Dengue remains a major public health concern in Mexico, with incidence and clinical burden increasing substantially in recent years. Using national surveillance data from 2020 to 2024, this study provides a comprehensive overview of the changing epidemiological landscape, with an emphasis on geographic distribution, temporal trends, serotype dynamics, and disease severity. Over this period, Mexico saw an almost fivefold increase in dengue cases, reaching over 123,000 confirmed infections and 426 deaths in 2024, the highest annual number recorded. Seasonal patterns shifted, with sustained transmission extending into unusual winter months from late 2023. Serotyping data revealed a shift in predominant virus serotypes, with DENV2 predominating until 2022, DENV1 peaking in 2021, and DENV3 rising sharply from 2022 onward, becoming dominant in 2023 and almost exclusive by 2024. This shift coincided with a sustained rise in dengue with warning signs (from 16.9% in 2020 to > 42% in 2023-2024) and higher hospitalisation rates, while severe dengue remained below 5%. Although DENV3 dominated nationally, DENV1 and DENV2 persisted in specific states, and DENV4 circulated sporadically, particularly in southern and northern regions. Several traditionally low-prevalence states experienced atypical outbreaks, underscoring the potential for sudden epidemic expansion. Climatic analysis showed a consistent positive association between temperature and DENV3 prevalence, with precipitation effects varying by year. Odds ratio analysis suggested serotype-specific differences in severity across years. These findings underscore the heterogeneous and dynamic nature of dengue transmission in Mexico and highlight the need for regional surveillance, prevention, and clinical preparedness strategies.

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.

Oncogenic viruses are widely recognized for their pivotal role in malignant transformation; however, their capacity to induce neurological disorders has received comparatively less attention. Increasing evidence indicates that several oncogenic viruses, including human T-cell leukemia virus type 1 (HTLV-1), human papillomavirus (HPV), hepatitis B virus (HBV), hepatitis C virus (HCV), and Kaposi's sarcoma-associated herpesvirus (KSHV), are associated with a broad spectrum of neurological complications involving both the central and peripheral nervous systems. These manifestations arise through diverse mechanisms, including direct viral neuroinvasion, persistent infection, immune-mediated tissue injury, chronic neuroinflammation, and disruption of neurovascular integrity. Moreover, virus-induced molecular alterations, such as oxidative stress, mitochondrial dysfunction, epigenetic remodelling, and aberrant cytokine signalling, contribute t neuronal dysfunction and disease progression. In this review, we critically examine the current understanding of the neurological complications associated with major oncogenic viruses by integrating evidence from molecular, experimental, and clinical studies. We first discuss the general mechanisms by which viral infections induce neurological injury, highlighting pathways shared among neurotropic and non-neurotropic viruses. We then summarise the neurological manifestations and virus-specific pathogenic mechanisms associated with each oncogenic virus, emphasising both common and distinct molecular pathways underlying neuropathogenesis. Finally, we address current diagnostic challenges, emerging biomarkers, and therapeutic strategies while identifying critical knowledge gaps that limit causal interpretation and clinical translation. A comprehensive understanding of the complex interactions between oncogenic viruses, the immune system, and the nervous system will facilitate earlier diagnosis, improve patient management, and support the development of targeted therapeutic approaches for virus-associated neurological disorders.

Varicella zoster virus (VZV) and herpes simplex virus (HSV) are major causes of viral meningitis and encephalitis. Standard intermittent intravenous acyclovir requires hospitalisation, reducing patient comfort and prolonging admissions. Continuous infusion may maintain therapeutic plasma and cerebrospinal fluid (CSF) concentrations while enabling treatment through Outpatient Parenteral Antimicrobial Therapy (OPAT). Objectives to evaluate the feasibility, pharmacokinetic target attainment, and cost reduction of continuous intravenous acyclovir for HSV and VZV neurological infections in an OPAT setting. We conducted a case series of eight patients with HSV or VZV neurological infections who received continuous intravenous acyclovir through our OPAT programme after initial hospital-based therapy. Steady-state plasma concentrations were measured to assess pharmacokinetic target attainment. Costs were calculated based on daily costs of discontinued inpatient care and OPAT. Existing literature on continuous intravenous acyclovir and acyclovir in OPAT was reviewed. No persistent complications associated with continuous intravenous acyclovir administration were observed. All patients completed treatment with good clinical responses; one had persistent ptosis, and another developed postherpetic neuralgia. Acyclovir plasma concentrations remained above the therapeutic threshold in all seven measured cases, suggesting adequate CSF exposure. Hospital admissions were shortened, with no readmissions. The acyclovir OPAT programme led to cost savings of 3486 EUR per patient. Despite this small case series, continuous intravenous acyclovir appears to be feasible for treating HSV and VZV neurological infections in an OPAT setting, with potential benefits in patient comfort, healthcare costs, and hospital resource utilization. Larger studies are warranted to assess safety and efficacy.

