Human herpesviruses (HHV) remain latent after primary infection and may reactivate during critical illness. HHV reactivation has been associated with adverse clinical outcomes, yet its pathogenic significance and optimal management remain unclear. This review summarizes the dysregulated immune mechanisms and risk factors for HHV reactivation in critical illness, treatment options, outcomes, current diagnostic challenges, and emerging precision medicine approaches. Critical illness induces profound immune dysregulation characterized by an initial hyperinflammatory response followed by immunosuppression, T-cell exhaustion, impaired natural killer cell function, and disrupted antiviral surveillance. These changes facilitate reactivation of latent HHV, including herpes simplex virus type 1 (HSV-1), cytomegalovirus (CMV), Epstein-Barr virus (EBV), and human herpesvirus 6 (HHV-6). HSV and CMV reactivation in mechanically ventilated and septic patients have been associated with prolonged mechanical ventilation, longer intensive care unit (ICU) stay, secondary infections, and increased mortality. However, the distinction between clinically significant disease from asymptomatic reactivation remains challenging. Current evidence does not support routine antiviral prophylaxis in immunocompetent ICU patients. Emerging approaches including metagenomic next-generation sequencing, host transcriptomics, immune phenotyping, and multi-omics integration may improve risk stratification and identify patient subgroups that are most likely to benefit from targeted intervention. HHV reactivation may serve as a biomarker and potential mediator of adverse outcomes. Improved understanding of host-virus interactions, coupled with precision medicine that integrates virological and immunological data, is required to differentiate clinically relevant reactivation from epiphenomena and to guide individualized therapeutic strategies.

CO2 sorbents play a central role in many carbon capture technologies. Visual monitoring of the sorbent behavior during CO2 capture could provide direct feedback and enable the optimization of both the sorbent and the reactor, which remains largely unexplored. In this work, we develop a self-reporting CO2 sorbent, prove its quantitative indication of CO2 absorption and desorption, and apply this method to evaluate different methods of sorbent regeneration. A pH indicator, thymol blue (TB), was embedded into polyethyleneimine (PEI) hydrogel particles, revealing a clear color transition from blue to green, yellow, and orange during CO2 absorption. This optical response was quantified by extracting Hue, a color coordinate in the Hue, Saturation, Value (HSV) space, from the particle images. Time-resolved analysis of the CO2 absorption revealed that Hue closely follows the measured CO2 uptake. A previously developed diffusion-reaction model was employed to investigate the relationship between the optical response and the internal chemistry of the particles. The measured Hue evolution more closely follows the modeled protonation response averaged over a substantial fraction of the particle volume than that of the shallow near-surface regions, supporting its potential use as an optical indicator for CO2 uptake. The robustness of the optical response was further confirmed by evaluating particles with different water contents, and excellent reversibility of the optical response was demonstrated during steam regeneration. As a final step, microwave regeneration was optically evaluated via this method, and shown to be much faster but less complete than steam regeneration. These results demonstrate that PEI/TB hydrogel particles can provide a timely, direct, and convenient optical signal during CO2 absorption and regeneration, enabling pathways for optimization at particle and potentially reactor scales.

A DFT-assisted Raman framework integrating difference-derivative-PCA highly distinguishable Raman bands screening and difference visualization (DD-PCA-HSV), characteristic peak correlation analysis, and machine learning classification was developed for three milled rice types (SXJ-100, FYXZ, and BJR) from the Taihu Lake Basin. Five independent lots were analyzed for each type. Lots L1-L4 formed the development dataset, and L5 was reserved for independent testing. DFT calculations on simplified amylose and amylopectin models, together with literature, supported the assignment of 22 characteristic Raman peaks. Grouped four-fold cross-validation of DD-PCA-HSV on L1-L4 reproducibly retained six bands at 439, 576, 939, 1126, 1262, and 1460 cm[-1]. Z scores of these bands characterized spectral differences among the three rice types in the development dataset, and the same relative trends were reproduced in L5. Differences between BJR and SXJ-100/FYXZ were mainly associated with pyranose-ring and glycosidic-linkage vibrations, whereas differences between SXJ-100 and FYXZ were mainly associated with CO and CCO stretching vibrations. Linear correlation analysis combined with a dual-threshold rule identified 1080/1106 and 524/615 cm[-1] as discriminative peak pairs. Subsampling analysis indicated that 30 spectra were sufficient for repeatable R[2] estimation. The corresponding linear correlation features were reproduced in L5. Among RF, DT, and SVM models, SVM using normalized spectra achieved the best independent test performance, with accuracy, macro-precision, macro-recall, and macro-F1 all reaching 0.98. Overall, the framework distinguished the investigated rice types while linking discriminative Raman features to molecular vibrations, thereby providing a chemically interpretable basis for Raman-based rice characterization.

