Search Results (162)

The rapid evolution of SARS-CoV-2 has underscored the need for a detailed understanding of antibody binding mechanisms to combat immune evasion by emerging variants. In this study, we investigated the interactions between Class I neutralizing antibodies—BD55-1205, BD-604, OMI-42, P5S-1H1, and P5S-2B10—and the receptor-binding domain (RBD) of the SARS-CoV-2 spike protein using multiscale modeling, which combined molecular simulations with the ensemble-based mutational scanning of the binding interfaces and binding free energy computations. A central theme emerging from this work is that the unique binding strength and resilience to immune escape of the BD55-1205 antibody are determined by leveraging a broad epitope footprint and distributed hotspot architecture, additionally supported by backbone-mediated specific interactions, which are less sensitive to amino acid substitutions and together enable exceptional tolerance to mutational escape. In contrast, BD-604 and OMI-42 exhibit localized binding modes with strong dependence on side-chain interactions, rendering them particularly vulnerable to escape mutations at K417N, L455M, F456L and A475V. Similarly, P5S-1H1 and P5S-2B10 display intermediate behavior—effective in some contexts but increasingly susceptible to antigenic drift due to narrower epitope coverage and concentrated hotspots. Our computational predictions show strong agreement with experimental deep mutational scanning data, validating the accuracy of the models and reinforcing the value of binding hotspot mapping in predicting antibody vulnerability. This work highlights that neutralization breadth and durability are not solely dictated by epitope location, but also by how binding energy is distributed across the interface. The results provide atomistic insight into mechanisms driving resilience to immune escape for broadly neutralizing antibodies targeting the ACE2 binding interface—which stems from cumulative effects of structural diversity in binding contacts, redundancy in interaction patterns and reduced vulnerability to mutation-prone positions. Full article

Herpes simplex virus 2 (HSV-2) remains a significant cause of morbidity and mortality in immunocompromised individuals, despite the availability of effective antivirals. Infections caused by drug-resistant isolates are an emerging concern among these patients. Understanding evolutionary aspects of HSV-2 resistance is crucial for designing improved therapeutic strategies. Here, we characterized 11 HSV-2 isolates recovered from various body sites of a single immunocompromised patient suffering from a primary HSV-2 infection unresponsive to acyclovir and foscarnet. The isolates were analyzed phenotypically and genotypically (Sanger sequencing of viral thymidine kinase and DNA polymerase genes). Viral clone isolations, deep sequencing, viral growth kinetics, and dual infection competition assays were performed retrospectively to assess viral heterogeneity and fitness. Sanger sequencing identified mixed populations of DNA polymerase mutant variants. Viral clones were plaque-purified and genotyped, revealing 17 DNA polymerase mutations (K533E, A606V, C625R, R628C, A724V, S725G, S729N, I731F, Q732R, M789T/K, Y823C, V842M, R847C, F923L, T934A, and R964H) associated with acyclovir and foscarnet resistance. Deep-sequencing of the DNA polymerase detected drug-resistant variants ranging between 1 and 95%, although the first two isolates had a wild-type DNA polymerase. Some mutants showed reduced fitness, evidenced by (i) the frequency of variants identified by deep-sequencing not correlating with the proportion of mutants found by plaque-purification, (ii) loss of the variants upon passaging in cell culture, or (iii) reduced frequencies in competition assays. This study reveals the rapid evolution of heterogeneous drug-resistant HSV-2 populations under antiviral therapy, highlighting the need for alternative treatment options and resistance surveillance, especially in severe infections. Full article

Pediatric high-grade gliomas (pHGGs), particularly diffuse midline gliomas (DMGs), are among the most lethal brain tumors due to poor survival and resistance to therapies. DMGs possess a distinct genetic profile, primarily driven by hallmark mutations such as H3K27M, ACVR1, and PDGFRA mutations/amplifications and TP53 inactivation, all of which contribute to tumor biology and therapeutic resistance. Developing physiologically relevant preclinical models that replicate both tumor biology and the tumor microenvironment (TME) is critical for advancing effective treatments. This review highlights recent progress in in vitro, ex vivo, and in vivo models, including patient-derived brain organoids, genetically engineered mouse models (GEMMs), and region-specific midline organoids incorporating SHH, BMP, and FGF2/8/19 signaling to model pontine gliomas. Key genetic alterations can now be introduced using lipofectamine-mediated transfection, PiggyBac plasmid systems, and CRISPR-Cas9, allowing the precise study of tumor initiation, progression, and therapy resistance. These models enable the investigation of TME interactions, including immune responses, neuronal infiltration, and therapeutic vulnerabilities. Future advancements involve developing immune-competent organoids, integrating vascularized networks, and applying multi-omics platforms like single-cell RNA sequencing and spatial transcriptomics to dissect tumor heterogeneity and lineage-specific vulnerabilities. These innovative approaches aim to enhance drug screening, identify new therapeutic targets, and accelerate personalized treatments for pediatric gliomas. Full article

