Antibiotic resistance in foodborne bacteria poses a substantial global health challenge. Reports indicate that antibiotic overuse in middle-class and low-income countries is a significant factor in the ever-increasing resistance. Resistance mechanisms have developed through enzymatic hydrolysis, reduced membrane permeability, efflux pumps, and target site mutations. Preventive measures like proper hygiene and safe food preparation, vaccination, antibiotic stewardship and surveillance, implementing infection prevention and control (IPC) measures, good agricultural practices, and investigating novel approaches like CRISPR, NGS, nanotechnology, and bacteriophages may be employed to address this challenge. Naturally occurring preservatives (e.g., nisin) are alternatives to antibiotics for food preservation. Prebiotics, probiotics, nanobiotics, phage treatment, and antimicrobial peptides are also substitutes for antibiotics. Furthermore, plant-derived compounds, such as essential oils and plant extracts, are promising substitutes for antibiotics in animal production. This review focuses on the mechanisms of underlying antibiotic resistance in foodborne pathogens, necessary preventive measures, and the challenges associated. Graphical abstract Created using BioRender https://www.biorender.com/

In endemic areas, hepatitis C virus (HCV)/hepatitis B virus (HBV) coinfection is common, and patients with coinfection have a higher risk of developing liver disease such as hepatocellular carcinoma, liver fibrosis and cirrhosis. In such cases, HCV predominates, and HBV replication is suppressed by HCV. HCV core proteins and interferons that are activated by HCV are responsible for the suppression of HBV. Immunosuppression is also seen in patients with HCV and HBV coinfections. A decrease in HCV-neutralizing antibody response and circulation of Th1-like Tfh cells is observed in patients with HCV and HBV coinfection. Both viruses interacted in the liver, and treatment of HCV/HBV coinfection is genotype-based and complex due to the interaction of both viruses. In HCV-dominant cases, direct-acting antiviral drugs and peg interferon plus ribavirin are used for the treatment, with continuous monitoring of AST and ALT. HBV-dominant cases are less common and are treated with peg interferon and nucleoside nucleotide analogues with monitoring of AST and ALT. The SVR rate in HCV-HBV coinfection is higher than that in monoinfection when treated with direct-acting antiviral drugs. But there is a risk of reactivation of HBV during and after therapy. The rate of reactivation is lower in patients treated with direct-acting antiviral drugs as compared to those treated with peg interferon plus ribavirin. Biomarkers of HBV such as HBcrAg, HBV DNA and HBVpg RNA are not effective in the prediction of HBV reactivation; only the hepatitis B surface antigen titre can be used as a biomarker for HBV reactivation. HCV can also be reactive, but this is found in very rare cases in which HBV is present and is treated first.