Research on herpes simplex virus (HSV) infections has highlighted the complex interplay between viral mechanisms and host immune responses. A study by Shankar et al. utilized cryoelectron microscopy to elucidate the structures of HSV DNA polymerase, revealing conformational dynamics that contribute to antiviral drug resistance, particularly against clinically used antivirals (ref: Shankar doi.org/10.1016/j.cell.2024.07.048/). Ford et al. expanded on immune responses by demonstrating that immunotherapeutic HSV-2 vaccination significantly increased the representation of HSV-2-specific T cell receptors in the skin, suggesting a localized immune enhancement at sites of reactivation (ref: Ford doi.org/10.1172/jci.insight.179010/). In contrast, Tessema et al. found that mouse guanylate-binding proteins did not mediate antiviral activity against HSV in vitro or in mouse models, indicating potential limitations in the role of these proteins in HSV immunity (ref: Tessema doi.org/10.1038/s42003-024-06748-8/). Furthermore, Yeh et al. reported a long-term association between herpes zoster and subjective cognitive decline, suggesting that HSV infections may have broader implications beyond immediate clinical symptoms (ref: Yeh doi.org/10.1186/s13195-024-01511-x/). Overall, these studies underscore the multifaceted nature of HSV infections, where immune responses can be both enhanced through vaccination and complicated by viral resistance mechanisms.

Cytomegalovirus (CMV) infection research has focused on the immune dynamics that govern both primary and chronic infections. Hederman et al. utilized systems serology to differentiate humoral immune profiles in pregnant women with primary versus chronic CMV infections, revealing distinct antibody responses that could inform maternal-fetal health strategies (ref: Hederman doi.org/10.1172/JCI180560/). In a complementary study, Schaenman et al. assessed the coordination of adaptive and innate immune responses in kidney transplant recipients, finding that a robust immune profile was crucial for controlling CMV infection, validated across multiple cohorts (ref: Schaenman doi.org/10.1016/j.kint.2024.07.003/). Zamora et al. further contributed by demonstrating that preemptive antiviral therapy significantly increased the presence of polyfunctional T cells and NK cells, correlating with reduced CMV disease incidence post-transplant (ref: Zamora doi.org/10.1172/jci.insight.180115/). Additionally, Mahmud et al. explored the role of the US28 receptor in establishing quiescent HCMV infections in monocytes, highlighting the mechanisms that facilitate viral persistence (ref: Mahmud doi.org/10.1126/scisignal.adn8727/). Collectively, these findings emphasize the importance of understanding immune responses to CMV in various clinical contexts, particularly in vulnerable populations such as transplant recipients.

The research surrounding Epstein-Barr virus (EBV) has unveiled its significant role in modulating immune responses and contributing to various cancers. Landman et al. demonstrated that EBNA3A, an EBV nuclear antigen, interacts with the interferon regulatory factor 3 to inhibit IFN-β expression, thereby affecting antiviral responses (ref: Landman doi.org/10.1016/j.jbc.2024.107645/). Veronese et al. focused on Kaposi's sarcoma-associated herpesvirus (KSHV), revealing that the ORF48 protein is essential for optimal lytic replication, indicating a potential target for therapeutic intervention (ref: Veronese doi.org/10.1371/journal.ppat.1012081/). Additionally, Zhang et al. identified that lncRNA BC200 promotes nasopharyngeal carcinoma development by upregulating TYMS expression, linking EBV infection to tumorigenesis (ref: Zhang doi.org/10.1016/j.ijbiomac.2024.134837/). Furthermore, Paudel et al. highlighted the role of EBV-encoded RNA EBER1 in enhancing oxidative phosphorylation, suggesting a mechanism by which EBV supports its own persistence and the survival of infected cells (ref: Paudel doi.org/10.1002/jmv.29869/). These studies collectively illustrate the multifaceted interactions between EBV and host cellular mechanisms, emphasizing the virus's role in cancer development and immune evasion.

Research on herpes zoster (HZ) has increasingly focused on vaccine acceptance and the factors influencing postherpetic neuralgia (PHN). Wang et al. conducted a scoping review that identified key predictors of vaccine hesitancy, emphasizing the need for targeted interventions to improve vaccination rates and public health outcomes (ref: Wang doi.org/10.3389/phrs.2024.1606679/). Liu et al. explored the relationship between sensory neuron involvement in HZ and its association with PHN, providing insights into the clinical characteristics that may predispose individuals to more severe outcomes (ref: Liu doi.org/10.1002/jmv.29821/). Pino-Belmar et al. examined the role of autophagy in host defense against HSV-1, suggesting that enhancing autophagic processes could be a potential therapeutic strategy to mitigate HZ-related complications (ref: Pino-Belmar doi.org/10.3390/cells13151256/). Together, these studies highlight the importance of understanding both the immunological and clinical dimensions of HZ and PHN, paving the way for improved prevention and management strategies.