KRAS is a pivotal oncoprotein that regulates cell proliferation and survival through interactions with downstream effectors such as RAF1. Despite significant advances in understanding KRAS biology, the structural and dynamic mechanisms of KRAS allostery remain poorly understood. In this study, we employ microsecond molecular dynamics simulations, mutational scanning, and binding free energy calculations together with dynamic network modeling to dissect how engineered DARPin proteins K27, K55, K13, and K19 engage KRAS through diverse molecular mechanisms ranging from effector mimicry to conformational restriction and allosteric modulation. Mutational scanning across all four DARPin systems identifies a core set of evolutionarily constrained residues that function as universal hotspots in KRAS recognition. KRAS residues I36, Y40, M67, and H95 consistently emerge as critical contributors to binding stability. Binding free energy computations show that, despite similar binding modes, K27 relies heavily on electrostatic contributions from major binding hotspots while K55 exploits a dense hydrophobic cluster enhancing its effector-mimetic signature. The allosteric binders K13 and K19, by contrast, stabilize a KRAS-specific pocket in the α3–loop–α4 motif, introducing new hinges and bottlenecks that rewire the communication architecture of KRAS without full immobilization. Network-based analysis reveals a strikingly consistent theme: despite their distinct mechanisms of recognition, all systems engage a unifying allosteric architecture that spans multiple functional motifs. This architecture is not only preserved across complexes but also mirrors the intrinsic communication framework of KRAS itself, where specific residues function as central hubs transmitting conformational changes across the protein. By integrating dynamic profiling, energetic mapping, and network modeling, our study provides a multi-scale mechanistic roadmap for targeting KRAS, revealing how engineered proteins can exploit both conserved motifs and isoform-specific features to enable precision modulation of KRAS signaling in oncogenic contexts. Full article

The underlying structural features of the mismatch between catalytic and cytostatic properties in L-asparaginase from Rhodospirillum rubrum (RrA) and three of its mutants were investigated. The rationale for selecting the specific mutations (RrA_{A64V, E67K}; RrA_{R118H, G120R}; RrA_{E149R, V150P, F151T}) is to elucidate the role of inter-subunit interaction in RrA and its impact on catalytic efficiency and stability. Bioinformatic modeling revealed a predominantly negative surface charge on RrA with limited positive charge clusters in the vicinity of the interface region. Thus, some negatively charged groups were replaced with positively charged ones to enhance the electrostatic interactions and stabilize the enzyme quaternary structure. RrA_{A64V, E67K} and RrA_{R118H, G120R} additionally contained an N-terminal 17-amino acid capsid peptide derived from the bacteriophage T7 (MASMTGGQQMGRGSSRQ), which could potentially affect the conformational stability of theenzymes. Circular dichroism (CD) spectroscopy was applied to the kinetic parameters analysis of Asn hydrolysis and showed that native RrA displayed a V_max of 30 U/mg and a K_M of 4.5 ± 0.5 mM. RrA_{E149R, V150P, and F151T} exhibited a substantially increased V_max of 57 U/mg. The catalytic efficiency of V_max/K_M also improved compared to the native enzyme: the V_max/K_M increased from approximately 7 U/mg × mM⁻¹ (for the native enzyme) to 9 U/mg × mM⁻¹ for Mut3. Other mutants exhibited less pronounced changes. Thermo-denaturation studies allowed us to determine the phase transition parameters of the RrA variants in comparison with commercial reference sample EcA. RrA_{A64V, E67K} and RrA_{R118H, G120R} exhibited the most favorable phase transition parameters, with melting temperatures (T_m) of 60.3 °C and 59.4 °C, respectively, exceeding that of the wild-type RrA (54.6 °C) and RrA_{E149R, V150P, F151T} (52 °C). The EcA demonstrated a slightly superior thermal stability, with a T_m of 62 °C. The mutations showed a significant effect on protein stability during trypsinolysis. Therefore, RrA_{E149R, V150P, F151T} showed higher resistance (45% activity remaining after 30 min of trypsin exposure) compared to the native RrA retained 20% activity. EcA preparations exhibited lower stability to trypsinolysis (losing over 90% activity in 15 min). The cytostatic effects were evaluated using MTT assays against K562 (leukemic) and A549 (lung carcinoma) cell lines. The MTT assays with K562 cells revealed that RrA_{E149R, V150P, F151T} (IC₅₀ of 10 U/mL) and RrA_{R118H, G120R} (IC₅₀ of 11.5 U/mL) exhibited superior antiproliferative activity compared to native enzymes RrA (IC₅₀ of 15 U/mL) and EcA (24 U/mL). RrA_{E149R, V150P, F151T} showed the most significant improvement in cytostatic activity. The results obtained indicate that the substitutions in RrA_{E149R, V150P, F151T} resulted in the improvement of the enzyme biocatalytic properties and an increase in the resistance to aggregation and trypsinolysis. This highlights the role of electrostatic interactions in stabilizing the oligomeric structure of the enzyme, which eventually translates into an improvement in cytostatic efficiency and antiproliferative forces. Full article

