Moreover, the role of viral ubiquitin deconjugases in regulating translational stress responses has been explored, revealing that while EBV, HCMV, and KSHV can counteract ribosomal quality control mechanisms, HSV-1's vDUB exhibits distinct limitations (ref: Liu doi.org/10.1111/febs.70278/). The reactivation of human cytomegalovirus (HCMV) from latency is also critical, with the UL78 gene identified as necessary for efficient reactivation, highlighting the complex interplay between viral latency and immune evasion (ref: Medica doi.org/10.1128/jvi.01402-25/). Collectively, these studies underscore the multifaceted challenges posed by herpesviruses and the imperative for continued research into their molecular mechanisms and therapeutic interventions.

In addition, the dynamics of immune surveillance against viremia have been explored, revealing the critical coordination between liver-resident immune cells and their role in controlling herpesvirus infections (ref: Zhang doi.org/10.1016/j.celrep.2025.116488/). The impact of herpesvirus reactivation on systemic inflammation in women living with HIV has also been investigated, demonstrating a complex relationship between viral shedding and inflammatory biomarkers post-antiretroviral therapy initiation (ref: Ssempijja doi.org/10.1093/ofid/). These findings collectively highlight the intricate interplay between herpesviruses and host immune responses, paving the way for potential therapeutic strategies targeting immune modulation.

The role of CMV in exacerbating tuberculosis severity and treatment outcomes has also been highlighted, indicating that CMV exposure may worsen TB disease progression (ref: Dasan doi.org/10.3389/fimmu.2025.1612709/). Furthermore, genetic variants associated with NK cell responses have been linked to CNS disease development due to HSV-2 and VZV, underscoring the genetic factors influencing herpesvirus-related health outcomes (ref: Graninger doi.org/10.1002/jmv.70667/). These findings emphasize the need for ongoing surveillance and vaccination strategies to mitigate the public health burden of herpesviruses.

Moreover, the complete seropositivity of EBV in pediatric-onset multiple sclerosis (POMS) patients compared to controls suggests a strong association between EBV and MS pathogenesis (ref: Monte doi.org/10.1007/s00415-025-13477-3/). The burden of CMV in kidney transplant recipients has also been documented, highlighting the need for effective management strategies to mitigate the risks associated with CMV infections in this vulnerable population (ref: Gill doi.org/10.3389/fimmu.2025.1618748/). These studies collectively underscore the diverse clinical manifestations of herpesvirus infections and the necessity for targeted therapeutic approaches.

The effectiveness of RZV in the U.S. Medicare population has also been assessed, demonstrating its efficacy in preventing herpes zoster and related complications, particularly among individuals with prior live zoster vaccine (ref: Vielot doi.org/10.7326/ANNALS-24-02409/). Furthermore, the role of letermovir in targeting human cytomegalovirus has been explored, revealing insights into its mechanism of action and resistance mutations, which could inform future antiviral strategies (ref: Gourin doi.org/10.1016/j.antiviral.2025.106289/). These findings emphasize the importance of ongoing vaccine research and the need for adaptive strategies to enhance immunization rates against herpesviruses.

The effects of Epstein-Barr virus on circadian rhythms and behavior have also been explored, demonstrating how viral infections can disrupt host physiology (ref: Naim doi.org/10.1186/s12993-025-00286-x/). Furthermore, the low frequency of N-methyl-D-aspartate receptor autoimmunity following tick-borne encephalitis suggests that such antibodies may not significantly impact cognitive outcomes in most cases (ref: Morén doi.org/10.1371/journal.pone.0334438/). These studies underscore the complexity of herpesvirus interactions with host genetics and the implications for disease outcomes.

The role of EBV tegument protein BRRF2 in suppressing innate immune responses has also been highlighted, indicating how herpesviruses evade host defenses (ref: Hu doi.org/10.1038/s41467-025-64037-2/). Furthermore, the association of biological age acceleration with mortality in HSV-positive adults underscores the long-term health impacts of herpesvirus infections (ref: Wei doi.org/10.1371/journal.pone.0334621/). These findings collectively emphasize the need for continued exploration of the neurological implications of herpesvirus infections and the potential for targeted therapeutic strategies.