Antiviral treatment (ART) resistance is an emerging global phenomenon that reduces the effectiveness of antiviral therapies and raises strong challenges for public health systems. This literature review focuses on the factors that contribute to developing antiviral drug resistance and the scope of pharmacogenetics. Studies have shown that inefficient use of antiviral therapies, genetic mutations in virus strains, and a limited healthcare framework are the main factors that increase resistance rates. Specifically, the poor adherence in HIV patients, combined with the virus high mutation, are the primary driver of drug-resistant strains development. The mutations in NS5A region reduce the efficacy of HCV direct-acting antivirals (DAAs). Where Influenza virus resistance to neuraminidase inhibitors (NAIs) like oseltamivir has been identified in seasonal strains, most notably the H275Y mutation in H1N1. Consequently, development of these resistant strains demands multidisciplinary strategies, global coordination, effective resistance monitoring systems, and public health initiatives to overcome this phenomenon. The paper aims to present a full picture of the antiviral drug resistance, which may provide better insights for clinicians and researchers.

Oncogenic viral pathogens, such as human papillomavirus (HPV), Epstein-Barr virus (EBV), hepatitis B and C viruses (HBV, HCV), and Kaposi's sarcoma-associated herpesvirus (KSHV), are involved in a significant proportion of human cancers worldwide. While genetic and epigenetic mechanisms underlying viral oncogenesis have been thoroughly investigated, emerging evidence underscores a critical role for epitranscriptomic regulation in virus-host interactions and their clinical consequences. RNA modifications such as N6-methyladenosine (m6A), 5-methylcytosine (m5C), and pseudouridine (Ψ) dynamically modulate RNA stability, translation, and immune recognition, thereby regulating viral replication and persistence. The present review describes current knowledge on the epitranscriptomic landscape of oncogenic viral pathogens and its functional implications. This review discusses how viral and host transcripts are selectively modified by cellular writers, erasers, and readers, shaping key stages of the viral life cycle, including replication, latency, and reactivation. Particular emphasis is placed on the role of RNA modifications in maintaining chronic infection and promoting tumourigenesis through the regulation of oncogenic pathways, cell proliferation, and apoptosis. Additionally, the present review examines how epitranscriptomic marks contribute to immune evasion by altering innate immune sensing and interferon responses. Finally, it explores the therapeutic potential of targeting epitranscriptomic machinery, highlighting recent advances in small-molecule inhibitors and the challenges associated with specificity and off-target effects. A deeper understanding of epitranscriptomic regulation in oncogenic viruses may reveal novel biomarkers and therapeutic strategies for virus-linked malignancies.

The interaction between the human immunodeficiency virus (HIV) and the gut microbiota is attracting growing interest due to its potential role in the progression of infection and the development of comorbidities. This review provides a comprehensive and critically appraised synthesis of current evidence on the bidirectional relationship between HIV infection and gut microbiota disruption, structured around four central themes: the mechanistic basis of HIV-associated gut dysbiosis and mucosal immune dysfunction and its link to chronic inflammation; the effects of different antiretroviral therapy (ART) classes on the intestinal ecosystem; the emerging role of the microbiota-gut-brain axis in the pathogenesis of HIV-associated neurocognitive disorders (HAND); and the therapeutic potential of microbiota-targeted interventions, including probiotics, prebiotics, synbiotics, faecal microbiota transplantation (FMT), and dietary strategies in people living with HIV (PLWH). By synthesising the current mechanistic, clinical, and translational evidence, this review aims to delineate the critical knowledge gaps and define the research priorities that will drive the next generation of microbiota-informed strategies for improving long-term outcomes in PLWH. This summary highlights the importance of considering the gut microbiota as a key player in the overall management of HIV infection.

Herpes zoster (HZ, shingles) constitutes a significant public health concern, particularly in ageing populations, and there is growing global interest in the recombinant zoster vaccine (RZV) from a public health perspective. In this systematic review with meta-analysis, we assessed the efficacy and effectiveness of RZV against HZ and its complications, including a possible association with a reduced risk of dementia, among immunocompetent individuals aged 50 years and older. We synthesised the latest evidence on long-term effects, incorporating recent data from both trials and real-world effectiveness studies. A total of 27 publications based on 18 primary studies, 3 randomised controlled trials (RCTs) and 15 observational studies, were included. RZV provides very high protection against HZ in immunocompetent adults ≥ 50 years in RCTs, with approximately 95% efficacy and high certainty of evidence (CoE) according to GRADE. Observational studies also consistently indicate substantial protection, but effect estimates vary across settings (high CoE). Among vaccinated individuals who develop HZ, RZV is associated with reduced loss of quality of life and decreased analgesic use. The vaccine also substantially reduces the risk of herpes zoster ophthalmicus (HZO) (high CoE) and likely postherpetic neuralgia (PHN) (moderate CoE). Long-term follow-up suggests durable protection for at least 11 years (low CoE). RZV may be associated with a reduced risk of dementia (low CoE), due to uncertainty the true effect may be substantially different, and similar associations have been observed with other vaccines and may be confounded by healthy vaccinee bias.

