Hantaviruses are increasingly regarded as an important emerging risk to global health, with an estimated annual impact on more than 200000 people worldwide. These pathogens are single-stranded RNA viruses belonging to the family Han taviridae and are known to cause two major clinical syndromes in humans: Hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). The so-called old world hantaviruses, which are associated with HFRS, are predominantly distributed across Asia, Europe, and parts of Africa. In contrast, new world hantaviruses, responsible for HPS, are largely confined to North and South America. Each year, approximately 150000-200000 HFRS cases require hospitalization globally, with the greatest burden occurring in developing regions. The mortality rate of HFRS ranges from below 1% to about 12%, depending on the infecting strain. Both disease forms are characterized by increased capillary permeability, leading to clinical features such as hypotension, thrombocytopenia, and leukocytosis. While HFRS has a broader geographic distribution, HPS carries a higher risk of death.. Moreover, the detection of new viral strains and the steady rise in reported cases have intensified global concern. Enhancing surveillance systems and expanding laboratory diagnostic capacity are therefore essential for effective monitoring and control of hantavirus diseases.
BACKGROUND The discontinuation of nucleos(t)ide analog (NUC) therapy remains controversial in hepatitis B e antigen-negative chronic hepatitis B (CHB) patients who have not attained hepatitis B surface antigen loss. AIM To assess re-treatment rates and risk factors in non-cirrhotic hepatitis B e antigen-negative CHB patients after the cessation of NUC. METHODS Demographic, clinical, and laboratory data were prospectively collected before to and following the discontinuation of NUC. RESULTS Eighty-seven patients were included in the follow-up from January 2015 to September 2025; 57 were male, with a mean age of 41.3 ± 10.8 years old. The baseline median values of alanine aminotransferase (ALT) and hepatitis B viral deoxyribonucleic acid (DNA) were 87 IU/L and 37211 IU/mL, respectively. The median histologic fibrosis score was 2. The median length of treatment and consolidation therapy was 69 months and 46 months, respectively. The median duration of follow-up following the cessation of therapy was 39 months. Of the 56 patients deemed qualified for assessment based on the suggested re-treatment criteria, 29 (51.7%) underwent re-treatment. The median duration until relapse was 11 months. The cumulative virological relapse rates, defined as HBV DNA over 2000 IU/mL, were 25%, 52%, 58%, and 61% at 6 months, 12 months, 24 months, and 36 months, respectively. The cumulative retreatment rates at 6 months, 12 months, 24 months, and 36 months were 19%, 25%, 28%, and 35%, respectively. Thirty-eight patients (43%) returned to NUC treatment after an average interval of 9 months (range 1 months to 42 months). The risk factors influencing clinical relapse in patients included gender, baseline HBV DNA levels, treatment method, and alanine aminotransferase and aspartate aminotransferase levels at the end of treatment, Ishak fibrosis score > 2, and at the conclusion of treatment. In multivariate analysis, Ishak fibrosis score > 2 is the unique factor for retreatment. CONCLUSION In resource-constrained areas, discontinuing NUC may be considered for early-stage patients with low baseline hepatitis B viral DNA and alanine aminotransferase levels after a lengthy consolidation treatment. A higher pretreatment liver biopsy fibrosis score predicts relapse.
Viral encephalitis requires rapid etiological assessment, yet targeted polymerase chain reaction, serology, culture, and multiplex panels leave many cases unresolved because they depend on prespecified pathogens, sampling time, and specimen biology. Metagenomic next-generation sequencing (mNGS) can interrogate DNA and RNA in cerebrospinal fluid without a predefined target and may detect unexpected, rare, opportunistic, or emerging viruses. Its clinical performance, however, is not uniform. In published cohorts, diagnostic yield varies with case selection, reference standards, pathogen burden, specimen volume, pretreatment, laboratory workflow, sequencing depth, bioinformatic thresholds, and contamination control. Short-read Illumina workflows currently have the largest clinical evidence base, whereas real-time nanopore sequencing offers speed and portability but still requires site-specific validation. The strongest role for mNGS is therefore not routine first-line replacement of polymerase chain reaction or serology, but early complementary use in severe, progressive, unexplained, atypical, or immunocompromised cases after urgent targeted testing and empirical treatment have begun. A positive result requires assessment of read distribution, genome coverage, controls, clinical plausibility, and orthogonal confirmation; a negative result cannot exclude a low-titer, serology-defined, or tissue-restricted infection. This minireview critically compares the available evidence, identifies causes of between-study variation, and proposes a practical decision pathway for integrating mNGS into the diagnosis of viral encephalitis.
The study by Jaho et al published in the World Journal of Virology highlights a compelling paradox in occupational health: While a robust 86.6% of 134 Albanian health sciences students demonstrate seroprotection (antibody to hepatitis B surface antigen ≥ 10 IU/L), a staggering 64.5% report at least one needlestick injury during training. This high prevalence of exposure is compounded by a culture of silence, with one-third of incidents remaining unreported. This editorial analyzes why high seroprotection rates should not lead to institutional complacency. It argues that the specific vulnerability observed among midwifery students and the lack of systematic post-vaccination serological testing represent critical system gaps. Instead of relying solely on historical vaccination records, institutions should adopt guideline-based strategies for assessing hepatitis B immune status before clinical exposure, while fostering non-punitive reporting pathways. Bridging the gap between immunological protection and clinical behaviour is essential to safeguard those at the frontline of care.
Arboviral encephalitis remains a major public health concern in tropical Asia, where the etiology of a substantial proportion of central nervous system infections remains undetermined despite endemic circulation of dengue virus (DENV) and Japanese encephalitis virus. Laboratory confirmation is frequently absent in clinically suspected encephalitis. Perera et al recently published a study in World Journal of Virology , highlight this diagnostic gap by identifying DENV infection in 6.06% of encephalitis cases, including molecular evidence of DENV-3 neuroinvasion. These findings add to the growing evidence that DENV can cause encephalitis and meningoencephalitis across age groups. However, encephalitis in endemic settings is etiologically heterogeneous, and dengue represents only one of several infectious and immune-mediated contributors. Neurological dengue is likely under-recognized due to overlapping clinical presentations and limited diagnostic capacity. The identification of DENV-3 is noteworthy given its recurrent association with neurological disease. Limited concordance between reverse transcription polymerase chain reaction and immunoglobulin M assays reflects challenges related to viral kinetics, timing of specimen collection, and flaviviral serological cross-reactivity. Strengthening surveillance through integrated molecular and serological diagnostic strategies, including multiplex polymerase chain reaction and metagenomic next-generation sequencing, is essential to reduce undiagnosed encephalitis and improve clinical management and public health preparedness in tropical Asia.
