The human immunodeficiency virus (HIV) infection can cause damage to multiple systems within the body, and the interaction among these various organ systems means that pathological changes in one system can have repercussions on the functions of other systems. However, the current focus of treatment and research on HIV predominantly centers around individual systems without considering the comprehensive relationship among them. The central nervous system (CNS) and cardiovascular system play crucial roles in supporting human life, and their functions are closely intertwined. In this review, we examine the effects of HIV on the CNS, the resulting impact on the cardiovascular system, and the direct damage caused by HIV to the cardiovascular system to provide new perspectives on HIV treatment.

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Background Colon adenocarcinoma (COAD) is the most common type of colorectal cancer. Disulfidptosis is a novel method of disulfide-dependent cell death. Previous evidence suggested that targeting disulfidptosis may be a novel therapeutic strategy for cancer therapy. LncRNA also plays a key role in COAD. However, the mechanisms of disulfidptosis-related lncRNAs remain unknown, and the disulfidptosis-related lncRNAs-based signature for COAD remains less studied. Methods The transcriptional profile and clinical information of COAD were downloaded from The Cancer Genome Atlas (TCGA). Disulfidptosis-related gene (DRGs) expression profiles were analyzed. A correlation test, Cox regression analysis, and selection operator (LASSO) method were performed to determine a disulfidptosis -related lncRNA prognostic signature. Survival and predictive performance were analyzed according to Kaplan-Meier and receiver operating characteristic (ROC) curves. Nomograms and calibration curves were established. Gene set enrichment analysis (GSEA) was utilized to analyze the biological function. Tumor Immune Analysis was also employed to analyze the tumor immune microenvironment, immune cell infiltration, and immune function. Additionally, drug sensitivity analysis was employed to predict the sensitivity of antitumor drugs. Results We identified six DRGs as differentially expressed DRGs (DE-DRGs). Six disulfidptosis-related lncRNAs were identified and included in the novel prognostic signature. The Kaplan–Meier, and ROC curves demonstrated that the feature had acceptable predictive validity in the TCGA training, test, and complete sets. The disulfidptosis-related lncRNA model had higher diagnostic efficiency compared to other clinical features. Besides, significant differences in biological functions and pathway activities were observed between the low- and high-risk groups. The study constructed a disulfidptosis-related lncRNA signature for COAD. Additionally, six drugs were sensitive to COAD. Conclusion The six disulfidptosis-related risk profiles for lncRNA may help assess the prognosis and molecular profile of COAD patients and improve treatment options that can be further applied in the clinic.

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