Pseudorabies virus (PRV), an important member of the Alphaherpesvirinae subfamily, shares high evolutionary homology with other members of the same subfamily, including human herpes simplex virus (HSV) and varicella-zoster virus (VZV). However, significant differences exist among them in terms of host range, pathogenicity, and immune evasion strategies. This review systematically compares the roles of PRV, HSV type 1 (HSV-1), and VZV in modulating host innate immune responses, encompassing the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling, RIG-I-like receptor (RLR) signaling, NOD-like receptor (NLR) signaling, Toll-like receptor (TLR) signaling, Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway, apoptosis, and autophagy. By summarizing and comparing the interactions of these three viruses with the host innate immune response, this review aims to provide a theoretical reference for understanding the conserved and unique mechanisms of immune evasion among alphaherpesviruses, and to offer insights for the development of novel antiviral strategies.

Exposure to environmental risk factors has been considered a major contributor to neurodegenerative diseases. As biological factors, infectious pathogens pose health concerns in the development of numerous aging-associated neurological defects. Emerging evidence continuously demonstrates the association between viral infection and the deterioration of brain function, such as dementia, multiple sclerosis, and microcephaly in infants. As intracellular pathogens, viruses demand macromolecules and energy by hijacking the host cell and reprogramming cellular metabolism. This study focuses on alterations in lipid metabolism in virus-infected neuronal cells using the DNA virus HSV-1 and the RNA virus ZIKV. We found that both HSV-1 and ZIKV downregulate lipid metabolism, sphingolipid metabolism, glycerophospholipid, and plasmalogen pathways in iPSC-derived neuronal cells, which may contribute to the pathogenesis of neurological diseases. The metabolomic dataset and analysis results will provide a valuable reference in studying the role of viral infection in neurodegeneration in vitro and in vivo .

Herpes simplex virus 1 (HSV-1) infections of the central nervous system cause encephalitis and are associated with increased risk of neurodegeneration, yet the molecular consequences of lytic infection in human neurons remain incompletely defined. We map the transcriptomic, proteomic, and surface-proteome changes induced by HSV-1 across the lytic infection cycle in human induced pluripotent stem cell-derived cortical glutamatergic neurons. HSV-1 drives extensive plasma-membrane remodeling, including the removal of voltage-gated sodium, potassium, and calcium channels, resulting in a profound loss of synchronous calcium signaling. We identify the viral ubiquitin-ligase adaptor pUL56 as the principal effector of this process: pUL56-dependent degradation of ion channels abolishes coordinated calcium signaling, whereas mutation of its E3-ligase-binding motifs preserves synchrony. Furthermore, expression of pUL56 alone is sufficient to abolish neuronal electrical activity. These findings establish pUL56 as a potent viral suppressor of neuronal excitability.

Viruses often hijack core host cell processes to optimize their replication. In the current study, we conducted comparative proteomics analyses of epithelial cells infected by the prevalent human pathogen herpes simplex virus type 2 (HSV-2), followed by experimental validation. The results reveal that HSV-2 infection induces significant reprogramming of the host cell cycle, characterized by a pronounced accumulation of cells in the synthesis (S)-phase. Mechanistically, we discovered that HSV-2 promotes gap 1 (G1)/S transition by downregulating the cyclin-dependent kinase inhibitor p21 via a proteasome-mediated pathway. Following this, the virus induces S-phase cell cycle arrest, characterized by reduced levels of cyclin-dependent kinase 2 (CDK2) and its active phosphorylated form and decreased activity of the cyclin A2-CDK2 complex. Consequently, this dysfunctional 'pseudo-S-phase' state significantly enhances HSV-2 replication. These findings reveal a previously unrecognized dual mechanism employed by HSV-2 to manipulate the host cell cycle, thereby advancing our understanding of how pathogens disrupt cellular homeostasis to facilitate their replication.

Patients in intensive care units (ICU) under mechanical ventilation, particularly those with SARS-CoV-2 infection, are highly susceptible to Herpes simplex virus (HSV) reactivation. Given the lack of data on the SARS-CoV-2 Omicron and Delta variants, this study aimed to assess the prevalence of pulmonary HSV reactivation in mechanically ventilated patients with SARS-CoV-2 pneumonia. The impact of HSV replication on SARS-CoV-2 replication, and conversely, was investigated, along with the susceptibility of HSV strains to antiviral therapies. This retrospective study included 381 mechanically ventilated ICU patients in Lyon. Overall, 103 patients (27.0%) experienced HSV reactivation, with a trend toward a higher prevalence among SARS-CoV-2-positive patients (32.8%) compared to SARS-CoV-2-negative (24.1%; p value = 0.058). HSV reactivation was significantly higher with the Delta variant (46.2%) compared to Omicron (27.1%; p value = 0.045); the Delta variant was associated with a 2.38-fold increased risk of HSV reactivation. HSV-positive patients exhibited a 1-log lower SARS-CoV-2 viral load compared to HSV-negative patients, a finding indicative of the natural course of SARS-CoV-2 infection followed by HSV reactivation, rather than viral interference. Unexpectedly, acyclovir resistance mutations appeared in the UL23 gene in at least 13.6% of HSV-1 strains in patients with an HSV load above 10[5] copies/mL. Complementary phenotypic and genotypic approaches allowed to identify three novel substitutions in UL30: Q217R, D741A, and E756K, classified as polymorphisms. Further optimization is needed in the management of mechanically ventilated ICU patients with pulmonary HSV reactivation, especially regarding antiviral resistance testing.

