This review explores the reactivation of Epstein–Barr virus (EBV) by various biological agents, including bacteria, viruses, and other pathogens. EBV, a ubiquitous human virus, can remain latent in cells but reactivate under stress, immunosuppression, or chemical induction. The review highlights the mechanisms by which these biological agents induce EBV reactivation, such as through direct or indirect host cell activation, and the resulting clinical implications. Key findings include: 1. **Bacteria**: Periodontal pathogens like *Aggregatibacter* and *Helicobacter pylori* can reactivate EBV by causing DNA damage, altering the cellular microenvironment, or triggering specific signaling pathways. 2. **Viruses**: Other viruses such as Human Simplex Virus-1 (HSV), Human Herpesvirus Type 6 (HHV-6), Cytomegalovirus (CMV), and Human Immunodeficiency Virus (HIV) can also reactivate EBV by modulating cellular microenvironments and immune responses. 3. **Other Pathogens**: Hepatitis viruses (HCV, HEV), Human Papillomavirus (HPV), and SARS-CoV-2 have been reported to reactivate EBV, often in immunocompromised individuals or during coinfections. The review emphasizes the need for further research to understand the specific mechanisms and clinical impacts of EBV reactivation by these biological agents, which could inform therapeutic strategies to prevent associated pathologies.This review explores the reactivation of Epstein–Barr virus (EBV) by various biological agents, including bacteria, viruses, and other pathogens. EBV, a ubiquitous human virus, can remain latent in cells but reactivate under stress, immunosuppression, or chemical induction. The review highlights the mechanisms by which these biological agents induce EBV reactivation, such as through direct or indirect host cell activation, and the resulting clinical implications. Key findings include: 1. **Bacteria**: Periodontal pathogens like *Aggregatibacter* and *Helicobacter pylori* can reactivate EBV by causing DNA damage, altering the cellular microenvironment, or triggering specific signaling pathways. 2. **Viruses**: Other viruses such as Human Simplex Virus-1 (HSV), Human Herpesvirus Type 6 (HHV-6), Cytomegalovirus (CMV), and Human Immunodeficiency Virus (HIV) can also reactivate EBV by modulating cellular microenvironments and immune responses. 3. **Other Pathogens**: Hepatitis viruses (HCV, HEV), Human Papillomavirus (HPV), and SARS-CoV-2 have been reported to reactivate EBV, often in immunocompromised individuals or during coinfections. The review emphasizes the need for further research to understand the specific mechanisms and clinical impacts of EBV reactivation by these biological agents, which could inform therapeutic strategies to prevent associated pathologies.