Porcine epidemic diarrhea virus (PEDV) is a major pathogen responsible for viral diarrhea in pigs, causing particularly high mortality in neonatal piglets. In recent years, genetic variations in PEDV have resulted in alterations in both its virulence and antigenicity, leading to a reduced efficacy of existing vaccines. In this study, diarrheal samples were collected from four commercial pig farms in the Hubei, Guangxi, and Jiangxi provinces, China, which experienced vaccine failure. RT-qPCR confirmed PEDV infection, and three PEDV strains, 2021-HBMC, 2024-JXYX, and 2024-JXNC, were successfully isolated. Sequence analysis and phylogenetic tree construction classified these strains into the G2c genotype, the predominant subtype in China. The neutralization assays revealed a significant reduction in the neutralizing titers of these strains against the immune serum compared with the AJ1102 reference strain. Further amino acid sequence analysis of the spike (S) protein identified several mutations in key neutralizing epitopes compared with the AJ1102 strain, including S27L, E57A, N139D, M214T, and P229L in the S-NTD epitope; A520S, F539L, K566N, D569E, G612V, P634S, E636V/K in the COE epitope; and Y1376H in the 2C10 epitope, along with several deletions at N-glycosylation sites (347NSSD and 510NITV). Additionally, whole-genome sequencing and recombination analysis indicated that the 2021-HBMC strain may have resulted from a recombination event. The findings of this study underscore the challenge posed by the continuous genetic evolution of PEDV to vaccine efficacy and provide valuable insights for future vaccine development and control strategies. Full article

Mammalian glutamate dehydrogenase (GDH) is an indispensable metabolic enzyme. GDH duplication has led to the presence of two paralogs, GDH1 and GDH2, in apes. Multiple GDH pseudogenes are also present in the human genome. The novel GDH2, supposed to be a target of positive selection, differs from GDH1 in regulation and is believed to be tightly linked to brain development. Although the differences of modern human GDH2 from GDH2 of other apes have been studied, the evolution of ancient human GDH2 remains a blank space. The goal of this work was to elucidate GDH2 evolution in the genus Homo using the accumulated data on the ancient genomes with high coverage—three Neanderthal and one Denisovan genome. Such analysis clarifies the difference between GDH2 of the last common ancestor of humans and chimpanzees and all Homo to be in M468L substitution, localized in the regulatory “antenna” region of the protein. A few novel missense mutations have been found in Denisovan and Altai Neanderthal GDH2, namely R76H, present in both genomes, and Denisovan-specific T154P, I358L, and S498A substitutions. Another mutation, R352K, has likely occurred independently in modern humans and later Neanderthals. The potential impact of these mutations was estimated using GDH2 structural data and evidence from contemporary medical data. All substitutions are supposed to be benign, with only the S498A GDH2 substitution connected to Parkinson’s disease with late onset. Additionally, the ancient genomes were revealed to have all GDH pseudogenes present in modern humans, including the RNA-coding ones. The GLUD1P3 RNA expression was found to correlate negatively with GDH1 in human tissues. A possible regulatory role has been proposed, and the GLUD1P3 RNA sequence identity in all the studied human genomes suggests its conservation in the genus Homo. Full article

