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Cellular and Molecular pathology > 17. Viruses and cancer 2 > Flashcards

17. Viruses and cancer 2 Flashcards

1. Describe how EBV and HPV cause cancer 2. Understand the life cycle of EBV and HPV 3. Give examples of proteins contributing to EBV and HPV infections 4. Describe vaccines and other treatments for viral infections

1
Q

When was EBV discovered?

A

1964

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2
Q

How was EBV discovered as an oncovirus?

A
  1. Burkitt noticed children were getting swollen jaws and lymph nodes.
  2. Predicted it was an infectious disease but it was actually a lymphoma
  3. Obtained a sample of the cancerous lymphoblasts
  4. did electron microscopy and saw dense structures inside the cells
  5. these were viral particles of EBV
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3
Q

What is Burkitt’s lymphoma?

A
  1. The cancer can be caused by EBV
  2. Cancerous cells growing the the jaw and the lymph nodes around it
  3. Mainly affects B cells
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4
Q

What is Epstein-Barr virus?

A
  1. A herpes virus with oncogenic potential
  2. It mostly proliferates in B cells or cells in the back of the throat.
  3. It was very early to be sequenced in 1983.
  4. It is transmitted through saliva.
  5. It can become latent in B cells.
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5
Q

What happens to EBV latently infected B cells?

A
  1. The DNA of EBV is carried throughout our life in B cells.
  2. Mostly infects B memory cells so they don’t proliferate but the viral DNA is still there.
  3. Similar to chicken pox that is latent in B cells and can reactivate into shingles.
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6
Q

What is the structure of EBV?

A
  1. Envelope with lots of membrane proteins.
  2. Tegument which is like the cytoplasm and full of proteins.
  3. DNA that is wrapped in a capsid made of hexagonal and pentagonal proteins.
  4. Portel vertex through which the DNA leaves the virus
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7
Q

What are the 2 main EBV surface proteins?

A
  1. gp350 which is 350KDa and the largest protein
  2. gH which is a glycoprotein
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8
Q

What kind of virus is EBV?

A

dsDNA virus

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9
Q

How does the EBV genome persist?

A
  1. As an episome
  2. This is like all herpes viruses.
  3. It doesn’t integrate into the host genome but it does enter the nucleus.
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10
Q

How does the EBV genome replicate in the host B cells?

A
  1. It can use the host machinery as it is a dsDNA virus.
  2. It replicates every time the B cells do.
  3. The viral genome is passed onto the daughter cells.
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11
Q

How does HIV enter the host genome?

A

Through random integration anywhere into the genome

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12
Q

What is the active infection of EBV?

A
  1. Infectious mononucleosis or glandular fever.
  2. It enters the lymph nodes and infects the B cells causing them to proliferate.
  3. It is very infectious and spreads easily.
  4. Also infects the epithelial cells at the back of the throat.
  5. Symptoms include fever, sore throat, fatigue, and swollen lymph nodes.
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13
Q

What are most EBV infections?

A
  1. Mostly harmless
  2. ill for a short period of time and then is cleared or becomes latent.
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14
Q

How often does EBV cause cancer?

A
  1. Rarely in the UK but causes about 1.5% of human cancer.
  2. this is due to genetic differences
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15
Q

Diseases associated with EBV primary infection

A
  1. Infectious mononucleosis
  2. Chronic infectious mononucleosis
  3. Fatal infectious mononucleosis
  4. immune dysfunction through exhausted b and t cells
  5. X-linked genetic T cell defect
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16
Q

Conditions associated with EBV B-cell lymphomas

A
  1. organ transplantation
  2. AIDS
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17
Q

Diseases associated with EBV: endemic Burkitt’s lymphoma

A

15% of Burkitt’s lymphomas

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18
Q

Diseases associated with EBV: Nasopharyngeal carcinoma

A
  1. HLA linkage
  2. most cases found in SE asia
19
Q

Diseases associated with EBV T-cell lymphomas

A

Nasal T-cell lymphoma

20
Q

What are the 3 groups of EBV genes?

A
  1. Latent genes
  2. Switch genes
  3. Lytic cycle genes
21
Q

How many proteins make EBV?

