Awadh Alanazi

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.

Background: The human microbiome is a dynamic and diverse community of microorganisms that affects susceptibility to illness and promotes wellness. Dysbiosis, or disruption of this delicately regulated microbial ecology, has been identified as a major factor in the emergence and development of systemic and organ‐specific disorders. Objective: With an emphasis on dysbiosis‐driven illness processes and therapeutic intervention implications, this study attempts to critically analyze host–microbiome interactions across key human organ systems. Methods: Using predetermined microbiome‐related keywords, a systematic literature search (2001–2025) was carried out in PubMed, Scopus, Web of Science, and Google Scholar. To assess microbiome formation, organ‐specific distribution, disease correlations, and therapeutic implications, English‐language peer‐reviewed original papers, meta‐analyses, and clinical or validated animal studies were chosen and methodically compiled. Results: Microbiome dysbiosis is linked to cardiovascular, metabolic, inflammatory, neurological, hepatic, renal, and cancer‐related illnesses by interfering with immune modulation, metabolic balance, and epithelial barrier integrity, according to evidence from human and verified animal research. Modified production of short‐chain fatty acids, immunological signaling imbalance, chronic inflammation, and communication between the gut–organ axis are examples of mechanistic linkages. Immune and metabolic indicators improved condition‐specifically with interventions such as probiotics, fecal microbiota transplantation, and diet‐based regulation. Conclusion: Collectively, current evidence supports the microbiome as a modifiable determinant of disease risk and therapeutic response, underscoring its translational potential for precision medicine.

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.

Dengue fever remains a significant public health issue in Saudi Arabia, with the majority of the infections occurring in the western urban centers. This st

We sincerely thank the authors of the comment for their interest in our study and for highlighting the issue of author name ambiguity in bibliometric research

Despite prolonged viral inhibition with combination antiretroviral therapy (ART), HIV-1 survives as genetically intact, replication-capable proviruses within durable CD4+ T-cell fractions, involving central memory, transitional memory, and stem cell-like memory populations, as well as within tissue-resident compartments including lymphoid follicles and gut-associated lymphoid tissue. Reservoir stability is preserved via clonal growth of infected cells and epigenetic processes that impose proviral transcriptional silencing. As a result, current therapeutic approaches seek to either directly alter proviral survival or to improve immune-driven elimination of infected cells. At the molecular level, investigational strategies such as CRISPR–Cas9 and CRISPR–Cas12 gene-editing systems are intended to remove or induce inactivating mutations inside embedded proviral DNA, as well as alter host entrance co-receptors such as CCR5 to provide cellular resistance to infection. In addition, pharmacologic latency regulation is being studied via histone deacetylase inhibitors, protein kinase C agonists, and bromodomain inhibitors to reverse latency, along with Tat inhibitors and other transcriptional repressors aimed to persistently silence proviral expression. Moreover, immunological techniques aim to counteract inefficient endogenous antiviral defenses. Broadly neutralizing antibodies with tailored Fc-driven effector functions are under examination for both neutralization and antibody-dependent cellular cytotoxicity. Therapeutic vaccine approaches seek to elevate polyfunctional HIV-specific CD8+ T-cell responses, while adoptive cellular approaches, involving CAR-T cells aiming HIV envelope epitopes, remain in early clinical research. Immune checkpoint blockade is also being investigated to reverse T-cell depletion inside reservoir-rich tissues. Nevertheless, the key obstacles continue to be the diverse reservoir composition, restricted tissue penetration, viral escape, and safety limitations. The molecular and translational obstacles that characterize attempts toward an HIV cure must be addressed through ongoing multidisciplinary research.

Background/Objectives: Predicting diseases based on the gut microbiome pattern is still difficult because of compositional shortcomings, batch heterogeneity, and scanty modeling of inter-taxon interactions. This study introduces a Dysbiosis-Aware Multiset Transformer Framework called DysbioFormer, which predicts state diseases by recognizing patterns of microbes. Methods: The current methods are mainly based on flat abundance representations or fixed-order models which limit the capability of describing intricate interactions of communities and evolutionary structure. Results: DysbioFormer is a solution to these shortcomings, in which each sample of the microbiome is modeled as a permutation-invariant multiset of taxonomic tokens with compositional, phylogenetic, and harmonized cohort data. Stacked Set Attention Blocks are used to learn relational dependencies between taxa, whereas Pooling-by-Multihead-Attention is used to aggregate global disease-level embeddings and this is not based on sequence assumptions. The model has been tested on MicrobiomeHD, which consists of a wide variety of human gut microbiome samples at a variety of disease conditions and healthy controls. Experimental results demonstrate strong diagnostic performance, achieving an accuracy of 97%, an AUC of 0.97, and an F1-score of 96%, consistently outperforming classical machine learning models under identical evaluation protocols. Attention-derived signatures also can give interpretable connections among predictive results and disease-linked microbial taxa, enhancing biological plausibility. Conclusions: The suggested architecture enables scalable, cohort-agnostic microbial diagnostics, and provides a principled route to transforming the complex information of the microbiome into reliable clinical information. DysbioFormer creates a universal basis of future microbiome-based disease screening and precision health uses. Its design allows extending towards multi-omics integration, longitudinal studies, and decision-support infrastructure, supporting microbiome-informed translational medicine in a variety of clinical research settings.