The gradual deterioration of the supporting periodontal tissues caused by periodontitis, a chronic multifactorial inflammatory disease, is thought to be triggered by the colonization of dysbiotic plaque biofilms in a vulnerable host. One of the most prevalent dental conditions in the world, periodontitis is now the leading factor in adult tooth loss. When periodontitis does develop, it is treated by scraping the mineralized deposits and dental biofilm off the tooth surfaces. Numerous studies have shown that non-surgical treatment significantly improves clinical and microbiological indices in individuals with periodontitis. Although periodontal parameters have significantly improved, certain bacterial reservoirs often persist on root surfaces even after standard periodontal therapy. Periodontitis has been treated with local or systemic antibiotics as well as scaling and root planning. Since there aren't many brand-new antibiotics on the market, several researchers are currently concentrating on creating alternate methods of combating periodontal germs. There is a delay in a study on the subject of nanoparticle (NP) toxicity, which is especially concerned with mechanisms of action, while the area of nanomedicine develops. The most promising of them are metal NPs since they have potent antibacterial action. Metal NPs may be employed as efficient growth inhibitors in a variety of bacteria, making them useful for the treatment of periodontitis. In this way, the new metal NPs contributed significantly to the development of efficient anti-inflammatory and antibacterial platforms for the treatment of periodontitis. The current therapeutic effects of several metallic NPs on periodontitis are summarized in this study. This data might be used to develop NP-based therapeutic alternatives for the treatment of periodontal infections. Graphical Abstract

MicroRNAs (miRNAs) are a group of small non-coding RNAs that regulate gene expression by targeting mRNA. Moreover, it has been shown that miRNAs expression are changed in various diseases, such as cancers, autoimmune disease, infectious diseases, and neurodegenerative Diseases. The suppression of miRNA function can be easily attained by utilizing of anti-miRNAs. In contrast, an enhancement in miRNA function can be achieved through the utilization of modified miRNA mimetics. The discovery of appropriate miRNA carriers in the body has become an interesting subject for investigators. Exosomes (EXOs) therapeutic efficiency and safety for transferring different cellular biological components to the recipient cell have attracted significant attention for their capability as miRNA carriers. Mesenchymal stem cells (MSCs) are recognized to generate a wide range of EXOs (MSC-EXOs), showing that MSCs may be effective for EXO generation in a clinically appropriate measure as compared to other cell origins. MSC-EXOs have been widely investigated because of their immune attributes, tumor-homing attributes, and flexible characteristics. In this article, we summarized the features of miRNAs and MSC-EXOs, including production, purification, and miRNA loading methods of MSC-EXOs, and the modification of MSC-EXOs for targeted miRNA delivery in various diseases. Graphical abstract

Hepatitis A virus (HAV) is one of the well‐known viruses that cause hepatitis all around the globe. Although this illness has decreased in developed countries due to extensive immunization, numerous developing and under‐developed countries are struggling with this virus. HAV infection can be spread by oral‐fecal contact, and there are frequent epidemics through nutrition. Improvements in socioeconomic and sanitary circumstances have caused a shift in the disease’s prevalence worldwide. Younger children are usually asymptomatic, but as they become older, the infection symptoms begin to appear. Symptoms range from slight inflammation and jaundice to acute liver failure in older individuals. While an acute infection may be self‐limiting, unrecognized persistent infections, and the misapplication of therapeutic methods based on clinical guidelines are linked to a higher incidence of cirrhosis, hepatocellular carcinoma, and mortality. Fortunately, most patients recover within two months of infection, though 10–15% of patients will relapse within the first six months. A virus seldom leads to persistent infection or liver damage. The mainstay of therapy is based on supportive care. All children from 12–23 months, as well as some susceptible populations, should receive routine vaccinations, according to the Centers for Disease Control and Prevention and the American Academy of Pediatrics. Laboratory diagnosis of HAV is based on antigen detection, checking liver enzyme levels, and antibody screening. Furthermore, polymerase chain reaction (PCR) technology has identified HAV in suspected nutrition sources; therefore, this technique is used for preventative measures and food‐related laws.

Viruses communicate with their hosts through interactions with proteins, lipids, and carbohydrate moieties on the plasma membrane (PM), often resulting in viral absorption via receptor-mediated endocytosis. Many viruses cannot multiply unless the host’s cholesterol level remains steady. The large endo/lysosomal membrane protein (MP) Niemann-Pick C1 (NPC1), which is involved in cellular cholesterol transport, is a crucial intracellular receptor for viral infection. NPC1 is a ubiquitous housekeeping protein essential for the controlled cholesterol efflux from lysosomes. Its human absence results in Niemann-Pick type C disease, a deadly lysosomal storage disorder. NPC1 is a crucial viral receptor and an essential host component for filovirus entrance, infection, and pathogenesis. For filovirus entrance, NPC1’s cellular function is unnecessary. Furthermore, blocking NPC1 limits the entry and replication of the African swine fever virus by disrupting cholesterol homeostasis. Cell entrance of quasi-enveloped variants of hepatitis A virus and hepatitis E virus has also been linked to NPC1. By controlling cholesterol levels, NPC1 is also necessary for the effective release of reovirus cores into the cytoplasm. Drugs that limit NPC1’s activity are effective against several viruses, including SARS-CoV and Type I Feline Coronavirus (F-CoV). These findings reveal NPC1 as a potential therapeutic target for treating viral illnesses and demonstrate its significance for several viral infections. This article provides a synopsis of NPC1’s function in viral infections and a review of NPC1 inhibitors that may be used to counteract viral infections. Graphical Abstract

According to a paper released and submitted to WHO by IARC scientists, there would be 905,700 new cases of liver cancer diagnosed globally in 2020, with 830,200 deaths expected as a direct result. Hepatitis B virus (HBV) hepatitis C virus (HCV), and hepatitis D virus (HDV) all play critical roles in the pathogenesis of hepatocellular carcinoma (HCC), despite the rising prevalence of HCC due to non-infectious causes. Liver cirrhosis and HCC are devastating consequences of HBV and HCV infections, which are widespread worldwide. Associated with a high mortality rate, these infections cause about 1.3 million deaths annually and are the primary cause of HCC globally. In addition to causing insertional mutations due to viral gene integration, epigenetic alterations and inducing chronic immunological dysfunction are all methods by which these viruses turn hepatocytes into cancerous ones. While expanding our knowledge of the illness, identifying these pathways also give possibilities for novel diagnostic and treatment methods. Nuclear factor erythroid 2-related factor 2 (NRF2) activation is gaining popularity as a treatment option for oxidative stress (OS), inflammation, and metabolic abnormalities. Numerous studies have shown that elevated Nrf2 expression is linked to HCC, providing more evidence that Nrf2 is a critical factor in HCC. This aberrant Nrf2 signaling drives cell proliferation, initiates angiogenesis and invasion, and imparts drug resistance. As a result, this master regulator may be a promising treatment target for HCC. In addition, the activation of Nrf2 is a common viral effect that contributes to the pathogenesis, development, and chronicity of virus infection. However, certain viruses suppress Nrf2 activity, which is helpful to the virus in maintaining cellular homeostasis. In this paper, we discussed the influence of Nrf2 deregulation on the viral life cycle and the pathogenesis associated with HBV and HCV. We summed up the mechanisms for the modulation of Nrf2 that are deregulated by these viruses. Moreover, we describe the molecular mechanism by which Nrf2 is modulated in liver cancer, liver cancer stem cells (LCSCs), and liver cancer caused by HBV and HCV.