Recent studies have highlighted the complex interplay between herpes simplex virus (HSV) and the immune system, particularly in the context of neurological disorders and other infections. One significant finding is the role of HSV-1 in Alzheimer's disease, where it has been shown that anti-herpetic tau can preserve neurons via the cGAS-STING-TBK1 pathway, suggesting a potential link between HSV-1 and neurodegenerative processes (ref: Hyde doi.org/10.1016/j.celrep.2024.115109/). Furthermore, research indicates that HSV-1 can manipulate mitochondrial nucleic acid-sensing pathways to reactivate from latent infection, with the UL12.5 protein being crucial for this process. This protein not only promotes viral lytic gene expression but also requires intact RNA- and DNA-sensing pathways, demonstrating HSV-1's ability to exploit antiviral responses for its benefit (ref: Krakowiak doi.org/10.1073/pnas.2413965122/). Additionally, a population study has established a significant association between HSV-2 infection and high-risk human papillomavirus (HR-HPV) infections, with an odds ratio of 1.46 for those with HSV-2, emphasizing the importance of preventive measures against HSV infections (ref: Liu doi.org/10.1093/infdis/). These findings collectively underscore the need for further investigation into the mechanisms by which HSV interacts with host immune responses and its implications for disease pathology.

Epstein-Barr virus (EBV) has been implicated in various malignancies, and recent research has focused on its role in nasopharyngeal carcinoma and other cancers. A first-in-human clinical trial of VK-2019, a small-molecule inhibitor targeting EBV nuclear antigen 1 (EBNA1), demonstrated promising results in patients with EBV-positive nasopharyngeal cancer, with pharmacokinetic and pharmacodynamic studies revealing significant changes in EBV DNA plasma levels (ref: Colevas doi.org/10.1158/1078-0432.CCR-24-2814/). Another study explored how EBV-driven cardiolipin synthesis supports metabolic remodeling during B cell transformation, highlighting the virus's ability to alter host cell metabolism to facilitate its own replication and oncogenic potential (ref: You doi.org/10.1126/sciadv.adr8837/). Additionally, a cohort study revealed that EBV-seronegative kidney transplant recipients have a markedly increased risk of posttransplant lymphoproliferative disease (PTLD), with an age-adjusted hazard ratio of 30.7 compared to seropositive individuals, emphasizing the need for vigilant monitoring in this population (ref: Ludvigsen doi.org/10.1016/j.ajt.2025.01.035/). These studies collectively highlight the multifaceted role of EBV in cancer pathogenesis and the importance of targeted therapeutic strategies.

Cytomegalovirus (CMV) remains a critical concern in transplantation, particularly regarding its impact on patient outcomes. A population-based screening program for congenital CMV (cCMV) revealed that 0.13% of newborns screened positive, with a significant proportion confirmed through urine PCR, underscoring the necessity for early detection and management to prevent long-term sequelae such as sensorineural hearing loss (ref: Dunn doi.org/10.1001/jamapediatrics.2024.5562/). In kidney transplantation, recent findings indicate that human CMV infection induces long-term changes in the cytokine milieu of recipients, with elevated levels of IL-6 and IL-10 persisting for months post-transplant, which could have implications for graft function and patient management (ref: Redondo doi.org/10.1002/jmv.70178/). Additionally, a retrospective cohort study highlighted the risks associated with EBV donor and recipient serostatus, revealing that nearly half of EBV D+/R- recipients developed EBV DNAemia, with a notable incidence of PTLD occurring at a median of 202 days post-transplant (ref: Potluri doi.org/10.7326/ANNALS-24-00165/). These findings emphasize the importance of monitoring viral infections in transplant recipients to optimize outcomes.

