Herpesvirus infections eliminate safeguards against breast cancer and its metastasis: comparable to hereditary breast cancers

Abstract

AbstractBreast cancer has no simple explanation. I tested the hypothesis that Epstein-Barr (EBV) infections promote the disease because they disable breast cancer safeguards. I used bioinformatics of public information from approximately 2100 breast cancers. Results demonstrate that chromosome breakpoints in breast and ovarian cancer cluster around the same breakpoints in diverse EBV-associated cancers. Cancers unrelated to EBV do not have these clusters. Breast cancers overexpress a methylation signature caused by active EBV infection. EBV remnants interspace between MHC genes and piRNA clusters as CRISPR- like evidence of past infection. I then found breast cancer breakpoints cluster around EBV docking sites. This clustering occurs because EBV breaks chromosomes and then damages breast cancers safeguards: BRCA1/2 pathways, SMC5/6, and mitotic controls. Finally, EBV causes the same losses that drive breast cancer metastasis. Activated EBV bypasses all these safeguards without large numbers of particles or continuing presence. Immunizing against EBV proteins may prevent breast, ovarian, and other cancers.SummaryHuman papilloma virus promotes cervical cancer because it disables tumor suppressors. EBV in breast cancer resembles this model. EBV variants disable a variety of molecular and cellular safeguards that protect against breast cancer.