Table 1 The role of viral infection in the enhancement of CSCs
Viral infection | Cancer type | Effects on CSCs | Ref. |
|---|---|---|---|
HPV | Head and neck squamous cell carcinoma | There is a correlation between HPV status and the percentage of CSC in HNSCC. The fact that CSC response to cisplatin treatment is unaffected by HPV status raises the possibility that additional variables account for the superior prognosis for people with HPV(+) cancer | [49] |
HPV | Head and neck squamous cell carcinoma | No link was seen between differences in CSC density between HPV groups and the improved clinical results observed in the HPV-positive status | [50] |
HCV and HBV | Liver cancer | In comparison to the control group, the percentages of LCSCs that express CD133/EpCAM were higher in viral hepatitis and cirrhosis groups. In the etiology of liver cirrhosis and HCC, CD133/EpCAM-expressing cells emerged due to either chronic HCV or HBV infection | [25] |
HBV | Hepatocellular carcinoma (HCC) | HBx promotes gene expression alterations that indicate CSCs, which at least in part lead to hepatocarcinogenesis | [56] |
HBV | HCC | Through PI3K/Akt signaling, miR-124 overexpression or lncRNA-MALAT1 silencing prevented HBx-induced CSC generation, stemness-related factor activation, and tumorigenicity | [58] |
HCV | HCC | Through the induction of DCAMKL-1 and hepatic progenitor and stem cell-related factors, chronic HCV infection appears to predispose cells towards acquiring CSC-like traits | [60] |
HCV | HCC | Treatment with stattic plus sorafenib showed a more robust impact on HCV-associated CSC mortality | [24] |
HCV | HCC | HCV infection causes the CSC state by activating AKT in hepatocytes via PAI-1 | [62] |
EBV | Gastric carcinoma | Cancer cells that were CD44v6/v9+/+ had a higher concentration of CSC characteristics, indicating that CD44v6/v9 is a specific CSC marker for EBVaGC. The LMP2A-NFB route was used to activate the capacity to form spheres, and EBVaGC might target this pathway as a potential therapeutic target | [65] |
EBV | Nasopharyngeal carcinoma | EBV, LMP1, which is linked to human cancers, including nasopharyngeal carcinoma (NPC), promotes tumor cell invasion, metastasis, and EMT. LMP1 allows NPC to develop CSC-like traits by turning on the mTORC1 and mTORC2 pathways | [64] |
HCMV | Glioblastoma (GBM) | The phenotypic flexibility that HCMV infection causes in GBM cells to boost GCSC characteristics may increase the tumor’s aggressiveness | [68] |
HCMV | Breast cancer | HCMV + TAMs promote proliferation, invasion, colony formation, and BCSC characteristics in inflammatory breast cancer cells via promoting the phosphorylation of p-STAT3, p-AMPK, p-PRAS40, and p-SAPK/JNK intracellular signaling molecules | [71] |
ADV | GBM | NEAT1 knockdown reduced the stemness of ADV-induced GSCs. Finally, HMGB1, a DAMP that activates TLR signaling, increased the expression of stemness markers in glioma cells | [77] |