Mucormycosis, triggered by fungi of the order Mucorales, represents a potentially fatal invasive mycosis, with death rates over 50% despite intensive therapy. The COVID-19 pandemic brought a sharp increase in cases, especially in individuals with diabetes mellitus and those undergoing immunosuppressive treatment, emphasizing significant gaps in our comprehension of disease pathogenesis. Emerging molecular studies have highlighted key virulence factors, such as the CotH family of invasins that facilitate endothelial invasion via interaction with glucose-regulated protein 78 (GRP78), complex iron acquisition systems necessary for fungal growth, and the release of mucoricin, a ricin-like toxin that impairs vascular integrity. Host defense depends mainly on innate immunity, with neutrophils and macrophages working as critical effector cells, while adaptive Th1 and Th17 responses aid in the fungal removal. Mucorales use a variety of immune evasion techniques, such as pathogen-associated molecular pattern (PAMP) masking via cell wall transformations, resistance to phagocytic death, and metabolic utilization of host factors including hyperglycemia and increased free iron in diabetic ketoacidosis (DKA). This review summarizes current evidence of the molecular processes underlying mucormycosis pathogenesis, underscoring host–pathogen interactions at the cellular and molecular levels, immune evasion tactics, and translational potential for new diagnostic and therapeutic approaches. Comprehending these molecular processes is crucial for creating efficient therapies against mucormycosis in an era of growing immunocompromised patients and expanding infectious disease synergies.

The Andes virus (ANDV, Orthohantavirus, andesense) is unique among hantaviruses in that it may transfer from person to person and cause severe vascular damage. The evidence on host–virus immunological interactions and their importance in disease progression, transmission, and public health is compiled in this narrative review. ANDV mostly affects pulmonary endothelial cells and does not result in widespread cell loss. Rather, the loss of vascular barrier integrity is caused by vascular endothelial growth factor (VEGF) signaling, Ras homolog family member A (RhoA) activation, breakdown of vascular endothelial (VE)-cadherin, hypoxia-related pathways, and mediators produced from infected pericytes. Additionally, the virus interferes with early antiviral defenses involving protein kinase R (PKR), TANK-binding kinase 1 (TBK1)–interferon regulatory factor 3 (IRF3), mitochondrial antiviral-signaling protein (MAVS), and retinoic acid-inducible gene I (RIG-I)/melanoma differentiation-associated protein 5 (MDA5). The intensity or outcome of the disease has been associated with increased interleukin-6 (IL-6), altered complement activity, thrombocytopenia, neutralizing-antibody reactions, and specific host genetic variations; nevertheless, significant T-cell activation does not necessarily correspond with viral clearance. Blood and a number of mucosal and secretory samples have been found to contain ANDV ribonucleic acid (RNA), albeit RNA discovery by itself does not prove the presence of an infectious virus. Epidemiological evidence indicates that Secondary transmission is rare and mostly linked to extended close or intimate contact. Genomic sequencing, when paired with epidemiological evidence, can shed light on transmission chains. Recent outbreaks linked to travel further emphasize the significance of worldwide surveillance and coordinated contact tracing. Prospective studies integrating genomic analysis, serial virological sampling, and standardized exposure evaluation are required to more effectively define the infectious phase and transmission patterns

Ebola virus disease (EVD) has traditionally been conceptualized as an acute, fulminant illness culminating in either death or apparent systemic viral clearance. However, clinical, virological, and genomic evidence gathered since the 2013–2016 West African epidemic demonstrates that Ebola virus (EBOV) can persist for months to years within immunologically privileged anatomical compartments, particularly the central nervous system, eye, and male reproductive tract, after blood viremia becomes undetectable. Importantly, the strength of evidence differs by endpoint: RT-PCR positivity demonstrates persistence of viral RNA, recovery in culture demonstrates replication-competent virus, and documented transmission requires epidemiological and, where available, genomic linkage. Persistent infection has been associated with clinically important outcomes, including relapsing meningoencephalitis, genomically supported sexual transmission long after recovery, and outbreak resurgence linked to persistent human viral lineages. Synthesizing evidence across human cohort studies, case reports, non-human primate models, and organoid systems, this review examines the anatomical, molecular, and immunological factors that may permit EBOV survival in privileged niches. Structural barriers and local immunoregulatory environments are established features of these compartments, whereas the contributions of defective viral genomes, cell-type-specific interferon responses, exosome- or cell-mediated spread, host immunogenetic variation, and acute-phase treatment to long-term reservoir establishment remain supported to differing degrees and, in several cases, are still mechanistic hypotheses. Although monoclonal antibodies and direct-acting antivirals have transformed acute-phase outcomes, their effects on established tissue reservoirs remain incompletely defined. key knowledge gaps establishing the relationship between viral RNA detection and true infectivity, defining correlates of protection against relapse, and determining how acute-phase therapeutic choice influences reservoir establishment remains essential for developing compartment-penetrant treatments, updating survivor care guidelines, and preventing future outbreak resurgences.