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Block 3 > Lecture 9.0 Oncogenic Viruses > Flashcards

Lecture 9.0 Oncogenic Viruses Flashcards

1
Q

List the factors that trigger oncogenesis

A
  • Environmental carcinogens:
    (Nicotine, radiations, chemicals, hormones, diet, etc)
    – Human genetic predispositions
    – Immunodeficiency
    – Loss of tumor immunity
    (mutation acquired over a period of time)
    – Infectious pathogens
    (i.e., Viruses)
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2
Q

Name 3 classes of regulatory genes contributing to oncogenesis

A
  • Tumor-suppressor genes / anti-oncogenes
    *e.g: p53 (Nuclear protein); pRb (Retinoblastoma protein)

– Proto-oncogenes
* e.g: c-myc (promoting cell growth & differentiation)

– Apoptosis regulating genes:
Induced cell death (mutation, DNA damage, ect)

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2
Q

Discuss the mechanism of oncogenic viruses

A
  • Inactivate tumor-suppressor genes
    *E.g: HPV proteins → promote the degradation of p53 & pRb
    → cervical cancer

– Activates cell proto-oncogenes
*E.g: Epstein Barr virus proteins → immortalization of B-
lymphocytes

– Inhibit apoptosis of damaged cells by inducing bcl-2

– DNA mutations due viral integration & error-prone viral RNA Polymerase
– Immune modulation → chronic activation of inflammation

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2
Q

List the DNA tumour viruses

A
  • Human papillomavirus
    (HPV)
  • Hepatitis B virus (HBV)
  • Herpes viruses
    *Epstein-Barr virus (EBV)
    *Kaposi sarcoma virus
  • Polyomaviruses
    *Merkel cell polyomavirus
    *JC virus
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2
Q

List the RNA tumour virus

A
  • Hepatitis C virus (HCV)
  • Human retroviruses
    -Human T-cell leukemia
    virus I (HTLV-I)
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3
Q

Discuss features of HPV

A

Have over 200 types:

– High risk types: associated with malignancy (16 & 18)
– Low risk types: warts (6 and 11)

– Predominant HPV types in SA: 16, 18 followed by 35 & 45

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3
Q

HPV transmission routes

A
  • Sexual transmission
  • In utero or perinatal
  • Autoinoculation or
    indirectly i.e fomites
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4
Q

Discuss the oncogenesis of HPV

A
  • Integration of HPV DNA into
    the host chromosomes
  • Viral proteins interfere with the
    control of cell cycle
    – E6 binds to p53
    – E7 binds to pRb
  • Activation of c-myc by nearby
    integration of HPVDNA
  • Cause a range of mucosa & cutaneous lesions
    – Majority clear the infection within 1-2 years
    – ~5–10% of cases → persistent
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5
Q

HPV screening tests, and appropriate samples

A

HPV screening tests
– Molecular assays
* DNA PCR
– Reflex testing
* Cytology

Sample
* Liquid-based cytology
* Self sampling (vaginal swab)

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5
Q

What are the risk factors for persistent infection & cervical cancer?

A

 Multiple sexual partners
 Immunosuppressive states
 Early age at first delivery; High parity
 Long-term oral contraceptive use
 STIs i.e., Bacterial vaginosis

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6
Q

Name the 2 HPV screening test

A
  • Molecular assays
    DNA PCR
  • Reflex testing
    Cytology
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6
Q

General measures and clinical prevention methods ze HPV

A
  • Behavior change:
    –Limiting high risk exposure
  • VACCINATION:
    –Cervarix (serotypes 16 and 18 )
    o Virus-like particle vaccine
    o Two doses, administered 6 months apart to girls aged 9-12 or up to 15 yrs
  • Private sector:
  • Gardasil 4 (serotypes 6,11, 16 & 18) or 9
  • HPV screening (SA Guidelines)
    – All women should initiate HPV screening from the earliest age of 25 years or at the time of a positive HIV diagnosis
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6
Q

Replicates via an RNA intermediate
– Partially dsDNA. Therefore, uses reverse transcriptase

A

HBV

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7
Q

Explain the progression of HBV

A

Acute infection with HBV»Chronic infection»Liver cirrhosis»Hepatocellular carinoma or just liver failure will result»eventually you die from either outcomes

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7
Q

What disposes an individual to HBV Oncogenesis?

A
  • Chronic or persistent infection with HBV
    -Early childhood HBV infection can result to chronic HBV infection (in 90% of
    cases)
  • Adults majority clear the infection; only 1-8% have chronic HBV
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8
Q

Interpretation of HBV surface markers:

What can you learn from the presence of HBV surface antigen in patient serum?

A

The presence of HBsAg indicates that the person is infectious
– HBsAg is detected in high levels in serum during acute or chronic hepatitis B virus infection

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8
Q

What;s the appropriate treatment for hepatitis b v?

A

ARVs: for HIV / HBV co-infected pts

– HBV mono-infection; refer pts to hepatitis clinic

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8
Q

Discuss the oncogenesis of HBV

A

– Viral integration to host DNA or viral proteins
- Random mutagenesis (insertional mutations)
- Transactivation of cellular oncogens
- Inactivation of tumour suppressor genes

– HBV chronic infection leading to liver damage

9
Q

How is HBV transmitted?

A

Sexual; Blood/ Parenteral; Perinatal; Horizontal

9
Q

How to diagnose HBV?