Missense mutations in the BCR::ABL1 kinase domain are found in approximately 12–80% of patients with chronic myeloid leukemia (CML). Clinically significant mutations include T315I, M244V, Y253H/F, E255K/V, V299L, and F359V. The aim of this study was to create a diagnostic system for rapid and inexpensive detection of the above mutations. We used genomic DNA and RNA from peripheral blood and bone marrow cells of 57 patients with a Ph-positive CML diagnosis established in the chronic phase. We have developed a method to detect mutations in the BCR::ABL1 gene based on allele-specific real-time polymerase chain reaction (AS-PCR). In parallel, we analyzed the RNA sequence of the protein kinase domain of the same samples by next-generation sequencing (NGS) covering the points of putative mutations. In this work, we compared the results obtained by both methods for mutation detection and variant allele frequency (VAF) estimation of mutated vs. normal alleles. The sensitivity and specificity of our diagnostic system were also evaluated. It was found that AS-PCR gives reliable results at VAF up to 0.01%. AS-PCR has high sensitivity and may serve as an alternative for the more time-consuming NGS in some cases, as well as for monitoring CML treatment and for analyzing archival material. Full article

Antibiotic resistance in Helicobacter pylori is increasing rapidly and emerging as a major factor in treatment failure. We aimed to identify genetic mutations associated with resistance to clarithromycin (23S rRNA peptidyl transferase), fluoroquinolones (gyrA), and metronidazole (rdxA), and to explore their mechanisms of action through molecular modeling. H. pylori detection and the molecular characterization of genes were conducted directly on gastric biopsies by real-time PCR followed by nucleotide sequencing. A 3D model was used to evaluate molecular interactions between the antibiotics and respective target proteins. H. pylori was identified in 66.7% of 33 patients. An analysis of 23SrRNA revealed novel mutations that, by in silico analysis, do not appear to contribute to clarithromycin resistance. In gyrA, mutations in amino acid residues 87 and 91 had an incidence of 27%, and the in silico analysis revealed that these positions are relevant in the binding and resistance to fluoroquinolones. It is also reported for other mutations, some of which are never described. All rdxA mutations were missense, with R16H, M56V, H97T, G98S, A118T, V123T, and R131K predicted by in silico analysis to impact metronidazole resistance. Monitoring H. pylori gene mutations is crucial for tailoring effective antibiotic therapies. Our study advances personalized medicine by introducing novel methods to detect resistance-related mutations and uncovering the molecular mechanisms driving this resistance. Full article

Background/Objectives: New anti-tuberculosis compounds are needed to treat patients infected with multi- or extensively drug-resistant Mycobacterium tuberculosis strains. Studies based on spontaneous in vitro mutagenesis can provide insights into the possible modes of action and resistance mechanisms of such new compounds. We evaluated the primary response of M. tuberculosis in vitro to the action of new aroylhydrazones and nitrofuroylamides. Methods: The reference strain H37Rv was cultured on solid media with compounds at increased concentrations relative to MIC. Resistant clones were investigated using whole-genome sequencing and bioinformatics tools to assess the role and potential impact of identified mutations. Results: Some of the mutations are significant (based on in silico analysis), located in essential genes, and therefore of particular interest. Frameshift mutations were observed in (i) Rv2702/ppgK, which is associated with starvation-induced drug tolerance and persistence in mice, and (ii) Rv3696c/glpK, which has been described as a switch on/off mutation associated with drug tolerance. Nonsynonymous substitutions were found in Rv0506/mmpS2, which belongs to the Mmp protein family involved in transport and drug efflux, and in infB, encoding the translation initiation factor IF-2. Conclusions: The primary adaptation of M. tuberculosis to the selective pressure of the tested compounds is complex and multifaceted. It involves multiple unrelated genes and pathways linked to non-specific drug tolerance, efflux systems, or mechanisms counteracting oxidative stress. Full article

