Oncogeneic viruses

• Oncogenic viruses are a type of virus that can cause cancer.
• Cancer is a large group of diseases characterized by the development of abnormal cells that divide uncontrollably and have the ability to infiltrate and destroy normal body tissue.
• Cancer is one of the leading causes of death and can affect almost every cell, organ in the human body.
• Malignant conversion is a stage in carcinogenesis.
• Carcinogenesis is the process of tumour formation.
• Oncogenic viruses are a type of carcinogen that can cause tumour formation.
• Viral infection is the leading contributor to the global cancer disease burden.
• Tumour promotion is a stage in carcinogenesis.
• Chromosomal nondisjunction is a type of event in multistage carcinogenesis.
• Manipulation of the cell cycle is a mechanism used by oncogenic viruses to cause cancer.
• Proto-oncogenes code for growth factors, growth factor receptors (tyrosine kinase or RTK), and transcription factors that increase cyclins and CDKs.
• Tumour suppressor genes are in charge of negative regulation of the cell cycle, protein products stop cell cycle progression, promote apoptosis and cell death, and are involved in DNA repair mechanisms.
• Proto-oncogenes are normal genes in charge of positive regulation of the cell cycle.
• Oncogenes lead to overexpression of genes, code for hyperactive proteins, and avoidance of apoptosis, leading to uncontrolled growth and division.
• Ultimately, the increased transcription of genes that code for special proteins leads to more of these proteins being made.
• Growth factors bind to growth factor receptors in the cell’s membrane, which activates signal transduction proteins.
• Oncogenes are mutated versions of proto-oncogenes.
• Examples of oncogenic viruses include Epstein-Barr virus, Hepatitis B virus, Human T-lymphotropic virus-1, Human papilloma viruses, Hepatitis C virus, Kaposi’s sarcoma-associated herpesvirus, and Merkel cell polyomavirus.
• Hepatitis B Virus also targets the liver as its major site of viral replication, with 25% of infections becoming chronic and 10-25% of chronic carriers at risk of developing Heptocellular carcinoma (HCC).
• Viral protein expression in Epstein-Barr Virus leads to the emergence of cell lines that are capable of infinite growth.
• Epstein-Barr Virus is transmitted via kissing (saliva), fomites.
• Infection with Epstein-Barr Virus is usually asymptomatic, but can lead to mononucleosis and a wide range of cancers.
• Human Papilloma Virus targets the liver as its major site of viral replication, with 25% of infections becoming chronic and 10-25% of chronic carriers at risk of developing Hepatocellular carcinoma (HCC).
• Latency in B cells, oral epithelial cells and NKs or T cells leads to malignancies in Epstein-Barr Virus.
• Latency membrane protein 1 (LMP1) is essential for B-lymphocyte transformation in Epstein-Barr Virus.
• Epstein-Barr Virus is the first human virus implicated in human tumours, including lymphomas and epithelial cell cancers.
• Increased replication rate of cells accumulating mutations
• Latency membrane protein 1 (LMP1) is considered the major Epstein-Barr Virus oncogene.
• Oncogenic viruses include Human Papilloma Virus, Hepatitis B Virus, and Epstein-Barr Virus.
• Mechanisms of cell transformation by retroviruses include retroviral transduction of oncogene, oncogene activation by retroviral insertion, and oncogenesis mediated by essential retroviral proteins.
• The Tax protein is a transcriptional factor for HTLV-1 genome and a promiscuous trans-activator that binds to cellular transcription factors to enhance their binding to cellular promoters.
• Slowly transforming retroviruses require months to produce tumours and produce tumours within the host’s lifespan.
• Tumour induction by DNA viruses is a diverse group of DNA tumour viruses that induce tumours in natural hosts, for example, HBV, and in experimental systems, for example, SV40.
• HTLV-1 doesn’t carry a cellular derived oncogene, doesn’t mediate cis-activation of oncogene, and has a unique regulatory protein, the Tax protein, which is essential for viral replication.
• The tag-along material is a proto-oncogene, for example, the src gene, which has been mutated and became a cancer-causing oncogene.
• Oncogenic viruses use envelope proteins to bind to growth factor receptors on the cell surface, triggering a growth-stimulating signal by mimicking normal ligand-receptor interaction.
• Insertional mutagenesis is a process where an oncogene becomes overactive and a tumour suppressor gene becomes inactive.
• The interaction can expand the available target pool and promote viral replication.
• Acutely transforming retroviruses produce tumours within weeks and require no further genetic changes after infection.
• The virus subsequently infects another cell, integrates its genome and the ‘tag-along’ material into the next cell.