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Oncovirus and Prions Group4
Oncovirus and Prions Group4
Oncovirus and Prions Group4
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
HEPATITIS B
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
HEPATITIS B
PATHOGENECITY AND PATHOLOGY
• Transmission: Sexual, perinatal, and parenteral routes are the most common modes of transmission. The
most common routes of transmission in the United States are heterosexual and male homosexual sexual
intercourse.
• HBV reaches the body via the bloodstream and infects the hepatocytes in the liver. The HBV-infected
hepatocytes are then attacked by cytotoxic T cells.
• The incubation period for HBV infection ranges from 2 to 6 months.
• Symptoms such as fever, anorexia, and hepatic tenderness appearing gradually. Jaundice affects only
about 10% of children under the age of five, although it is much more frequent in older children and
adults (32 percent to 54 percent ).
• The virus is gradually removed from the bloodstream as the immune response is triggered, and most
patients become noninfectious.
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
HEPATITIS B
• The presence of HBsAg in a patient's
serum means that he or she is infected with
HBV, is a chronic carrier, or is in the
incubation phase. Early in the course of the
disease, IgM anti-HBc emerges, indicating
an acute infection. The presence of IgM
anti-HBc supports the diagnosis of acute
HBV infection in patients that do not have
HBsAg and have not yet developed anti-
HBs.
• HCV is a ssRNA virus belonging to the Hepacivirus genus in the Flaviviridae family.
• A main protein, two envelope glycoproteins, and several nonstructural proteins are
encoded by the genome, which is 9.4 kb in size.
• Positive stranded RNA virus
• Six genotypes and more than 100 subtypes
• Hepatitis C virus (HCV) has a very narrow species and tissue tropism
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
HEPATITIS C
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
HEPATITIS C
Transmission
• While infection can be transmitted via perinatal and sexual transmission, and
parenteral transmission has been identified as a major route of infection, HCV
antibody has been found in patients whose transmission routes are unknown or who
have no identifiable risk factors.
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
HEPATITIS C
PATHOGENESIS
• HCV is a non-cytopathic virus that enters the liver cell and replicates at the same time,
causing cell necrosis through a variety of mechanisms, including immune-mediated
cytolysis, as well as hepatic steatosis, oxidative stress, and insulin resistance.
Irshad, M., Mankotia, D. S., & Irshad, K. (2013). An insight into the diagnosis and pathogenesis of hepatitis C virus infection. World journal of
gastroenterology, 19(44), 7896–7909. https://doi.org/10.3748/wjg.v19.i44.7896
HEPATITIS C
Diagnostic Test
• Enzyme immunoassay
• Recombinant immunoblot assay
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
HEPATITIS C
TREATMENT
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
HUMAN T-LYMPHOTROPIC VIRUS (HTLV-1)
• HTLV-1 can infect different cell types (T cells, B cells, dendritic cells, fibroblasts,
etc.) in tissue culture. However, it can transform only T cells both in vitro and in vivo.
• HTLV-1 induces the clonal proliferation of T lymphocytes, mainly CD4-positive T
cells, and to a lesser extent, CD8-positive T cells
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
HUMAN T-LYMPHOTROPIC VIRUS (HTLV-1)
PATHOGENESIS
• Virus enters T-cell and copies the two strands of RNA into double-stranded DNA that
can incorporate into the host cell's genes (much like HIV)
• -It's thought to be sexually transmitted or passed on by breastfeeding.
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
HUMAN T-LYMPHOTROPIC VIRUS (HTLV-1)
DIAGNOSTIC TEST
• HPVs, which belong to the genus Papillomavirus in the family Papillomaviridae, cause
papillomas, or warts. Some HPV forms have been related to cancer, including cervical cancer,
despite their association with the common wart.
• There are over 100 different types of these small dsDNA viruses, with over 40 of them being
sexually transmitted and referred to as genital types. Both children and young adults are believed
to be infected with HPV 1, 2, 3, and 4, with no major consequences.
• Different HPV forms have different tissue tropism depending on whether the viruses preferentially
invade cutaneous or mucosal epithelial cells. Based on their association with genital tract cancers,
genital HPVs are further classified as medium, intermediate, or high risk.
