The human virome represents a fundamental yet understudied component of the microbiome, influencing immune regulation and disease. Given the profound immune dysregulation and microbial imbalance associated with HIV infection, understanding virome alterations during HIV and antiretroviral therapy is essential. This narrative review seeks to integrate and discuss the latest evidence regarding the structure and behavior of the human virome in healthy individuals, in the context of HIV infection, and under antiretroviral therapy. A comprehensive literature search was performed in MEDLINE and Google Scholar for peer-reviewed English-language articles published up to November 2025. Studies describing virome composition, diversity, and interactions in people living with HIV, as well as antiretroviral-induced changes, were included. Reference lists of relevant papers were screened to identify additional sources. Data were extracted and synthesized narratively, emphasizing human studies and supported by evidence from primate models where applicable. HIV infection induces profound alterations in the human virome, notably an expansion of eukaryotic viruses such as Anelloviridae, Adenoviridae, and Parvoviridae, accompanied by reduced bacteriophage diversity. Antiretroviral therapy partially restores virome balance but fails to fully re-establish pre-infection diversity, with persistent enrichment of Anelloviridae reflecting incomplete immune reconstitution. Virome perturbations correlate with immune activation, microbial translocation, and inflammation, contributing to comorbidities despite virological suppression. Emerging evidence suggests regimen-specific effects, with integrase inhibitor-based therapies showing more favorable viromic recovery. HIV and antiretroviral therapy profoundly remodel the human virome, with lasting implications for immune homeostasis and chronic inflammation. The ongoing disruption of the virome highlights its promise as both a biomarker and a potential therapeutic target in the management of HIV. Longitudinal, multi-omic studies are needed to clarify the causal role of virome alterations and guide future interventions.

Background: Influenza A(H3N2) viruses remain a major public health concern due to their rapid antigenic evolution and association with severe disease, particularly among high-risk populations. During the 2025–2026 influenza season, a marked epidemiological shift was observed in Europe, with the emergence and predominance of the A(H3N2) subclade K (J.2.4.1). Objectives: This narrative review aims to provide an integrated overview of the epidemiology, evolutionary dynamics, and public health implications of subclade K, with a particular focus on its impact on vaccine effectiveness, in comparison with the 2024–2025 influenza season. Methods: A non-systematic literature review was conducted using major scientific databases and official public health sources, including WHO and ECDC reports. Recent surveillance data, genomic analyses, and epidemiological updates were included. Given the rapidly evolving evidence base, selected preprint studies were also considered and interpreted with caution. Results: The 2025–2026 influenza season in Europe was characterized by a relative genetic convergence, with subclade K accounting for the majority of A(H3N2) sequences. This variant demonstrated a clear selective advantage and was associated with an earlier and more intense epidemic peak. Molecular analyses indicate the accumulation of multiple mutations in the hemagglutinin protein, particularly within key antigenic sites, contributing to immune escape. These evolutionary changes have important implications for vaccine effectiveness, with current estimates suggesting moderate protection against infection but preserved effectiveness against severe outcomes. Antigenic mismatch, manufacturing constraints, and host-related factors further contribute to reduced vaccine performance. Conclusions: The emergence and rapid spread of subclade K highlight the dynamic nature of influenza virus evolution and its impact on public health. Continuous genomic surveillance and timely vaccine updates remain essential. Despite suboptimal effectiveness against infection, influenza vaccination continues to provide significant protection against severe disease and should remain a cornerstone of prevention strategies.

Background: Torque teno virus (TTV) is a ubiquitous, non-pathogenic component of the human virome whose role in people living with HIV (PLWH), particularly during antiretroviral therapy (ART)-mediated immune reconstitution, remains unclear. This systematic review aimed to synthesize available evidence on TTV viral load in PLWH, focusing on its relationship with immunological markers. Methods: This systematic review followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines. A comprehensive literature search was conducted in MEDLINE, Web of Science, and Scopus in January 2026 to identify studies assessing plasma TTV viral load before and/or during ART and reporting immunological outcomes. Eligible studies included prospective and retrospective longitudinal studies, cross-sectional studies, and mixed designs assessing plasma TTV viral load in relation to ART status and immune recovery markers. Results: Thirteen studies (n = 1700 PLWH) were included, predominantly observational and conducted in adult populations. Most studies (76.9%) reported a significant inverse association between TTV viral load and CD4 T-cell count, while all studies assessing HIV viral load found a direct correlation with TTV levels. An inverse relationship with the CD4/CD8 ratio was consistently observed where evaluated. Higher TTV loads were reported in ART-naïve individuals and in those with advanced immunosuppression, with longitudinal studies indicating a general decline during ART. Overall, methodological heterogeneity and moderate risk of bias were common. Conclusions: TTV viral load shows a consistent inverse association with CD4 cell count and may reflect global immune dysfunction in PLWH beyond conventional markers. However, its clinical utility remains investigational due to the heterogeneity in the study design, limited data on longitudinal dynamics, and lack of standardized assays and thresholds.