2026年 · 第139卷第19期

The global human immunodeficiency virus (HIV) epidemic remains a major public health challenge, with an estimated 40.8 million people living with HIV (PLWH) worldwide by the end of 2024. Despite expanding combination antiretroviral therapy (cART) coverage to 31.6 million in 2024, HIV-related illnesses still caused approximately 630,000 global deaths.^[1]

Influenza viruses are a significant challenge to the health of the global population, and are responsible for millions of severe cases and hundreds of thousands of deaths each year. The outbreaks of pandemics can result from the rapid antigenic drift and shift of the virus, which can also affect the effectiveness of the existing vaccines. Despite the availability of antiviral drugs like neuraminidase inhibitors, the rise in resistant strains is indicative of the urgent need for novel therapeutic strategies with distinct mechanisms of action. Developing treatment approaches that target host-directed pathways essential for viral replication and the immune response could be a pivotal step in mitigating this issue. The key pathway central to this strategy is the innate immune-sensing pathway mediated by retinoic acid-inducible gene I (RIG-I) and its adaptor protein mitochondrial antiviral-signaling protein (MAVS).^[1]This axis serves as the first line of intracellular defense, recognizing viral RNA (vRNA) and triggering a potent antiviral state through the induction of type I interferons (IFN-I) and hundreds of interferon-stimulated genes (ISGs). The fundamental function of the RIG-I/MAVS pathway in regulating influenza A and B virus replication in the respiratory epithelium is well-established.^[2]However, the activation of this pathway is complex and not merely a simple on/off switch. To play its role in eradicating the virus without causing excessive inflammation and immunopathology, it must be succinctly and tightly regulated. Notably, a diverse array of non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), has been identified as key regulators of this delicate balance.^[3]This editorial highlights the complex regulatory networks orchestrated by ncRNAs on the RIG-I/MAVS signaling hub during influenza infection and discusses their translational potential as targets for next-generation, host-directed antiviral therapies.

To the Editor: Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of non-Hodgkin’s lymphoma, and exhibits significant morphologies and biological heterogeneity, which can be classified into germinal center B-cell-like (GCB) and activated B-cell-like (ABC) subtypes based on cellular origin and gene expression profiles.^[1]Although rituximab-based regimens have markedly improved patient survival, 30-40% of patients still develop treatment resistance and relapse. Rituximab exerts its anti-lymphoma activity through CD20 binding, mediating complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and direct apoptosis induction.^[2]However, primary and acquired resistance significantly constrain its therapeutic efficacy in DLBCL, with the underlying mechanisms remaining not fully elucidated. Emerging evidence highlights metabolic reprogramming, particularly aerobic glycolysis, whereas lactate is the main metabolic product, and it is related to the resistance of tumor cells.^[3]Therefore, understanding the mechanism of this metabolic shift could contribute to the development of strategies for overcoming rituximab resistance in DLBCL. Detailed methods are provided in the Supplementary Materials, http://links.lww.com/CM9/C974.

To the Editor: Lung cancer (LC) is the leading cause of cancer-related deaths worldwide.^[1]Chronic lung diseases, such as chronic obstructive pulmonary disease (COPD), interstitial lung disease (ILD), pulmonary tuberculosis (PTB), bronchiectasis, and asthma, are non-malignant disorders of the respiratory system.^[2]The associations between chronic lung diseases and LC risk reported by previous studies remain controversial, possibly due to geographical differences, genetic differences, and inherent biases of observational studies caused by confounding factors, small sample size, reverse causality, etc. Therefore, we conducted a bidirectional two-sample Mendelian randomization (MR) study [Supplementary Table 1, http://links.lww.com/CM9/D4] to analyze the causal relationship between chronic lung diseases and LC, aiming to enhance clinicians’ understanding of this association.^[3]In addition, as current epidemiological data vary across populations, this study separately analyzed the potential causal association between these diseases in European and East Asian populations and explored the possible genetic mechanisms involved in this relationship [Supplementary Figure 1, http://links.lww.com/CM9/D4].

To the Editor: Histologic transformation of epidermal growth factor receptor (EGFR)-mutant lung adenocarcinoma (LUAD) into small cell lung cancer (SCLC) represents a recognized mechanism of resistance to EGFR tyrosine kinase inhibitors (TKIs).^[1]This transformation is frequently associated with an aggressive clinical course and rapid deterioration. Although inactivation of tumor protein p53 (TP53) and retinoblastoma 1 (RB1) has been implicated in this process,^[2]the comprehensive clinicopathological features and molecular mechanisms remain to be elucidated. This retrospective cohort study aimed to describe the clinical characteristics and prognosis of patients with transformed SCLC (T-SCLC), and to investigate the genetic alterations associated with this phenomenon.

To the Editor: Lung cancer (LC) is the most common solid tumor and the leading cause of tumor-related deaths worldwide.^[1]Survival among patients with LC is influenced not only by the progression and treatment of the tumor itself but also by complications. Venous thromboembolism (VTE) is one of the main causes of cancer-related death, with cancer patients complicated by VTE showing a 3-4-fold increase in mortality compared with patients without VTE. Pulmonary embolism (PE) is a subtype of VTE in which an embolus blocks the blood vessels of the pulmonary artery tree. The risk of PE is nearly 20 times greater among cancer patients than among cancer-free patients.^[2]

To the Editor: Brain health is essential for overall well-being, as the brain regulates bodily functions. Cerebral blood flow (CBF) plays a crucial role in sustaining brain function and metabolism, making it a vital parameter for evaluating brain health and diagnosing and monitoring various neurological disorders.^[1]Magnetic resonance imaging (MRI) supports the diagnosis and monitoring of neurological disorders by quantifying CBF.^[1]Arterial spin labeling (ASL) perfusion MRI non-invasively labels arterial blood water magnetically, using it as an endogenous tracer.^[1]In clinical settings, the pseudo-continuous ASL (pCASL) technique represents the standard ASL approach to labeling inflowing blood.^[1]