This latent virus in 90% of the human body causes chromosome breakage and promotes cancer
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Nature: This latent virus in 90% of the human body causes chromosome breakage and promotes cancer.
Epstein-Barr virus (EBV) is one of the most common viruses in the world, and EBV is easily transmitted through bodily fluids (mainly saliva) , such as kissing, sharing drinks or eating utensils. According to statistics, 90%-95% of people worldwide have been infected, usually in childhood.
EBV infection can cause infectious mononucleosis or a similar illness, but this is usually asymptomatic. Most EBV infections are mild and disappear, but the virus persists in the body, dormant, and can and can be reactivated. In recent years, some studies have shown that long-term latent EBV virus is related to some chronic inflammation and various cancers , and some studies have found that EBV may be the causative factor of multiple sclerosis (MS) .
On April 12, 2023, the team of Professor Don Cleveland of the University of California, San Diego published a research paper entitled: Chromosomal fragile site breakdown by EBV-encoded EBNA1 at clustered repeats in Nature .
The study describes for the first time how the Epstein-Barr virus (EBV) exploits a vulnerable site in the human genome to cause chromosome breakage, trigger cancer, and simultaneously reduce the body’s ability to suppress cancer.
In every human genome there are sites of vulnerability, specific chromosomal regions that are more prone to mutations, breaks or deletions as DNA replicates. These changes can all be associated with disorders and diseases, can lead to genetic diseases, and can lead to cancer.
Professor Don Cleveland , the corresponding author of the paper , said that this study reveals how EBV induces the breakage of human chromosome 11 and triggers a series of genomic instability, which may activate oncogenes that cause leukemia and disable major tumor suppressor genes.
This is also the first demonstration of how breaks at fragile DNA sites can be selectively induced.
In this latest study, the research team focused on the EBNA1 protein, a viral protein that persists in human cells infected with EBV.
Previous studies have shown that EBNA1 binds to specific genomic sequences at the initiation of EBV genome replication.
The study found that EBNA1 also binds a cluster of EBV-like sequences at a vulnerable site on human chromosome 11, where increased abundance of the protein triggers chromosome breakage.
Previous studies have shown that EBNA1 can inhibit the p53 gene, which is known as the “guardian of the genome” and plays a key role in controlling cell division and cell death. Under normal circumstances, p53 can inhibit the occurrence and development of tumors, while mutant p53 is related to the growth of cancer cells.
The research team also examined whole-genome sequencing data from 2,439 cancers across 38 cancer types from the Whole Genomes Pan-Cancer Analysis Project, and they found that tumors with detectable EBV infection showed higher levels of chromosome 11 abnormalities, especially It is a case of head and neck cancer .
For a virus that is ubiquitous and harmless to most people, identifying those at high risk for disease associated with latent infection is still an ongoing effort, says postdoctoral fellow Julia Su Zhou Li , first author of the paper .
This study demonstrates that susceptibility to EBNA1-induced chromosome 11 breakage depends on control of EBNA1 protein levels produced in latent infection, as well as genetic variation in the number of EBV-like sequences on chromosome 11 in each individual.
Going forward, this finding paves the way for screening for risk factors for the development of diseases associated with EBV infection.
Furthermore, blocking the binding of EBNA1 to EBV-like sequences on chromosome 11 could be used to prevent the development of EBV-associated diseases.
Paper link :
https://www.nature.com/articles/s41586-023-05923-x
This latent virus in 90% of the human body causes chromosome breakage and promotes cancer
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