The mechanisms by which viruses establish latency and promote pathogenesis are critical areas of research. A study on gammaherpesvirus demonstrated that intrinsic p53 activation restricts the expansion of germinal center B cells during latency establishment, indicating a complex interaction between viral gene expression and host tumor suppressor pathways (ref: Owens doi.org/10.1038/s41467-025-56247-5/). Additionally, the intratumoral injection of the oncolytic virus OH2 in sarcoma patients showed promising tolerability and efficacy, suggesting that oncolytic viruses could be a viable therapeutic option for difficult-to-treat cancers (ref: Tan doi.org/10.1136/jitc-2024-010543/). Furthermore, research on pseudorabies virus revealed that the UL46 protein mediates the phosphorylation of connexin-43, leading to the closure of gap junctions, which facilitates intercellular virus spread while simultaneously hindering immune responses (ref: Tishchenko doi.org/10.1371/journal.ppat.1012895/). These studies collectively illustrate the diverse strategies employed by viruses to manipulate host cellular environments and evade immune detection.

The relationship between viral infections and autoimmune diseases has garnered increasing attention, particularly in understanding how viral components may contribute to disease pathogenesis. A comprehensive analysis of the blood DNA virome in a cohort of individuals with autoimmune diseases and COVID-19 revealed significant associations between viral presence and immune dysregulation, suggesting that specific viral components may exacerbate autoimmune conditions (ref: Sasa doi.org/10.1038/s41588-024-02022-z/). In the context of HIV-associated primary effusion lymphoma, the development of a prognostic score (PEL-PS) has provided valuable insights into patient outcomes, with significant differences in overall survival based on the presence of negative prognostic factors (ref: Lurain doi.org/10.1002/ajh.27580/). Additionally, the interaction between HIV-1 Vpu and SARS-CoV-2 proteins with the STING pathway highlights how these viruses can disrupt antiviral signaling, further complicating the immune response in infected individuals (ref: Rui doi.org/10.1126/scisignal.add6593/). These findings underscore the intricate connections between viral infections and autoimmune diseases, warranting further exploration of therapeutic interventions.

The development of viral vaccines and therapeutics is a rapidly evolving field, with recent studies highlighting innovative approaches to combat viral infections. The oncolytic virus talimogene laherparepvec (T-VEC) has shown efficacy in a phase II trial for patients with difficult-to-resect basal cell carcinomas, achieving a 50% resectability rate after just six cycles of treatment, indicating its potential as a neoadjuvant therapy (ref: Ressler doi.org/10.1038/s43018-024-00879-x/). Furthermore, the association between HSV-2 and high-risk HPV infections emphasizes the need for preventive strategies, including vaccination, to mitigate the risks associated with these viral infections (ref: Liu doi.org/10.1093/infdis/). Additionally, the co-option of mitochondrial nucleic acid-sensing pathways by HSV-1 for reactivation from latency illustrates the virus's ability to manipulate host immune responses, which could inform future therapeutic strategies targeting viral reactivation (ref: Krakowiak doi.org/10.1073/pnas.2413965122/). These studies collectively highlight the importance of continued research in viral therapeutics and the potential for innovative vaccine strategies to address viral diseases.

Herpesviruses, particularly HSV-1, have been implicated in various neurological disorders, with emerging evidence suggesting their role in neurodegenerative diseases such as Alzheimer's. A study found that HSV-1-associated proteins were detected in human brain samples, linking the virus to the pathophysiology of Alzheimer's disease through mechanisms involving tau pathology and the cGAS-STING-TBK1 pathway (ref: Hyde doi.org/10.1016/j.celrep.2024.115109/). Additionally, research indicates that herpesviruses can mimic zygotic genome activation to enhance their replication, showcasing their ability to exploit host cellular mechanisms for viral advantage (ref: Neugebauer doi.org/10.1038/s41467-025-55928-5/). The co-option of mitochondrial nucleic acid-sensing pathways by HSV-1 during reactivation from latency further illustrates the virus's sophisticated strategies to evade immune detection and promote its lifecycle (ref: Krakowiak doi.org/10.1073/pnas.2413965122/). These findings underscore the need for further investigation into the role of herpesviruses in neurological disorders and their potential impact on neurodegenerative disease progression.