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Biology of Cancer > Viruses and Cancer > Flashcards

Viruses and Cancer Flashcards

1
Q

What did Peyton Rous discover?

A
  • Chicken Sarcoma Virus in 1909
  • Tumours found in the muscles of chickens which are transmissible by viruses
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2
Q

How did he discover chicken sarcoma virus?

A
  • Removed sarcoma from the breast of a chicken
  • Broke it up into small chunks of tissue
  • Ground it with sand
  • Passed it through a fine pore filter to collect filtrate
  • Injected filtrate into young chickens
  • Observed sarcoma in injected chicken
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3
Q

What is rous sarcoma virus?

A
  • a retrovirus which has an extra gene called SRC
  • Causes sarcoma in chickens
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4
Q

What is the difference between a DNA virus and a retrovirus

A

A DNA virus injects its own DNA into a host cell straight into the genome, however a retrovirus is a type of RNA virus which has RNA that needs to be reverse transcribed into DNA before it can enter the genome

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5
Q

What is an acute/chronic virus?

A
  • Acute = occur suddenly and either resolve quickly or result in death
  • Chronic = persists over a long period of time (6+ months)
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6
Q

Give an example of an acute and a chronic virus

A
  • Acute = SARS-CoV2 (Covid)
  • Chronic = Human Immunodeficiency Virus (HIV)
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7
Q

What is a cytopathic/non-cytopathic viru

A
  • Cytopathic = either completely eliminated by the immune system or they kill the infected organism
  • Non-cytopathic = can establish long-lasting infections and successfully evade complete destruction by the immune system
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8
Q

Give an example of a cytopathic and a non-cytopathic virus?

A
  • Cytopathic = influenza virus
  • Non-cytopathic = Hepatitis C virus (HCV)
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9
Q

What are examples of chronic virus infections associated with human cancer?

A
  1. Hepatitis B virus (HBV)
  2. Hepatitis C virus (HCV) (RNA virus)
  3. Epstein Barr virus (EBV)
  4. Human herpes virus-8 (HHV-8)
  5. Human papilloma virus (HPV)
  6. Human T cell lymphotropic virus (HTLV-1)
  7. Polyoma virus
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10
Q

What are 2 ways in which chronic viral infections cause cancer?

A
  • Immortalisation of cells followed by secondary mutation due to DNA damage
  • Chronic inflammation leading to multiple cycles of tissue repair
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11
Q

What is immortalisation?

A

The ability of a cell line to reproduce indefinitely. The cells escape from the normal limitation of a finite number of division cycles which can lead to tumour formation

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12
Q

What percentage of human cancers are associated with viral infections?

A
  • Approx 40%
  • specifically liver and cervical cancers and Lymphomas
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13
Q

What did Hansen discover between HPV and cervical cancer?

A
  • Cervical carcinoma lesions derived from benign lesions are histologically similar to warts and other papillomas
  • Found that HPV DNA is found within cervical carcinomas
  • Now it’s known that approx 80-90% of cervical cancers are associated with HPV16 and/or HPV18
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14
Q

What are some characteristics of HPV?

A
  • Known to consist of 150+ genotypes
  • Sexually transmitted
  • Some of these genotypes (eg HPV16/HPV18) are associated with cervical cancer
  • Some are associated with warts of specific tissues
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15
Q

What are some cancers that oncogenic HPV is associated with?

A
  1. Anogenital
  2. Oropharyngeal
  3. Oesophageal
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16
Q

How does HPV cause cancer?

A
  • Causes cells to undergo change and if they’re not treated they can, over time, become cancer cells.
  • Once oncogenic HPV infects cells, it interferes cell communication, causing infected cells to multiply in an uncontrolled manner leading to tumours
17
Q

How does HPV infiltrate the body?

A
  • Virus infects a basal keratinocyte in the epidermis with the use of early (E) genes
  • The virus and cells replicate together
  • Viral DNA is amplified in non dividing cells
  • Using late (L) genes, the virus is made ready for infection of the individual
18
Q

What vaccines are there to protect from HPV?

A
  • Cervarix -> HPV16/18
  • Gardasil -> HPV16/18/6/11
  • Has lead to a large reduction in cervical cancer
19
Q

Does SV40 polyoma virus cause cancer in humans?

A
  • Simian virus 40 (SV40) is a type of Polyoma virus
  • Infects monkeys and causes cancer in hamsters
  • In US 1955-1963 90% children and 60% adults were inoculated with SV40-contaminated polio vaccines
  • However there were no epidemiological links to cancer
  • SV40 does infect human lung mesothelial cells, not sure if it causes mesotheliomas
20
Q

Do JCV/BKV polyoma viruses cause cancer?

A
  • Both cause brain tumours in hamsters
  • Both infect nearly all humans by 11 years
  • JCV can cause progressive multifocal leukoencephalopathy (PML) seen in AIDS
  • JCV is associated with astrocytomas that arise in JCV-PML lesions
  • Both cancers are very rare
21
Q

Does MCV polyoma virus cause cancer?