A

around 36 structural proteins

22
Q

What is the pre latent phase?

A
  1. Once it has entered the B cell.
  2. EBV starts to shut off genes and proteins that are not needed.
23
Q

What is latency 0?

A
  1. No EBV proteins are being produced.
  2. Only the episome is being produced.
  3. This prevents the infected B cells from being recognised by T cells.
24
Q

When are LMP1 and LMP2 produced?

A

In latency 2 and 3

25
Q

What does EBNA1 do?

A

allows the episome to replicate in the B cell

26
Q

What causes EBV to exit the latent phase?

A

no one really knows.
could be immunosuppression

27
Q

What do the EBV pre-latency proteins do?

A

Survival and invasion of the immune system

28
Q

What do the EBV latency 3 proteins do?

A

B cell proliferation

29
Q

What do the EBV latency 2 proteins do?

A

Mimic T cells stimulation and BCR signalling to activate the B cells and cause lymphoma and carcinoma

30
Q

What do the EBV latency 1 proteins do?

A

Viral replication and B cell proliferation causing burkitt’s lymphoma and gastric carcinoma

31
Q

What do we know about EBV reactivation?

A
  1. The BZLF1 transcription factor is needed.
  2. it causes the expression of all other viral proteins.
  3. We don’t know what triggers BZLF1 in vivo.
32
Q

EBV and nasopharyngeal carcinoma

A
  1. Epithelial tumour at the back of the throat.
  2. 80,000 new cases every year
  3. mainly SE Asia due to genetic variation and diet.
33
Q

EBV and endemic Burkitt’s lymphoma

A
  1. B-cell lymphoma in the jaw.
  2. Coincident with malaria but not sure of the link.
  3. All patients have antibodies to the virus.
  4. Viral DNA and proteins are in the patient’s tumour cells.
  5. This proves the link between EBV and cancer.
34
Q

How does EBV work with H.pylori to cause gastric cancer?

A
  1. H.pylori attaches to gastric epithelial cells and injects proteins like CagA.
  2. CagA is phosphorylated by Src and Abl.
  3. This causes proliferation.
  4. Normally this is stopped by SHP1 which dephosphorylates CagA and prevents its function.
  5. When EBV is present, it prevents SHP1 expression.
  6. Leads to proliferation and cancer
35
Q

What is SHP1?

A

A Tumour Suppressor Gene with SH2.

36
Q

What are EBV gp350 vaccines?

A
  1. Prevented infectious mononucleosis but not EBV infection.
  2. Antibodies to gp350 were made post vaccination.
  3. new vaccines are being developed especially cocktail vaccines against different strains.
36
Q

What is HPV?

A
  1. Another oncovirus.
  2. Over 200 types.
  3. most are low risk and cause benign warts.
  4. HPV-16 and HPV-18 are responsible for 70% of cervical cancer cases
  5. 20% of oral cancers are HPV+
37
Q

How does HPV infect cells?

A
  1. It enters through a wound in squamous epithelium.
  2. Gets into the basal stem cells that proliferate.
  3. The virus is carried through all the progeny.
  4. Viral replication continues in the non-dividing cells until about 50-100 copies per cell.
  5. Assembly and release in the top cells of the epithelium.
  6. No cell death so there is no inflammation so it remains undetected for years.
38
Q

How do HPV genome persist?

A

As episomes but it makes replication proteins so it can divide in non-dividing cells.

39
Q

What are the HPV vaccines?

A
  1. Use the L1 capsid protein.
  2. Development started in the 1990s.
  3. Cervarix by GSK against types 16 and 18.
  4. Gardasil by Merck against types 6, 11, 16, 18.
  5. immunisation 12-13 years old.
40
Q

How many cervical cancer death are due to HPV?

A

90%

41
Q

Why is the HPV vaccines not a magic bullet?

A
  1. some countries don’t have good access.
  2. expensive
  3. don’t have the infrastructure to distribute it.
42
Q

What does HPV-6 and 11 cause?

A

Genital warts

43
Q

what does HPV-16 and 18 cause?

A

cervical cancer

Cellular and Molecular pathology (25 decks)

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