Multiple sclerosis (MS) is a complex, multifactorial neurodegenerative disease with an aetiology that is still partially elusive. Several risk factors are associated with MS development including genetic predisposition and various environmental stressors; however, recently, viral infections have gained significant attention as a crucial environmental trigger. Despite the well-established link between Epstein-Barr virus (EBV) and MS susceptibility, a single-pathogen model fails to clearly characterise the molecular cascades driving the disease, suggesting that the transition from infection to autoimmune response involves more than one viral agent. In this review we examine the speculation that the interactions among different neurotropic viruses could serve a collective causative role in MS, which is under-researched in the literature at present. We summarise contradictory evidence on the role of different viral agents, including the Herpesviridae family (Human Cytomegalovirus, EBV, Herpes Simplex Viruses HSV-1 and HSV-2, and Varicella Zoster Virus), Paramyxoviridae family (Measles Virus and Rubella Virus), Influenza virus, SARS-CoV-2, and Human Endogenous Retroviruses (HERVs). Through interplay within shared molecular pathways, immune modulation, and activation of latent infections, these viruses may collectively influence the inflammatory and demyelinating processes that characterise MS. This review evaluates the etiological role of viral interplay in MS through the cumulative and interactive effects of these pathogens. The available epidemiological, immunological, and experimental data converge on the concept that viral co-exposures act synergistically to shape MS susceptibility in genetically predisposed individuals. Characterising these viral interactions presents a new research direction for the identification of novel biomarkers and the development of preventative strategies through the targeted control of viral networks.

Current cancer immunotherapy predominantly targets CD8+ T cells, leaving NK cell surveillance largely unaddressed. We report that lactylation of the membrane checkpoint ligand CD112 serves as a convergent mechanism for dual immune escape. In contrast to T cell-centric checkpoints such as PD-L1, CD112 functions as a shared inhibitory ligand for both CD8+ T cells and NK cells through TIGIT/CD112R signaling. Mechanistically, the lactyltransferase AARS2 catalyzes CD112 lactylation at lysine 412 in response to tumor lactate accumulation, competitively blocking the HECT E3 ligase UBE3C to suppress K48/K63-linked ubiquitination and lysosomal degradation. This stabilizes CD112 at the plasma membrane, enabling tumor cells to coordinately evade both adaptive and innate cytotoxic lymphocytes. Disrupting this axis restores dual immune surveillance and suppresses tumor growth. Tumors with high CD112 lactylation and surface enrichment are selectively vulnerable to TIGIT/PD-L1 bispecific antibody blockade and HSV-2 oncolytic virotherapy, nominating CD112 lactylation status as a predictive biomarker for combination immunotherapy.

In the early years of the AIDS epidemic, the occurrence and potential for heterosexual transmission of human immunodeficiency virus type 1 (HIV 1) in the United States were uncertain. To better understand infection among women and the possible role of prostitution in the emerging epidemic, the Centers for Disease Control and Prevention established CDC AIDS Project 72, a multisite study of 1 410 women with recent histories of prostitution recruited from eight areas of the United States during 1986 and 1987. Participants were interviewed, examined, and tested for serologic markers of HIV 1, hepatitis B virus (HBV), syphilis, herpes simplex virus types 1 and 2 (HSV 1 and HSV 2), and human T cell lymphotropic virus types I and II (HTLV I/II). HIV 1 antibodies were detected in approximately 12% of women tested, but prevalence varied considerably across study sites. HSV 2 was the most commonly detected infection, followed by HSV 1, HBV, syphilis, HIV 1, and HTLV I/II. HIV 1, HBV, and HTLV I/II were strongly associated with injection drug use, whereas syphilis and HSV 2 followed different patterns related to sexual exposure. Among women without evidence of injection drug use, infrequent condom use during vaginal intercourse with clients was associated with HIV 1 infection. Project 72 showed that prostitution alone did not explain infection risk among these women. Injection drug use, sexual and injection networks, local prevalence of infection, and the social circumstances in which women lived and worked were also important. The project contributed to an evolving public health approach that emphasized epidemiologic evidence, cooperation with affected communities, and practical strategies for reducing risk rather than assumptions about stigmatized populations.