Respiratory syncytial virus (RSV) and human metapneumovirus (hMPV) are seasonal respiratory viruses that can cause severe outcomes, particularly in older adults; however, their burden remains under-captured. The World Health Organisation (WHO) recommends expanding surveillance over pathogens, such as RSV and hMPV, through the Mosaic Respiratory Surveillance Framework. Although COVID-19 accelerated RSV surveillance, similar advancements for hMPV are lacking. This study evaluated and compared RSV and hMPV surveillance across multiple countries. A comparative qualitative analysis of RSV and hMPV surveillance was conducted in France, Germany, Italy, Japan, Spain, the United Kingdom, and the United States using a framework based on the WHO guidance. Surveillance systems were mapped across seven modules: non-medically attended community, virological, community, outbreak, primary care, hospital, and mortality surveillance. Each was assessed using five criteria: granularity, timing, representativeness, sampling strategy, and communication. Sources included public health institution webpages, surveillance subsystems, and peer-reviewed publications. Most countries have dedicated RSV surveillance frameworks, with the United States and Spain having the most comprehensive systems. Key areas for potential improvement included limited adult-centric data and severe outcome reporting. No country had robust surveillance for hMPV (Germany reported hMPV-specific hospital data, whereas France, Germany, and the United Kingdom published sentinel positivity rates), and detection was mainly through influenza or COVID-19 virological surveillance. The absence of hMPV reporting from active sentinel surveillance, year-round monitoring, demographic and severity data, and restricted public information dissemination are common limitations. Significant limitations persist in RSV and particularly hMPV surveillance, highlighting the need for more robust, comprehensive systems.

Nipah virus (NiV) has emerged as a high-consequence zoonotic pathogen, posing a significant threat to global health security. Characterised by extreme virulence and case-fatality rates that can exceed 70%, it is recognized as a WHO priority pathogen. This review examines the multifaceted challenges posed by recurring NiV outbreaks, spanning the complex dynamics of unpredictable zoonotic spillover from Pteropus fruit bats, the rising risk of sustained human-to-human transmission, and the profound gaps in medical countermeasures. The epidemiological shift from events mediated by intermediate hosts to those involving direct spillover and efficient person-to-person spread in South Asia highlights the virus's evolving pandemic potential. In the absence of any licenced vaccines or therapeutics, public health responses are limited to supportive care and stringent infection control. Ultimately, this review concludes that mitigating the NiV threat is fundamentally a One Health challenge, requiring an integrated strategy that unites ecological surveillance, accelerated medical research, and coordinated global policy to secure against this formidable pathogen.

Between mosquitoes and birds, West Nile virus (WNV) is a neurotropic flavivirus, an arthropod-borne pathogen involved in an enzootic cycle. Additionally, it can infect both people and horses, leading to severe illness. Since 1999, WNV has spread across North and South America, including Mexico and the Caribbean. It is endemic in several regions of Europe, Africa, the Middle East, and Asia. WNV affects the central nervous system (CNS), causing severe disease in a small percentage of infected individuals, especially in immunocompromised or elderly hosts. This re-emerging pathogen was identified during an outbreak in July 2025 in the Lazio region of Italy, rekindling interest in an area where the virus had not circulated for some time and raising several questions about the WNV vector and its spread. Gammadelta T (γδ T) lymphocytes are innate cells that can respond rapidly and non-specifically to viral infections and other pathogens, thereby linking innate and adaptive immunity. Several studies in mice and humans suggest they play distinct roles in controlling WNV infection by communicating with other immune cells, underscoring their antiviral role, which is essential for containing viral dissemination in the host. This review will discuss recent studies on the role of γδ T cells in viral pathogenesis and in protective immunity during WNV infection.

Alphaviruses, including significant human pathogens like Chikungunya (CHIKV), Venezuelan Equine Encephalitis (VEEV), and the model Sindbis virus (SINV), pose a considerable global health threat. Their ability to establish infection and cause disease is critically dependent on successfully subverting the host's innate immune defenses, particularly the Type I Interferon (IFN-I) system. This review provides a comparative analysis of the molecular strategies employed by CHIKV, VEEV, and SINV to dismantle these antiviral pathways. We first outline the conserved principles that form a core alphavirus “toolkit” for evasion, such as the formation of membrane-bound replication factories to shield viral RNA from cytosolic sensors and NSP1-mediated mRNA capping to mimic host transcripts. The review then delves into the divergent, virus-specific tactics, highlighting the central role of the non-structural protein 2 (NSP2) as a master antagonist. We contrast the aggressive strategies of pathogenic alphaviruses—such as CHIKV NSP2-mediated cleavage of MAVS and degradation of STAT2, and VEEV-induced degradation of STAT1—with the more subtle, modulatory approach of SINV, which relies more on a global shutdown of host gene expression. These distinct molecular mechanisms are directly correlated with their varying pathogenic outcomes. Furthermore, we examine the remarkable adaptability of these strategies between vertebrate hosts, where suppressing the IFN system is paramount, and invertebrate vectors, where evading the RNAi pathway is the primary challenge. A comprehensive understanding of these commonalities and divergences in immune evasion is essential for the rational design of broad-spectrum antiviral therapeutics and next-generation vaccines.

Oncogenic viruses cause approximately 20% of cancers globally burden, with Epstein–Barr virus and high-risk Human papillomavirus recognized as major contributors to epithelial malignancies. Increasing evidence suggests that EBV–HPV co-infection may enhance tumour progression through overlapping molecular and immunological mechanisms, particularly in cervical, oropharyngeal, and nasopharyngeal cancers. This review critically summarizes current evidence regarding the cooperative role of EBV and HPV in carcinogenesis while distinguishing viral co-presence from biologically active co-infection. EBV latent proteins, including LMP1, LMP2A, and EBNA1, activate oncogenic signalling pathways such as NF-κB, PI3K/Akt, and JAK/STAT, whereas HPV oncoproteins E6 and E7 disrupt p53 and retinoblastoma (Rb) tumour suppressor pathways. Together, these alterations may promote genomic instability, chronic inflammation, immune evasion, epigenetic dysregulation, and epithelial–mesenchymal transition (EMT), thereby enhancing invasive and metastatic potential. Epidemiological studies report higher frequencies of EBV–HPV co-detection in advanced lesions and aggressive tumours; however, causal synergy remains insufficiently validated because of methodological heterogeneity and variability in viral detection techniques, including PCR, in situ hybridization, and immunohistochemistry. Emerging technologies such as spatial transcriptomics and single-cell profiling may improve characterization of biologically meaningful co-infection. In addition, circulating viral DNA, viral microRNAs, and HPV genotyping are being explored as biomarkers for disease monitoring and prognosis. Therapeutic strategies targeting viral oncogenes, immune checkpoints, and gene-editing technologies also represent promising investigational approaches. Overall, EBV–HPV co-infection represents a biologically plausible but incompletely understood contributor to tumour aggressiveness, emphasizing the need for standardized diagnostics, longitudinal studies, and functional experimental models.