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
HUMAN PAPILLOMAVIRUS (HPV)
• Papillomaviruses are small, non-enveloped, icosahedral DNA viruses that have a diameter of 52–
55 nm.
• The viral particles consist of a single double-stranded DNA molecule of about 8000 base-pairs
(bp) that is bound to cellular histones and contained in a protein capsid composed of 72
pentameric capsomers.
• Papillomaviruses are highly species and tissue restricted, and these viruses display both
mucosotropic, cutaneotropic or dual tropism for epithelial tissues
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
HUMAN PAPILLOMAVIRUS (HPV)
• It's spread by sexual intercourse and skin-to-skin contact; it's even spread (rarely)
during childbirth.
• Cancers and recurrent respiratory papillomatosis are caused by a variety of subtypes,
including types 16 and 18. (RRP)
• HPV types 6 and 11 are linked to genital warts. HPV is responsible for almost all
cervical cancers and all cases of genital warts.
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
HUMAN PAPILLOMAVIRUS (HPV)
PATHOGENESIS
• HPV infection occurs at the basal cell layer of stratified squamous epithelial cells.
• Infection stimulates cellular proliferation in the epithelium and infected cells display a broad
spectrum of changes, ranging from benign hyperplasia to dysplasia to invasive carcinoma.
• To effectively replicate, HPV must utilize the host cellular machinery.
• During the process, the viral protein product encoded by E6 binds to the p53 tumor
suppressor gene product, which results in the premature degradation of the p53 protein.
• The E7 protein binds to a tumor suppressor protein—the retinoblastoma protein—and
inhibits its function.
• These protein products mediate much of the virus’ oncogenic potential and their production
represents a key difference between the low- and high-risk strains of HPV.
• Jennings, C. Oncoviruses. https://www.vumc.org/chtn/sites/vumc.org.chtn/files/public_files/Oncoviruses!.ppt
HUMAN PAPILLOMAVIRUS (HPV)
DIAGNOSTIC TEST
• Human herpesvirus 8, a member of the Rhadinovirus family, has been found in all
types of Kaposi sarcoma, including AIDS-related, Mediterranean, HIV-1–negative
endemic to Africa, and post-transplantation.
• It's also been linked to the progression of primary effusion lymphomas and
multicentric Castleman disease.
• The majority of herpes genes contain upstream promoter and regulatory sequences, an
initiation site followed by a 5' nontranslated leader sequence, the open reading frame
(Orf) itself, some 3' nontranslated sequences, and finally, a polyadenylation signal.
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
KAPOSI SARCOMA HHV-8
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
KAPOSI SARCOMA HHV-8
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
KAPOSI SARCOMA HPV-8
• A type of virus that causes Kaposi sarcoma (a rare cancer in which lesions grow in the
skin, lymph nodes, lining of the mouth, nose, and throat, and other tissues of the
body). Human herpesvirus 8 also causes certain types of lymphoma (cancer that
begins in cells of the immune system).
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
KAPOSI SARCOMA HPV-8
PATHOGENESIS
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
KAPOSI SARCOMA HPV-8
DIAGNOSTIC TEST
• PCR: used to detect the virus in various specimen such as tissue, blood, bone marrow,
saliva and semen.
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
KAPOSI SARCOMA HHV-8
PREVENTION AND TREATMENT
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
EPSTEIN-BARR VIRUS (EBV)
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
EPSTEIN-BARR VIRUS (EBV)
PATHOGENESIS
• EBV can be obtained from the oropharynx of both symptomatic and healthy people,
and contaminated saliva can spread the virus to others.
• EBV can take anywhere from two weeks to two months to incubate. Infection is very
normal and leads to latency, much like the other herpes community viruses, and most
adults have antibodies to the virus. Infection in children under the age of five is almost
always asymptomatic. As the age at the time of infection rises to young adulthood, the
ratio of symptomatic to asymptomatic infections rises.
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
EPSTEIN-BARR VIRUS (EBV)
PATHOGENESIS
• In addition, the virus is becoming more widely known as a significant infectious agent
in transplant recipients. The initiation of a B-cell lymphoproliferative disorder or
lymphoma is the most serious clinical consequence of EBV infection in these patients.
• B cells and epithelial cells are infected; latency can be established.
