22, P = 0.001). The most prevalent virus genotype in the patients was type 16 (38.8%). The expression of p53 and RB were decreased while and inflammatory cytokines were increased in HPV-positive lung cancer and HPV-positive control tissues compared to HPV-negative lung cancer and HPV-negative control tissues. Also, the expression level of E-cad and PTPN-13 genes were decreased in HPV- positive samples while the expression level of SLUG, TWIST and N-cad was increased in HPV-positive samples compared to negative samples. CONCLUSION: Our study suggests that HPV infection drives the induction of inflammation and EMT which may promote in the development of lung cancer.
