Brief Report - (2018) Volume 3, Issue 1
Bajaj A*
Department of Histopathology, A.B.Diagnostics, A-1 Ring Road, Rajouri Garden, New Delhi, India
*Corresponding Author:
Mbamalu ON
Consultant, Department of Histopathology
A.B. Diagnostics, A-1 Ring Road
Rajouri Garden, New Delhi.
Tel: 00919811693956; 00911141446785
E-mail: anubha.bajaj@gmail.com
Received date: November 27, 2017; Accepted date: November 27, 2017; Published date: March 16, 2018
Citation: Bajaj A (2018) Viral Monitors in Generation, Maintenance and Perpetuation of Neoplasia. Insights Biomed. Vol.3 No.1:3
Universally, approximately 20% of the cancers are related to infectious agents. Intracellularly, viruses encode proteins to reprogramme signalling pathways for cell proliferation, differentiation, dissolution, genomic integrity and immune assimilation. Viral genomes are tightly crammed within the host structure to target cellular regulatory modes. Mostly these are key proteins and are subject to mutation and chromosomal re-arrangements in non-viral diseases and carcinomas. Many retroviruses integrate near c-oncogenes and express by proviral insertional mutagenesis and modulate cell growth and differentiation. Retroviruses that carry the viral oncogenes can engender a wide variety of neoplasia (abnormal growth and proliferation of abnormal cells or abnormal amount of cells which exceeds and is uncoordinated with that of the normal tissue and persists in the same excessive manner after the cessation of the stimuli which evoked the conversion, due to a benign or malignant process) in a short interval, chiefly haematopoietic and mesenchymal malignancies etc.
Keywords
Cancer; Genomic integrity; Mutations
Introduction
Oncogenic viruses, typecast RNA and DNA viruses promote cellular transformation and insuppressible cell growth to cause a lethal tumefaction. Viruses boosting fatal conversion induce the viral combined with the host genome, revise the host cell proliferation, synthesize new proteins and alter viral oncogenes.
Execution of viruses in the generation of cancer
Proto-oncogenes (cellular oncogenes) affecting cell growth/ development, may have mutations such as amplification, point mutations, deletions and chromosomal translocation. C-oncogenes are protein kinases, growth factors, growth factor receptors and DNA binding proteins [1].
Anti-oncogenes (tumor suppressor genes) lose their clamping and disorderly growth occurs
Oncogenes are classified as growth factors PDGF and sis gene encoding PDGF (beta). Growth factor receptors erbB, erbB2, fms, kit, met, ret, ros, trk. Signal transducers i.e., non-receptor protein kinases, tyrosine kinase (abl, lck and src) and serine threonine kinases (raf-1, mos, pim-1). GTP binding proteins monomeric (H-ras, K-ras, N-ras) and heterotrimeric (gsp, gip). Transcription factors erbA, ets, fos, jun.myb, c-myc. Apopotosis or programmed cell death Bcl-2. Tumor suppressor genes retinoblastoma gene and p53, Wilm’s tumor gene WT1, Von Hippel Landau VHL gene, NFI and NF2, APC, DCC in familial adenomatous polyposis [2].
Contrivance of oncogenesis
Cancerous mobilization by mutation, gene amplification and chromosomal rearrangements is a multistep process so more than one working instituted in the genesis. The internecine has the capacity for metastasis and a combination proto-oncogene propellment and anti-oncogene inactivation is insinuated. Nontransforming retroviruses activate oncogenes and expressions through proviral insertional mutagenesis, amplify sequences in the gene locus and customize gene expression. The appearance of the malignancies has a long latent period. The infected host cells grow rapidly, the cellular composition and morphology changes meaningfully. Methodologies include: Direct and catalytic growth with surface proteins binding to growth factor receptors, boosting growth and i) infecting the cells ii) increasing the number of target cells iii) enhancing viral replication. Long terminal repeats which have promoter/ enhancer attachments which mediate expression of sequence to be kept under control. This impinges upon the high levels of viral replication load and increases recombinant oncogenic potential [3].
Discussion and Conclusion
According to the survey conducted, the common, uncommon and isolated tumorigenesis with viral aetiology includes:
• EBV (Epstein Barr Virus) incorporating B cells and Oropharyngeal cells implicated in Burkitt’s lymphoma, nasopharyngeal carcinoma, Hodgkin’s lymphoma and Multicentric Castleman’s disease.
• Hepatitis B and C viruses found in hepatocytes and white blood corpuscles, insinuated in Hepatocellular carcinoma.
• Human Papilloma Virus (HPV) type 6, 11, 16, 18, 31, 45 in squamous epithelial cells, absolving cervical, anogenital, oral cancer, Merkel cell carcinoma and solid tumors.
• Human T-cell leukaemia virus (HTLV1) found in immune T cells, causative in Adult T cell leukemia.
• Kaposi sarcoma associated herpesvirus (KSHV) or Human Herpes Virus (HHV8) in immune B cells associated with Kaposi sarcoma, primary effusion lymphoma.
• Adenoviruses type 9, 12, 18, 31 begetting solid tumors in rodents.
• Polyoma viruses BK virus, JC virus, SV 40 (simian virus), cited in Brain Prostate, Bone, Mesothelioma, Merkel cell Polyoma virus.
• Poxviuses entailing Molluscum Contagiosum Viruses (MCV).
• Human Endogenous Retrovirus (HERV) entangled in Seminona, Breast, Melanoma and Ovarian.
• Human Mammary Tumor Virus (HMTV) hinted with breast.
• Torque Teno-Virus (TTV) included in gastrointestinal, lung, breast and melanoma.
• Alpharetrovirus (AEV, ALV, ASV) imputed in erythroblastosis, carcinoma and sarcoma.
• Deltaretovirus and Gammaretrovirus BLV, FC, LV, SV, MO, MLV, MSV included in lymphomas. Viral families are Hepnadenviridae, Flaviviridae, Retroviridae, Adenoviridae, Papillomaviridae, Alpharetrovirus, Deltaretovirus and Flaviviridae [4].