The exploration of viral mechanisms and drug resistance has revealed critical insights into the challenges posed by herpesviruses in clinical settings. Sallée et al. reviewed the management of refractory HSV infections in hematopoietic stem cell transplantation recipients, emphasizing the heightened risk of antiviral resistance due to compromised immune responses (ref: Sallée doi.org/10.1002/rmv.2574/). Finnen et al. investigated the role of pUL21 phosphorylation in HSV-2, demonstrating that disruption of this process impairs the secondary envelopment of viral nucleocapsids, which is crucial for viral egress (ref: Finnen doi.org/10.1128/jvi.00656-24/). Bergeman et al. further contributed by elucidating the role of the Rab6 post-Golgi secretory pathway in HSV-1 egress, highlighting the complexities of viral exit strategies (ref: Bergeman doi.org/10.1128/jvi.00599-24/). Li et al. examined the role of LKB1 in KSHV reactivation, suggesting that metabolic reprogramming by the virus is a key factor in its persistence and associated malignancies (ref: Li doi.org/10.1128/jvi.00604-24/). These findings underscore the intricate relationship between viral biology and host responses, emphasizing the need for innovative therapeutic approaches to combat drug resistance.

Vaccine development against herpesviruses has seen significant advancements, particularly in enhancing immune responses through innovative strategies. Li et al. demonstrated that heterologous prime-boost immunization using varicella-zoster virus gE mRNA and protein subunit vaccines elicited superior cellular immune responses in middle-aged mice, suggesting a promising approach for improving vaccine efficacy (ref: Li doi.org/10.2147/IJN.S464720/). Solera et al. conducted a multicenter study that highlighted the role of cell-mediated immunity in guiding prophylaxis for CMV infection in organ transplant recipients, with findings indicating that early identification of CMV-specific T cell responses could allow for the early discontinuation of antiviral prophylaxis (ref: Solera doi.org/10.1097/TP.0000000000005173/). Wang et al. also contributed to the discourse on vaccine acceptance, emphasizing the importance of understanding public perceptions to enhance immunization rates against herpes zoster (ref: Wang doi.org/10.3389/phrs.2024.1606679/). Collectively, these studies illustrate the dynamic landscape of vaccine research, where innovative strategies and public health considerations converge to improve outcomes in herpesvirus infections.

Research on congenital and perinatal viral infections has highlighted the implications of herpesviruses in maternal and neonatal health. Hofstadter et al. investigated the role of mitochondrial dynamics in infection-induced cellular responses, revealing that peripheral mitochondrial fission is crucial for maintaining bioenergetics during viral infections (ref: Hofstadter doi.org/10.1038/s41467-024-51680-4/). Charles et al. developed the HerpesDRG database, a comprehensive resource for tracking antiviral drug resistance mutations, which is essential for managing herpesvirus-associated diseases effectively (ref: Charles doi.org/10.1186/s12859-024-05885-5/). Liu et al. examined the association between active herpesviruses and ICU admissions in patients with pulmonary infections, finding that herpesvirus positivity correlated with dysbiosis in the respiratory microbiome, further complicating clinical outcomes (ref: Liu doi.org/10.3389/fmicb.2024.1441476/). These findings underscore the need for ongoing research into the mechanisms of viral transmission and the impact of herpesviruses on maternal and neonatal health.

The neurological impacts of herpesviruses have garnered attention, particularly in relation to herpes simplex encephalitis (HSE) and associated autoimmune responses. Asakura et al. reported elevated cerebrospinal fluid IgG indices in patients post-HSV-1 clearance, suggesting a potential link between immune responses and neurological outcomes in HSE (ref: Asakura doi.org/10.1002/jmv.29850/). Dumez et al. focused on anti-NMDA receptor autoimmune encephalitis following herpes encephalitis, revealing distinct clinical and radiological characteristics that may help identify patients at higher risk for severe outcomes (ref: Dumez doi.org/10.1007/s00415-024-12615-7/). Wang et al. conducted a multicenter study to assess the etiological and clinical characteristics of sexually transmitted infections, emphasizing the need for comprehensive approaches to manage STIs, including those caused by herpesviruses (ref: Wang doi.org/10.3389/fcimb.2024.1407124/). These studies highlight the complex interplay between herpesviruses and neurological health, underscoring the importance of early diagnosis and intervention.