The immune responses elicited by herpesviruses are complex and involve various mechanisms that viruses exploit to evade host defenses. For instance, Kaposi's sarcoma-associated herpesvirus (KSHV) utilizes its encoded Bcl-2 (vBcl-2) to induce mitochondrial fission, thereby impairing mitochondrial antiviral signaling and inhibiting interferon responses, which enhances viral production (ref: Zhu doi.org/10.1038/s41564-025-02018-3/). In contrast, the cGAS-STING pathway, crucial for initiating interferon responses, also induces autophagy during herpes simplex virus (HSV) infections, with TRIM23 identified as a key mediator of this process (ref: Acharya doi.org/10.1038/s41467-025-59338-5/). Furthermore, Epstein-Barr virus (EBV) infection leads to aberrant B cell migration through FAK-dependent chemotaxis pathways, which may contribute to its oncogenic potential (ref: Delecluse doi.org/10.1038/s41467-025-59813-z/). These studies highlight the diverse strategies employed by herpesviruses to manipulate host cellular processes for their benefit, emphasizing the need for further research into these interactions to inform therapeutic strategies. In addition to immune evasion, the methodologies employed in these studies reveal significant advancements in our understanding of herpesvirus biology. For example, the use of nano-flow cytometry has enabled the discrimination between human cytomegalovirus (HCMV) virions and extracellular vesicles, providing insights into their distinct roles in viral pathogenesis (ref: Bokun doi.org/10.1002/jev2.70060/). Moreover, the investigation of EBNA-1-specific antibodies during acute infectious mononucleosis has demonstrated their functional properties, including antibody-dependent cellular phagocytosis, which may play a role in controlling EBV infections (ref: Ganta doi.org/10.1016/j.celrep.2025.115709/). Collectively, these findings underscore the intricate interplay between herpesviruses and host immune responses, revealing potential targets for therapeutic intervention.

Epstein-Barr virus (EBV) is implicated in various diseases, including autoimmune disorders and cancers. Recent studies have shown that latent EBV enhances the efficacy of teplizumab, a monoclonal antibody used in type 1 diabetes treatment, suggesting that EBV seropositivity may influence therapeutic outcomes (ref: Lledó-Delgado doi.org/10.1038/s41467-025-60276-5/). Additionally, the dynamics of CD8+ T cell responses during latent EBV infection have been characterized, revealing the generation of diverse memory responses that are crucial for controlling viral reactivation (ref: Santosa doi.org/10.1084/jem.20242078/). These findings highlight the importance of understanding EBV's role in modulating immune responses and its potential impact on disease progression and treatment efficacy. Moreover, the exploration of the EBV-host chromatin interactome has unveiled the complex regulatory mechanisms governing gene expression during infection. Utilizing advanced 3D genome mapping techniques, researchers have delineated the spatial architecture of EBV within host cells, revealing critical interactions between EBV noncoding RNAs and host chromatin (ref: Tian doi.org/10.1038/s44318-025-00466-5/). This intricate interplay may contribute to the pathogenesis of EBV-associated diseases, including diffuse large B-cell lymphoma, where reactivation of latent EBV is being investigated as a therapeutic strategy (ref: Xu doi.org/10.1093/narcan/). Overall, these studies underscore the multifaceted role of EBV in disease and the potential for targeted therapies that leverage our understanding of its biology.

Cytomegalovirus (CMV) infections pose significant challenges, particularly in immunocompromised populations such as transplant recipients. Recent research has focused on the use of virus-specific T cells (VSTs) for the prophylaxis and treatment of CMV infections following hematopoietic stem cell and solid organ transplants. A scoping review highlighted the efficacy of CMV-VSTs in preventing and managing infections, emphasizing their potential as a therapeutic strategy (ref: Fung doi.org/10.1093/cid/). Furthermore, the role of CMV in cancer development has been underscored by studies linking HCMV infection to the formation of polyploid giant cancer cells, suggesting that HCMV gene products may manipulate cellular pathways associated with tumorigenesis (ref: El Baba doi.org/10.1016/j.canlet.2025.217824/). Additionally, the relationship between EBV infection and mental health has been explored, revealing a significant association between EBV levels and depression, supported by Mendelian randomization analysis (ref: Li doi.org/10.1016/j.jad.2025.119488/). This connection highlights the broader implications of viral infections on mental health and underscores the need for comprehensive approaches to patient care. Moreover, the discovery that gammaherpesvirus infection can trigger the formation of tRNA fragments from premature tRNAs adds another layer of complexity to our understanding of viral interactions with host cellular machinery (ref: Manning doi.org/10.1128/mbio.00875-25/). Collectively, these findings emphasize the need for continued research into CMV and its interactions with the immune system and its potential role in cancer and mental health.