• EBV can infect different cell types, including B cells and epithelial cells.
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
EPSTEIN-BARR VIRUS (EBV)
DIAGNOSTIC TEST
• (Eliason, 1940)Eliason, N. E. (1940). A Textbook. In American Speech (Vol. 15, Issue 3). https://doi.org/10.2307/486972
EPSTEIN-BARR VIRUS (EBV)
TREATMENT
• -Chemotherapy, immunotherapy, bone marrow transplant, stem cell transplant, surgery, and
radiation for Burkitt's lymphoma
• -For Hodgkin's disease, early stage treatment includes chemo and radiation, while late stage
treatment includes only chemo.
• Causative agents are protein molecules from within the cells of the host; no nucleic acid has been
found associated with them.
Carter, J., & Saunders, V. (2007). Chapter 26 Prions, Virology: Principles and Applications, 327-328 (1st ed.). Wiley.
PRIONS
• Prnp gene
It cycles between endosomes and the cell surface, where it is held in the plasma membrane by a
glycosyl-phosphatidyl-inositol anchor at its C terminus. It is found on many cell types, but
especially on cells of the central nervous system.
Carter, J., & Saunders, V. (2007). Chapter 26 Prions, Virology: Principles and Applications, 327-328 (1st ed.). Wiley.
PRIONS
Carter, J., & Saunders, V. (2007). Chapter 26 Prions, Virology: Principles and Applications, 328-329 (1st ed.). Wiley.
PRIONS
• Onset in the UK of bovine spongiform encephalopathy (BSE), and its apparent transmission to
humans as variant Creutzfeldt-Jakob disease (vCJD).
• Characteristic pathology in the central nervous system, with parts of the brain becoming
vacuolated or spongey, in many cases also with extensive deposits of extracellular protein
fibrils or plaques but with no sign of inflammation.
• Different brain regions are affected by the various spongiform encephalopathies.
Dimmock, N., Easton, A., & Leppard, K. (2007). Chapter 22 Prion Diseases, Introduction to Modern Virology, 401-402. Wiley.
PRIONS REPLICATION
• It has been suggested that a form of ‘evangelism’ may be involved, whereby molecules of the
misfolded protein ‘convert’ normal protein molecules and cause them to misfold.
• SEED - an aggregate of a number of misfolded protein molecules
• accumulates in endosomes and lysosomes, and quantities build up especially in neurons.
Carter, J., & Saunders, V. (2007). Chapter 26 Prions, Virology: Principles and Applications, 329-330 (1st ed.). Wiley.
PRIONS
Transmissible Spongiform Encephalopathies (TSE)
Carter, J., & Saunders, V. (2007). Chapter 26 Prions, Virology: Principles and Applications, 328 (1st ed.). Wiley.
PRIONS
PATHOLOGY
Carter, J., & Saunders, V. (2007). Chapter 26 Prions, Virology: Principles and Applications, 330 (1st ed.). Wiley.
PRIONS
SIGNS AND SYMPTOMS
Dimmock, N., Easton, A., & Leppard, K. (2007). Chapter 22 Prion Diseases, Introduction to Modern Virology, 402. Wiley.
PRIONS
DISEASES IN HUMANS
• CJD - Creutzfeld–Jakob disease - most common, occurring throughout the world at an incidence of
about 1.7 cases per million people per year
• Familial CJD - families whose genomes encode certain amino acids at particular codons in the Prnp
gene
• Fatal familial insomnia - families whose genomes encode certain amino acids at particular codons
in the Prnp gene
Carter, J., & Saunders, V. (2007). Chapter 26 Prions, Virology: Principles and Applications, 331 (1st ed.). Wiley.
PRIONS
DISEASES IN HUMANS
Carter, J., & Saunders, V. (2007). Chapter 26 Prions, Virology: Principles and Applications, 331 (1st ed.). Wiley.
PRIONS
DIAGNOSTIC TEST
• Virus strains are defined by differences in the sequences of their nucleic acids, but if TSE
agents do not contain nucleic acids how can strains with different phenotypic characters be
explained?
Carter, J., & Saunders, V. (2007). Chapter 26 Prions, Virology: Principles and Applications, 332 (1st ed.). Wiley.