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14 Cards in this Set
- Front
- Back
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Hepatitis D overview
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- Cytotoxic parasite of HBV - Only infects ppl with ACTIVE HBV infection
- "Defective virus" - HDV replication requires HBV replication - Same envelope, surface proteins as HBV - immunity against HBV = immunity against HDV - Cytotoxic, kills hepatocytes directly |
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Hep C overview
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- Flavivirus = enveloped, ssRNA (+), (flavus = yellow in latin, yellow fever!)
- Most common chronic blood born infection in US - leading cause of liver transplants - For unknown reasonts - Co-infection with HIV causes HCV to reach end-state, death much more quickly (from 20 yrs -> only 5ish) - NO VACCINE - More than 90 serotypes - very wide genetic variability - Transmission - primarily blood - (sexual, perinatal is low) - Diagnosis - screen for antibodies, PCR for viral genome - Treatment - Acute = Pegylated (PEG)interferon-α (IFN have short life, pegylation extends) - Chronic = PEG IFN-α, ribavirin - Prevention = universal precautions, screen blood products |
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Hep C chronic vs. acute
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- Opposite of HBV! >70% become chronic, 15% - rapid cirrhosis onset, 15% - clear completely
- Of chronic infections, 50% will progress to cirrhosis, hepatocellular carcinoma, failure - Other 50% of chronic will be asymptomatic... |
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Hepatitis E overview
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Calicivirus - (+)ssRNA, non-enveloped
- Very similar in transmission, outcome of HAV - Mortality in pregnant women = 20%! - Often seen in US in patients that have travelled to developing countries |
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Rous sarcoma virus (also RSV) overview
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Retrovirus - First virus known to cause tumors!
- Injected cell-free tumor sample from bird to other birds -> caused cancer! - Basically, discovery that viruses can cause cancer! |
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Oncovirus overview
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- 6 major viruses cause human cancer
- RNA, DNA = both integrate genome into human chromosomes - DNA viruses = HPV, HBV, EBV, HHV8 - HPV = cervix (also genital/anal warts, oral tumor) - HBV = liver - EBV = B-cell parasite = lymphoma, leukemia - HHV8 = B-cells, Kaposi's sarcoma - RNA (retro) viruses = HCV, HTLV-1 - HCV = liver - HTLV-1 = leukemia |
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Oncovirus tumor generation mechanism
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- Integrate into human genome
1) Unmodulated activation of oncogenes - uncontrolled proliferation (dominant mutations) - c-xxx = inherent cell gene, v-xxx indicates viral replacement 2) Suppression of tumor-suppressing genes (recessive mutations) - pRb, p53, etc. - 2-hit hypothesis! - Viral genome either replaces/alters expression of human gene |
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HPV tumor overview
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- E5, E6, E7 proteins
- E5 - growth factor - proliferation - E6 - p53 ubiquination - E7 - binds pRb, releases E2F -> cycle progresses - Cervical cancer mostly - some genital/anal warts, oral cancer - HPV 16 and 18 strains = immortalize cells = cancer - HPV 11, 16 = genital warts (doesn't progress to cancer) - Vaccine = L1 surface protein |
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HBV tumor mech
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- Ineffective immune response - no HBsAb produced
- Chronic, low-level infection -> virus not rapidly replicating, still incorporated into genome randomly - Random incorporation into genome turns activates oncogenes, can mess up suppressors - Other factors = alcohol use, chronic inflammation -> ROS DNA damage |
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Viral hepatitis, hepatocellular carcinoma (HCC)
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- Viral hepatitis infection (HBV or HCV)
- Surgically hard to remove, very poor outcomes... - Chronic alcohol use, aflotoxin (mold) exposure, fatty liver = other factors |
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EBV tumor overview
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B-cell parasite - Can immortalize B-cells
- Latent memory protein (LMP) - promotes proliferation, anti-apoptotic, promotes angiogenesis, etc. - EB nuclear antigen protein (EBNA) - activate growth transcription factors - Burkitt's lymphoma, Hodgkins's and non-Hodgkin's lymphoma, nasopharyngeal carcinoma and lymphoma - Treatment = Rituxan - monoclonal Ab of B-cell surface receptor CD-20 - Signal attack of B-cells, hopeful destruction of virus - AIDS patient B-cell lymphoma - probably EBV reactivation! |
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HHV-8 - Kaposi's Sarcoma
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- Also B-cell parasite
- Encodes to promote growth, inhibit apoptosis of infected cells - growths form all over body - Typically asymptomatic - problems in AIDS patients - Opportunistic infection of AIDS/immunosuppressed patients |
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HCV, hepatocellular carcinoma
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- Basically same as HBV mech
- Chronic, low-level infection -> virus not rapidly replicating, still incorporated into genome randomly - Random incorporation into genome turns activates oncogenes, can mess up suppressors - Other factors = alcohol use, chronic inflammation -> ROS DNA damage |
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Human T Lymphotrophic virus (HTLV-1)
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- Retrovirus - transmission, prevention = very similar to HIV
- Distinct pathogenesis - Tax gene = simulataneous expression of IL-2 and IL-2 receptors - Autocrine growth factor loop! - Also blocks CDK inhibitor p16, and p53 activity - T-cell leukemia, T-cell lymphoma - HTLV-1 DNA found in all adult T-cell leukemia - all have Abs to HTLV-1 |