Objectives: Annexin-A1 is a 37 kDa phospholipid-binding protein which is concentrated in a truncated 34 kDa form (AnnA1) in caveolae on the tumor vascular endothelial cell surface with expression in many tumor types. PRISM developed the monoclonal mouse antibody mAnnA1 against AnnA1 for evaluation of AnnA1 as a potential target for imaging and therapy in oncology. mAnnA1 was humanized to make hAnnA1 for translation to clinical studies. Both PRISM-produced mAnnA1 and cGMP contractor-produced hAnnA1 were investigated using noninvasive PET/CT imaging, and dosimetry was evaluated to enable clinical translation of this strategy and to investigate in vivo behavior of hAnnA1. Methods: Antibodies mAnnA1 and hAnnA1 (PRISM “hAnnA1-P” or contractor generated “hAnnA1-C”) were conjugated with the chelator deferoxamine and evaluated for immunoreactivity with ELISA. Conjugated antibodies were radiolabeled with zirconium-89. Naïve mice, rats, and non-human primates (NHP) were injected with [⁸⁹Zr]mAnnA1 or [⁸⁹Zr]hAnnA1 and imaged with PET/CT up to 10 days post injection. After imaging, mice and rats were euthanized and organs were collected, weighed, and radioactivity was quantified using a gamma counter. Dosimetry in mice and NHPs were calculated using OLINDA. Results: [⁸⁹Zr]mAnnA1 showed similar biodistribution to other antibodies with slow clearance through the liver. Transition to [⁸⁹Zr]hAnnA1-C during the dosimetry studies revealed substantial uptake in the spleen (130 ± 48% ID/g at day 5 post injection in female BALB/c), which was not observed with [⁸⁹Zr]mAnnA1 (5.6 ± 1.7% ID/g at day 7 PI). Further studies in multiple strains of mice showed variable elevated splenic uptake of [⁸⁹Zr]hAnnA1-C across mouse strains, with the highest uptake observed in female BALB/c mice (118.4 ± 23.1% ID/g) and the lowest uptake observed in male CD1 mice (34.7 ± 10.2% ID/g). Additionally, splenic uptake of hAnnA1-C was observed in Fischer rats (2.8 ± 0.6% ID/organ) and NHPs (1.6 ± 0.6% ID/organ), although at lower levels than what was observed in BALB/c mice (8.8 ± 1.8% ID/organ). Dosimetry results showed similar values between estimates based on mouse and NHP data, with the largest difference seen in the spleen (5.2 vs. 2.6 mSv/MBq in females respectively). Sequencing of hAnnA1-C revealed a frameshift mutation in the antibody sequence introduced during cGMP manufacture. Restoration of the antibody sequence by PRISM returned the antibody distribution into alignment with mAnnA1. Conclusions: An aberration introduced during cGMP production of hAnnA1-C resulted in increased splenic uptake and alteration of the biodistribution in mice. PET imaging enabled quantitative detection of the immunogenic behavior of hAnnA1, which led to detection of the sequence error. Restoration of the sequence resulted in an antibody which was non-immunogenic to mice. Full article

Despite recent advancements in radiotherapy for Diffuse Intrinsic Pontine Glioma (DIPG), the prognosis of this disease remains poor, highlighting the need for new treatment strategies to improve outcomes. Adding stereotactic biopsy to the diagnostic process for children with DIPG has been crucial in improving the management of this disease. Indeed, the discovery of the H3K27M mutation as a key driver of DIPG has led to the development of new drugs that are more effective than traditional ones. These include nimotuzumab (an anti-EGFR drug) and vinorelbine (a semisynthetic vinca alkaloid) in combination, Panobinostat (a histone deacetylase inhibitor), ONC201 (a drug that blocks the dopamine receptor D2 and inactivates Akt and ERK kinases), and chimeric antigen receptor (CAR) T cells. In terms of local therapy, identifying the H3K27M mutation can help us explore how genetic changes affect treatment response, recurrence patterns, and survival. Beyond the time to first recurrence, specific patterns of tumor recurrence, like leptomeningeal spread, can influence treatment plans. For example, radiotherapy can be adjusted in terms of doses and volumes, based on tumor aggressiveness. Because the H3K27M mutation is linked to higher malignancy, a slightly higher dose could be used for the second round of local irradiation. Additionally, irradiating the entire craniospinal axis could help control both local and leptomeningeal disease. Full article