A
  • Merkel cell polyoma virus (MCV) causes brain tumours in hamsters
  • Recently associated with Merkel cell carcinoma (aggressive skin cancer)
22
Q

What are human herpes viruses (HHVs)

A
  • 8 different viruses that all infect humans
  • Lifelong infections which are controlled by immunity
  • Are latent/reactivating = able to lie dormant in the cell for a period of time with no symptoms and then become reactivated and cause infections
23
Q

What are the 8 HHVs?

A
  1. Herpes simplex virus type 1 (HHV-1)
  2. Herpes simplex virus type 2 (HHV-2)
  3. Varicella zoster virus (HHV-3)
  4. Epstein-Barr virus (HHV-4)
  5. Cytomegalovirus (HHV-5)
  6. Human herpesvirus 6 (HHV-6)
  7. Human herpesvirus 7 (HHV-7)
  8. Human herpesvirus 8 (HHV-8)
24
Q

What is an example of symptoms caused by HHV-3?

A

Causes chicken pox in early life and then shingles in later life

25
Q

What is the life cycle of a HHV?

A
  1. Virus enters and infects cell
  2. Virus replicates inside the cell
  3. Lytic infection causes the cell to die and the newly made viruses are released
  4. Process repeats
26
Q

How does HHV become latent?

A

A HHV establishes latency inside a new cell by:
- It replicates closely to the host genome and only uses proteins it really needs
- This results in not many viral antigens being displayed on the cell surface
- The virus is then able to avoid immuno surveillance and replicate for years
- It can then reactivate and continue its usual life cycle

27
Q

What are characteristics of EBV and HHV-8?

A
  • Both gamma-herpes viruses
  • Both linear dsDNA genomes
  • long unique region of 140 kbp
  • 85-100 ORFs
28
Q

What are cancers associated with EBV?

A
  • majority of people are infected but most don’t develop anything further
  • there are rare cancers developed:
    1. Lymphoma in immunosuppressed patients (HIV/transplant)
    2. Burkitt’s lymphoma in Africa
    3. Nasopharyngeal cancer is Asia
29
Q

What are cancers associated with HHV-8?

A
  • up to 40% of populations infected usually only causing a mild fever
  • rare cancers include:
    1. Kaposi’s sarcoma
    2. Multi centric Castelman’s disease
    3. Primary effusion lymphoma (PEL)
30
Q

How do EBV and HHV-8 become latent?

A
  • both can immortalise peripheral B cells
  • they convert these cells into immortalised lymphoblastoid cells
  • HHV-8 can also infect and immortalise keratinocytes, epithelial cells and vascular endothelial cells
  • latent infection only requires a fraction of the viral genome to be expressed
31
Q

How do EBV and HHV-8 cause Burkitt’s lymphoma?

A
  • the immortalised lymphoblasts made by the virus continue to divide, making them prone to picking up secondary mutations
  • this is a problem for these cells as B cells have a potent recombinase system which allows them to perform chromosomal rearrangements and translocations
  • an overexpression of this causes translocations that result in the formation of oncogenes
  • Burkitt’s lymphoma is an example of this as a common translocation is bringing c-myc (ch8) next to an IgG loci (ch14) leading to the dysregulation of c-myc and its transformation into an oncogene
32
Q

How does HHV-8 cause skin cancer?

A
  • vascular endothelial cells can be infected by HHV-8 which triggers their transformation into spindle cells
  • HHV8 latently infect VE cells
  • HHV8 uses ephrin receptor A2, which is expressed on VE cells, that result in ligation that triggers angiogenesis and transformation
  • These lytically infected cells induce host production of paracrine factors which, with virus-encoded factors, promote proliferation of latently-infected cells, invasiveness and angiogenesis
33
Q

What is viral hepatitis?

A
  • An infection that causes liver inflammation
  • associated with several pathogens (Hepatitis A/B/C/D)
  • often acute infections, resolved by host immunity
  • sometimes chronic infections, kept under control by host immunity
  • chronic infections can lead to cirrhosis and eventually hepatic cancer
34
Q

What is Hepatitis B virus (HBV)

A
  • A DNA virus
  • it is chronic hepatitis that leads to cirrhosis and can eventually progress to hepatocellular cancer (HCC)
  • one of the most common malignancies in the world, especially Africa and Asia
35
Q

How successful is the HBV vaccine?

A
  • In Taiwan, carrier rate in children fell from 10% to 1.3% 10 years after mass vaccination
  • HCC rate is falling and is expected to decrease by 85% within 3-4 decades of mass vaccination
36
Q

What is Hepatitis C virus (HCV)?

A
  • an RNA virus (ssRNA flavivirus)
  • causes chronic hepatitis
  • no vaccine at the moment
  • good drugs to protect but are expensive
  • non-Cytopathic
  • associated with extensive liver infiltration of leukocytes
  • associated with generation and infiltration of CD8+ cells which attack and destroy infected cells
  • HCV persistence is due to variants which are not recognised by CD8+ cells
37
Q

What is human T-cell lymphotropic virus (HTLV-1)

A
  • an RNA virus (retrovirus)
  • isolated from adult T—cell leukaemia (ATL)
  • varies from smouldering leukaemia to aggressive lymphoma
  • inserts randomly and is able to transactivate the hosts oncogenes to immortalise T cells and induce leukaemia/lymphoma
  • less than 1 in 100 infected in a lifetime

Biology of Cancer (19 decks)

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