Orthohantaviruses (also known as hantaviruses) are pathogens that cause two distinct, yet related forms of severe human disease: hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). These diseases pose a significant threat to global public health due to their high case fatality rates, which can range from 1% to 50%. In recent years, an increasing number of countries and regions have reported human cases, underscoring the urgent need for improved understanding, prevention, and treatment strategies. Given the severity of these diseases and the lack of specific post-exposure antiviral treatments, preventive measures are critical. For several decades, substantial efforts have been dedicated to developing orthohantavirus vaccines, leading to significant advancements. The first large-scale deployment involved inactivated vaccines, which played a crucial role in reducing HFRS incidence in South Korea and China. Subunit vaccines, viral vector vaccines, and virus-like particle (VLP) vaccines have also been extensively researched. Nucleic acid vaccines, including both mRNA and DNA vaccines, hold the greatest potential for future development due to their rapid design and production cycles, ability to elicit robust immune responses, ease of storage and transportation, and adaptable production platforms. Ongoing advancements in computer technology and artificial intelligence promise to further enhance the development of more effective orthohantavirus vaccines.

Tuberculosis, induced by Mycobacterium tuberculosis (Mtb), continues to pose a significant global public health challenge. Ferroptosis has emerged as a pivotal factor in tuberculosis pathogenesis, however, the mechanism has not yet been fully clarified. Therefore, the aim of this study was to hypothesize and validate potential ferroptosis-related genes in Mtb infection through bioinformatics analysis, thereby offering insights for further investigation. The mRNA microarray expression profile datasets were sourced from the Gene Expression Omnibus. The differentially expressed genes (DEGs) were derived using GEO2R. Subsequently, the shared DEGs between the GSE174566 and GSE227851 datasets were intersected with the genes in the ferroptosis database. The ferroptosis-associated shared DEGs (Ferr-sDEGs) were validated in the GSE20050 dataset. They were subjected to PPI, Cytoscape and Friends analysis, the infiltration correlation of immune cells and qRT-PCR. A total of 11 Ferr-sDEGs were identified, and 9 genes were validated. These analyses revealed that the key Ferr-sDEGs contributed to ferroptosis during Mtb infection and these key Ferr-sDEGs were relatively independent, implying that ferroptosis may be triggered by various mechanisms. Concurrently, the infiltration and correlation analysis demonstrated that multiple types of immune cells could be activated by the key Ferr-sDEGs. Ultimately, qRT-PCR validated that the expression levels of key Ferr-sDEGs. In conclusion, ferroptosis serves a pivotal function in the pathogenesis of tuberculosis. IL1B, PTGS2, TNFAIP3, HMOX1, SOCS1, CD82, and NUPR1 may be vital genes associated with the ferroptosis induced by Mtb infection.

The pathogenesis of hemorrhagic fever with renal syndrome (HFRS) remains incompletely understood. Currently, the clinical diagnosis of HFRS primarily relies on epidemiological history and clinical presentation, while the confirmation of HFRS depends mainly on the detection of hemorrhagic fever antibodies. As a viral disease, etiological diagnosis has yet to be widely implemented in clinical practice. We conducted a prospective study to characterize the temporal pattern of viremia in patients with HFRS and to explore the relationship between viral load and key laboratory parameters. Demographic and clinical data were collected from HFRS patients admitted to Tangdu Hospital, The Fourth Military Medical University, between December 2021 and December 2022. Serum samples obtained at different illness stages were tested for viral load using RT‐PCR, and corresponding laboratory results were analyzed. A total of 61 patients were enrolled, providing 256 serum samples. Both viral detection rate and viral load decreased with disease progression, with viremia detectable up to day 22. Regardless of clinical severity, Hantaan virus (HTNV) RNA load declined over time. Viral load was positively correlated with white blood cell count, lymphocyte count, and monocyte count ( r = 0.428, 0.485, and 0.318, respectively; all p < 0.001), negatively correlated with platelet count ( r = −0.507, p < 0.001), and showed weak correlations with hemoglobin and neutrophil count. Additionally, viral load was negatively correlated with fibrinogen ( r = −0.502, p < 0.001) and weakly correlated with prothrombin time, activated partial thromboplastin time, and prothrombin activity; it was positively correlated with the aspartate aminotransferase‐to‐platelet ratio index ( r = 0.515, p < 0.001). In conclusion, viremia occurs early in HFRS onset, can persist for more than 2 weeks, and viral load is an important indicator for early diagnosis of HFRS.