Publications by Year: 2026

Monkeypox (MPOX) is an emerging zoonotic disease caused by monkeypox virus (MPXV), an orthopoxvirus closely related to smallpox. Initially confined to endemic regions in Central and West Africa, MPOX has recently gained global significance with outbreaks reported across multiple continents. MPXV is maintained in animal reservoirs but is increasingly transmitted from person to person, facilitated by close contact, respiratory droplets, and, in some cases, sexual transmission. Clinically, MPOX presents with fever, lymphadenopathy, and a characteristic vesiculopustular rash, though atypical manifestations have been observed in recent outbreaks, complicating diagnosis. Laboratory confirmation relies on molecular testing, while differential diagnosis must consider varicella, herpes, and other vesicular illnesses. Therapeutic options remain limited; supportive care is the cornerstone of management, but antivirals such as tecovirimat and brincidofovir, as well as smallpox vaccines, have shown efficacy in mitigating disease severity and preventing infection. The unprecedented global outbreak has underscored the importance of surveillance, rapid diagnostics, and coordinated public health responses to contain transmission. This review provides an overview of epidemiology, virology, clinical manifestations, modes of transmission, available diagnostics, and prophylactic and therapeutic strategies against MPOX. We also discuss the role of animal reservoirs, viral evolution, and human-to-human transmission in shaping the dynamics of recent MPOX outbreaks. By summarizing the latest evidence, this review aims to inform clinicians, researchers, and policymakers about key aspects of MPOX biology, clinical management, and prevention, while identifying gaps that warrant future investigation for the control of this and potentially other emerging zoonotic-related pathogens with an impact on human health.

The remaining unacceptably high mortality of influenza-induced acute respiratory distress syndrome underscores the urgent need to identify key cellular drivers of host responses. Endothelial cells (ECs) are increasingly recognized for their immunomodulatory roles, but whether they function as antigen-presenting cells (APCs) following respiratory viral infection remains unknown. Here, we show that influenza A virus H1N1 restrictively infects pulmonary microvascular ECs (PMVECs) during late-stage acute lung injury, triggering robust MHC class I (MHC-I) upregulation in vitro, in vivo, and in ex vivo human precision-cut lung slices. Infected PMVECs present H1N1 antigens via MHC-I and co-stimulatory CD40 to lung-resident CD8⁺ T cells, driving their proliferation and effector function (Granzyme B, IFNγ) to promote viral clearance and resolve inflammation. This process is IFNγ-dependent and STAT1-regulated, forming a positive feedback loop that enhances PMVEC antigen presentation and CD8⁺ T cells activation. By contrast, the emerging H5N1 (A/Texas/37/2024) infect pulmonary ECs earlier and more broadly but elicits weaker pulmonary EC-driven CD8 + T cell responses, potentially contributing to its higher pathogenicity. These findings reveal PMVECs as active APCs in antiviral defense and highlight new avenues for immunotherapeutic intervention.