Herpes simplex virus type 1 (HSV-1) is a prevalent pathogen known for its ability to establish latency and cause recurrent infections. Recent studies have investigated the impact of host metabolic pathways on HSV-1 infection dynamics, revealing that de novo lipogenesis is essential for HSV-1 infectivity. The virus upregulates fatty acid synthase (FASN), leading to increased lipid accumulation, which is crucial for viral replication (ref: Albano doi.org/10.1371/journal.ppat.1013068/). This finding suggests that targeting metabolic pathways may offer new therapeutic avenues for managing HSV-1 infections. In addition to metabolic interactions, the development of novel models has enhanced our understanding of HSV-1 pathogenesis. A porcine corneal explant model was utilized to study the initial events during acute HSV-1 infection, revealing that the infection is primarily restricted to the corneal epithelium (ref: Arshad doi.org/10.1371/journal.ppat.1013162/). This model provides valuable insights into the mechanisms underlying herpes keratitis, a leading cause of infectious blindness. Furthermore, the implications of COVID-19 vaccination on individuals with Long COVID have been explored, shedding light on the immune responses and symptomatology in this population (ref: Grady doi.org/10.1038/s43856-025-00829-3/). These studies collectively highlight the intricate dynamics of HSV-1 infection and the potential for innovative therapeutic strategies.

The development of effective vaccines against herpesviruses, particularly cytomegalovirus (CMV), remains a critical area of research. Recent studies have focused on the structural basis of neutralization by antibodies targeting glycoprotein B (gB) of CMV, revealing that specific antibody responses can significantly enhance neutralization efficacy (ref: Wu doi.org/10.1016/j.celrep.2025.115646/). This understanding is crucial for designing vaccines that can elicit robust immune responses in vulnerable populations, such as newborns and immunocompromised individuals. Moreover, innovative approaches such as heterologous prime-boost strategies combining mRNA vaccines with oncolytic viruses have shown promise in overcoming immune suppression within tumors, enhancing therapeutic efficacy in cancer treatment (ref: Zhang doi.org/10.1016/j.celrep.2025.115745/). Additionally, the use of CRISPR/Cas12a systems for the ultrasensitive detection of herpes simplex virus (HSV) highlights the potential for integrating advanced technologies into vaccine development and diagnostics (ref: Xu doi.org/10.1016/j.bios.2025.117597/). These advancements underscore the importance of continued research in vaccine development to combat herpesvirus infections effectively.

Herpesviruses, particularly Epstein-Barr virus (EBV) and cytomegalovirus (CMV), are associated with various malignancies, prompting extensive research into their roles in cancer pathogenesis. Recent studies have demonstrated that EBV can reactivate in diffuse large B-cell lymphoma (DLBCL), providing a potential therapeutic target for lytic induction therapy, which aims to sensitize tumor cells to treatment (ref: Xu doi.org/10.1093/narcan/). This approach highlights the potential for leveraging viral reactivation to enhance the efficacy of existing cancer therapies. Additionally, the impact of CMV on cancer development has been explored, with findings indicating that CMV infection can lead to genomic instability in non-replicative HSV-1 vectors, which are being investigated for gene therapy applications (ref: Basset doi.org/10.3390/ijms26104941/). Furthermore, the role of coagulation factors in herpes zoster patients has been examined, revealing differences in coagulation parameters that may influence disease outcomes (ref: Yuan doi.org/10.3389/fimmu.2025.1511901/). These studies collectively emphasize the intricate relationship between herpesviruses and cancer, underscoring the need for targeted research to develop effective therapeutic strategies.

The clinical implications of herpesvirus infections extend beyond acute disease, impacting chronic conditions and treatment outcomes. For instance, the effectiveness of the live zoster vaccine in patients with type 2 diabetes has been evaluated, demonstrating significant reductions in the risk of herpes zoster and associated complications (ref: Kim doi.org/10.1016/j.cmi.2025.05.003/). This finding underscores the importance of vaccination in high-risk populations to prevent herpesvirus-related morbidity. Moreover, the association between Epstein-Barr virus (EBV) infection and multiple sclerosis (MS) has been further elucidated, with evidence suggesting that EBV-induced B cell expansion correlates with early MS activity (ref: SoRelle doi.org/10.1172/jci.insight.188543/). This connection highlights the potential for targeting EBV in MS treatment strategies. Additionally, the comparative effectiveness of duloxetine and amitriptyline in managing postherpetic neuralgia has been investigated, revealing significant pain relief with both combinations, which may inform clinical decision-making for pain management (ref: Wang doi.org/10.1111/cns.70460/). These findings emphasize the need for a comprehensive understanding of herpesvirus infections to optimize patient care and treatment outcomes.

The interactions between herpesviruses and host metabolism are critical for understanding viral pathogenesis and developing therapeutic strategies. Recent studies have shown that gammaherpesvirus infections can manipulate host lipid metabolism, leading to exaggerated germinal center responses that facilitate chronic infection (ref: Schmalzriedt doi.org/10.1128/jvi.00757-25/). This manipulation of metabolic pathways underscores the importance of host-virus interactions in shaping immune responses and disease outcomes. Additionally, the impact of COVID-19 vaccination on individuals with Long COVID has been explored, revealing changes in immune phenotypes and symptomatology following vaccination (ref: Grady doi.org/10.1038/s43856-025-00829-3/). This research highlights the complex interplay between viral infections and host immune responses, emphasizing the need for targeted interventions to address the long-term effects of viral infections. Furthermore, the investigation of calycosin's inhibitory effects on KSHV lytic replication demonstrates the potential for natural compounds to modulate viral activity and offers insights into alternative therapeutic approaches (ref: Liu doi.org/10.1016/j.phymed.2025.156884/). Collectively, these findings illustrate the intricate relationship between viral infections and host metabolism, paving the way for innovative therapeutic strategies.