Correction: Identification, Functional Analysis, and Clinical Applications of Defective Viral Genomes

Xiaowei YanYitong PanPeiying LiLi ZhuJianhai YuChenguang ShenBao Zhang^*Wei Zhao^*

• Southern Medical University, Guangzhou, China

In the published article, there was an error in positions of figures as published. Due to an oversight during the proofreading stage, FIGURE 2 and FIGURE 3 were swapped in the published version, resulting in a mismatch between the figure and their actual content. The corrected positions of figures and captions appear below. The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated. The above image is FIGURE 2, with the the caption “High concentrations of DVGs significantly enhance type I/III interferon signaling by detecting and activating RIG-I-like receptors and MAVS signaling pathways. DVGs-rich cells activate the cell survival pathway by up-regulating TNF/TNFR2/TRAF1, and combine with a small amount of standard viral genome to maintain a persistent infection state.” The above image is FIGURE 3, with the the caption “Schematic diagram of how DIPs activate host immune defense. DVGs are present in DIPs. Retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated protein 5 (MDA-5) recognize copyback DVGs and then trigger the creation of interferons (IFNs) and other cytokines, which supports the activation of the innate immune response. These factors contribute to the maturation of dendritic cells, thus contributing to the adaptive immune response. Subsequently, DVGs can enhance the recognition between naive T cells and mature dendritic cells, promoting the cell-mediated immune process mediated by type I IFN signaling. This, in turn, stimulates B cells to produce corresponding antibodies, thereby exerting the function of humoral immunity.”