Epstein-Barr virus (EBV)-associated nasopharyngeal carcinoma (NPC) remains a clinically challenging malignancy, particularly in recurrent or metastatic disease where durable responses to chemoradiotherapy and immune checkpoint blockade are limited. The viral aetiology of NPC provides a strong biological rationale for immune-based treatment; however, translation of chimaeric antigen receptor (CAR) T-cell therapy into this solid tumour setting is constrained by poor tumour trafficking, antigen heterogeneity, limited surface accessibility of EBV latent antigens, T-cell exhaustion, and an immunosuppressive tumour microenvironment. This review critically evaluates the emerging therapeutic prospects of CRISPR-engineered CAR-T cell therapy for EBV-associated NPC. It synthesises evidence on EBV latency biology, NPC immune evasion, solid-tumour CAR-T limitations, and genome-engineering strategies including conventional CRISPR-Cas9, base editing, prime editing, and double-strand-break-sparing targeted integration. Particular attention is given to genotoxicity, chromosomal rearrangements, chromosome loss, bystander and off-target editing, manufacturing heterogeneity, and the regulatory and biological barriers that currently separate technical feasibility from NPC-specific clinical implementation. Available clinical evidence from checkpoint blockade, EBV-specific adoptive T-cell therapy, base-edited CAR-T cells in haematologic malignancy, and early CRISPR-edited T-cell trials supports the feasibility of immune and genetic redirection but does not establish efficacy of a clinically validated CRISPR-engineered CAR-T platform for NPC. Future development should prioritise surface-accessible antigen validation, fit-for-purpose selection of editing technology, genomic safety, scalable manufacturing, and biomarker-driven early-phase trials.

Respiratory syncytial virus (RSV) has long been underrecognized as a significant pathogen in older adults, despite accumulating evidence of its substantial morbidity and mortality burden in this population. While RSV vaccination is now well established as an effective intervention for preventing lower respiratory tract disease, this narrative review examines whether its public health value may extend beyond these primary clinical endpoints. A targeted search of Scopus and Web of Science from database inception to May 2026 was conducted to identify biological, epidemiological, observational, interventional, and modelling evidence relevant to potential downstream vaccine effects. The available evidence potentially supports hypotheses concerning possible reductions in cardiovascular complications and secondary bacterial infections, possible decreases in transmission to younger household contacts, and potential preservation of functional status and independence. However, the strength of evidence varies substantially across these outcomes. Cardiovascular protection has not been independently demonstrated in randomized trials, bacterial and antimicrobial-use outcomes have rarely been prespecified, real-world household transmission studies are unavailable, and functional trajectories may be strongly modified by baseline frailty and pre-existing disability. RSV vaccination in older adults therefore remains a well-validated strategy for preventing acute respiratory disease, whereas its proposed broader effects should be regarded as biologically plausible but incompletely demonstrated benefits. Future studies should incorporate prespecified cardiovascular, bacterial, transmission, geriatric, and functional outcomes, with particular attention to frailty, antimicrobial use, and longer-term follow-up.

Human cytomegalovirus (HCMV) is a globally prevalent virus that poses a significant public health concern, especially for newborns and immunocompromised patients, causing a wide range of infections. Clinical outcomes associated with HCMV infection include congenital disease, graft rejection in transplant recipients, and life-threatening systemic infections with significant morbidity and mortality. HCMV is a member of the Beta-herpesvirinae subfamily. Distinguishing characteristics of HCMV, in particular, and herpesviruses in general are their ubiquitous presence in nature and the initial infection that often results in lifelong latency. Over the past 40 years, the genetics of HCMV have been explored, leading to the isolation of various genotypes, including those of glycoprotein B, glycoprotein N, and UL144. Despite operational obstacles in isolating HCMV genotypes due to heterogeneity in the technologies used for genotyping the virus, studies have been able to describe their clinical implications across a variety of human hosts. This review summarises the genotypic variation of HCMV and discusses its clinical relevance and impact on antiviral resistance and vaccine development. Understanding the genetic diversity of HCMV genotypes is crucial for advancing drug development to combat resistant strains and for developing new vaccines and treatment modalities.

Oncolytic virotherapy has recently emerged as a promising immuno-oncological strategy, utilising the natural cytolytic potentials of viral pathogens to selectively target and destroy malignant cells. Although various engineered viruses, such as adenoviruses, vaccinia virus, and herpes simplex virus, are currently in clinical evaluation, emerging and re-emerging viruses with intrinsic oncolytic potential, including Zika virus (ZIKV), Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Dengue virus (DENV), and West Nile virus (WNV), have also shown promising results. These emerging and re-emerging viral pathogens show specific tumour tropism, immune evasion strategies, and immunogenic cell death mechanisms that could be harnessed for next-generation therapeutic platforms. Nonetheless, concerns related to safety, viral pathogenicity, host immune responses, and the risk of uncontrolled viral dissemination present significant translational challenges. The present review provides a comprehensive overview of novel viral candidates, including ZIKV, SARS-CoV-2, DENV, and WNV, in oncolytic virotherapy, their molecular mechanisms of tumour targeting, and current advancements in genetic engineering aimed at improving therapeutic efficacy and biosafety. Moreover, this review describes clinical perspectives, regulatory considerations, and future directions in integrating emerging virotherapeutic agents into precision oncology.