A

Serology
* HBV surface antigen (HBsAg) – marker of HBV infections
- Chronic HBV: sAg (+) for >6 months

– HBV viral load = monitoring

10
Q

Interpretation of HBV surface markers:

What can you learn from the presence of HBV surface antibodies in patient serum?

A
  • The presence indicates recovery and immunity from hepatitis B virus infection.
    – Anti-HBs also develops in a person who has been successfully
    vaccinated against hepatitis B (>10 IU/ml
11
Q

An oncogenic virus High in Egypt;
– Intermediate seen in
Ethiopia, Saudi Arabia,
Europe & Asia;
– Low incidence in SA

A

Hepatitis C

11
Q

3 ways to prevent for HBV infection

A
  1. Vaccination:
    – Infant immunization (EPI)
    oStandard practice – HBV vaccination at birth
    oCurrently – @ 6, 10 & 14 weeks then booster @ 18 months and @ 4-6 years

– Adult

  1. Hepatitis B Immunoglobulin:
    – Adult Post Exposure prophylaxis
    -Individual who lack of HBV immunity
    – Babies Post Exposure prophylaxis
    -For babies to HBV infected mothers
    -HB Ig + HB vaccine → administered within 12hrs of birth
  2. Prevention of high-risk behaviors:
    – Unprotected sexual intercourse
    – Intravenous drug users
    – Screening of blood
11
Q

Interpretation of HBV surface markers:

What can you learn from the presence of Hepatitis B core antigen IgM (anti-HBc IgM) in patient serum?

A

Its presence indicates acute/recent infection (<6 months)

12
Q

Interpretation of HBV surface markers:

What can you learn from the presence of Hepatitis B core antigen (anti-HBcA)in patient serum?

A

The presence indicates previous or ongoing infection (exposure) with hepatitis B virus in an undefined time frame and persists for life

13
Q

How to manage HCV?

A

Management
– No vaccine
– Antiviral therapy → viral clearance in 90% of cases

13
Q

Techniques to diagnise HCV in the lab

A

Lab Diagnosis
– Screening test: HCV Ab
– Confirmatory test: HCV RNA PCR

14
Q

Discuss oncogenesis of HCV

A

– Persistent HCV infection is a pre-requisite for tumor formation

15
Q

Common cause of infectious mononucleosis

A

Epstein Barr

*Infects and cause immortalization of B-lymphocytes into
lymphoblastoid cells
–Also infect T-lymphocytes, epithelial cells & smooth
muscle cells

16
Q

How is Epstein Barr Transmitted?

A
  • Infected oropharyngeal secretions
  • Blood
  • Transplant solid donor organ
16
Q

Tumour of the jawline resulting from infection with Epstein Barr

A

Bukirt lymphoma

*Lymphoma of childhood
*Occurs in children from tropical Africa & Papau New Guinea

16
Q

Discuss the oncogenesis of Burkit lymphoma

A

Oncogenesis:
- Result from the translocation between the c-myc on
Chromosome 8 & 14 or
Chromosome 2 & 22

o Associated with depressed CMI –due to burden of malaria
-Malaria – act as a co-factor

17
Q

Name other tumors associated with Epstein Bar virus

A
  • Post transplant lymphoproliferative disease (PTLD)
  • Nasopharyngeal ca
    – Cancer of the epithelial lining of the oro-nasal mucosa
    – Common in South East Asia – suggested co-factors
    o Genetic susceptibility
    o Chemical carcinogens in their diet
  • Hodgkin’s & Non- Hodgkin’s lymphoma
  • Primary CNS lymphoma
  • X-lymphoproliferative disease (Duncan syndrome)
  • Smooth muscle tumors 28
17
Q

Discuss the oncogenesis of Epstein Barr virus

A
  • Viral oncogenes: LMP, EBN-
    Ag & EBE-RNA causes
    widespread immortalization
    of B-cells
  • EBV linked cancers are
    associated with absence or
    depressed cell mediated
    immune response
18
Q

How tto diagnose Epsein bar?

A

EBV PCR / viral load → blood, plasma or CSF
– Excisional tumor biopsy or core needle biopsy

19
Q

Human herpes virus 8 neoplasia; 1st identified in 1994, in AIDS patients; prevalence higher in Sub-Saharan Africa

A

Kaposi sarcoma

19
Q

Treatment for Epstein Bar

A
  • No vaccine against EBV
  • Reducing immunosuppressive – PTLD
  • ARVs may be of benefit to HIV patients
  • Anecdotal support regarding the use of;
    oHerpes antivirals – acyclovir or ganciclovir
    oImmunoglobulin or monoclonal antibodies
    29
19
Q

How is HH8 transmitted?

A
  • Sexual
  • Blood
  • Organ transplant
20
Q

Discuss HH8 oncogenesis

A

LANA protein binds p53 & pRb

20
Q

Name other HH8 virus associated cancers

A
  • Kaposi sarcoma
    – Primary effusion / body cavity lymphoma
    – Multicentric Castleman’s disease
21
Q

How to diagnose kaposi sarcoma?

A

PCR on tumor biopsy

22
Q

Cancers associated with retroviruses

A
  • Human T-leukemia virus
    *Adult T-cell leukemia (ATLV)
22
Q

How to treat kaposi sarcoma?

A

Early ART for HIV patients

23
Q

Tumours caused by polyoma viruses:

A
  • Merkel cell polyomavirus:(polyomavirus 5)
    *Discovered in ~80% of Merkel cell Ca

– JC virus
*A causative link has been suggested between JC virus &
human colorectal Ca

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