Background/Objectives: Studies have shown that some mutations, especially M694V, are correlated with renal RI and/or AA. There are limited data about rare mutations on severity of the disease and RI. Today, evaluating genotype–phenotype correlations in rare mutations is important to better understand FMF. We aimed to evaluate clinical, demographic and genetic changes and genotype–phenotype correlations in pediatric patients with FMF over thirty years as well as the importance of the rare mutations. Methods: A total of 2765 pediatric patients with FMF were included in this study. Genetic results were firstly divided into ten groups including rare mutations. Rare mutations were seen in 2% of all patients and divided into eight groups. Results: There was a significant increase in compound heterozygous mutations, E148Q het/hom, R202Q het/hom, complex mutations and rare mutations in the last decade. RI wo AA was 5.8% and AA was 1% in the patients with rare mutations. While M694V and compound het with M694V were positively correlated with severe PRAS, E148Q and V726A were negatively correlated with severe PRAS (p < 0.05, R = 0.137, R = −0.077, R= −0.05, respectively). Although K695R mutation was negatively correlated with severe PRAS (p < 0.05, R = −0.04), the rate of RI was 20%. Although the rare mutation R761H was negatively correlated with severe PRAS (p < 0.05, R = −0.051), the colchicine resistance rate was 8.3%. Conclusions: It may be misleading for clinicians that mutations which have increased in frequency over the years are clinically mild. RI and AA rates in rare mutations are not less than the related rates in common mutations. Full article

Real-world data on HIV drug resistance (HIVDR) after transitioning to tenofovir disoproxil fumarate/lamivudine/dolutegravir (TLD) are limited. We assessed HIVDR rates and patterns in clients with virological failure (VF) after switching from an NNRTI-based regimen to TLD. A cross-sectional study was conducted in Gaza, Mozambique (August 2021–February 2022), including adults on first-line ART for ≥12 months who transitioned to TLD and had unsuppressed viral load (VL) ≥ 1000 copies/mL six months post-transition. After three adherence counseling sessions, participants with VF underwent genotyping for drug resistance mutations (DRMs) using the Stanford HIVdb Program. Of 717 participants (median age 39.2 years, 70.7% female), 217 (30.2%) had VF, 193 (88.9%) underwent genotyping, with 183 (94.8%) successfully genotyped. Intermediate–high dolutegravir (DTG) resistance was found in 19.6% (36/183). Unsuppressed VL before DTG transition was independently associated with VF (aOR: 2.14). Resistance patterns included 33.3% (12/36; 95% CI: 14.6–46.3) to all three TLD drugs, 55.6% (20/36; 95% CI: 39.3–71.9) to DTG and 3TC, and 11% (4/36; 95% CI: 0.8–21.3) to DTG only. Major drug resistance mutations to DTG included G118R (9.3%), R263K (6.6%), and Q148H/R/K (4.4%). This study highlights the need to consider virologic status before transitioning PLHIV to TLD and suggests that adherence counseling may not prevent resistance in those with unknown or prior VF. Full article

Erosive rainfall is essential for initiating surface runoff and soil erosion to occur. The analysis on its temporal and spatial distribution characteristics is crucial for calculating rainfall erosivity, predicting soil erosion, and implementing soil and water conservation. This study utilized daily rainfall observation data from 90 meteorological stations in Henan from 1981 to 2020, and conducted geostatistical analysis, M-K mutation test analysis, and wavelet analysis on erosive rainfall to reveal the spatiotemporal distribution characteristics over the past 40 years. Building on this foundation, the correlation between erosive rainfall, rainfall, and rainfall erosivity were further explored. The findings indicated that the average annual rainfall in Henan Province varied between 217.66 mm and 812.78 mm, with an average yearly erosive rainfall of 549.24 mm and a standard deviation of 108.32 mm. Erosive rainfall constitutes for 77% of the average annual rainfall on average, and the analysis found that erosive rainfall is highly correlated with rainfall volume. The erosive rainfall increased from northwest to southeast, and had the same spatial distribution characteristics as the total rainfall. The number of days with erosive rainfall was 20.5 days and the annual average sub-erosive rainfall was 26.86 mm. The average annual rainfall erosivity in Henan Province ranged from 1341.81 to 6706.64 MJ·mm·ha⁻¹·h⁻¹, averaging at 3264.63 MJ·mm·ha⁻¹·h⁻¹. Both the erosive rainfall and the rainfall erosivity are influenced by the monsoon, showing a unimodal trend, with majority of the annual total attributed to rainfall erosivity from June to September, amounting to 80%. The results can provide a basis for forecasting of heavy rainfall events, soil conservation and planning, ecological treatment, and restoration. Full article