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BDS Module 4 > OC 3 - virus aetiology > Flashcards

OC 3 - virus aetiology Flashcards

1
Q

What infectious agents (viruses) can cause oral cancer?

A
  • HPV
  • EBV
  • HIV
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2
Q

What do HPV alpha and HPV beta tend to effect?

A

Alpha - tends to effect the skin, warts etc

Beta - effects the oral mucosa

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3
Q

What is a papilloma?

A
  • benign, can be found anywhere from direct contact with the source
  • common on palate, mainly soft palate
  • easily treated by excision
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4
Q

What kind of cancers can high-risk types of HPV cause?

A
  • cervical
  • anal
  • oropharyngeal
  • vaginal
  • vulvar
  • penile
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5
Q

What are the high risk HPV types in head and neck cancer?

A

16 and 18

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6
Q

What gives HPV 16 its oncogenic properties?

A

E6 and E7, target tumour suppressor genes and knock out their function

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7
Q

What does HPV infect?

A

undifferentiated proliferative basal cells, which are capable of dividing

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8
Q

Where does HPV viral DNA localise?

A

viral DNA localises in to the nucleus and establishes itself as an episome

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9
Q

What do the viral proteins E6 and E7 do?

A

E6 and E7 may disturb the normal terminal differentiation by stimulating cellular proliferation and DNA synthesis

(E6 and E7 start disturbing the tumour suppressor genes (P53 and retinoblastoma), in doing so they take over cellular proliferation and DNA synthesis)

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10
Q

What are L1 and L2?

A

Capsid proteins

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11
Q

Where do L1 and L2 accumulate?

A

in the mature epithelium cells before they’re shed

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12
Q

Where does the assembly of infectious virions take place?

A

in terminally differentiated cells of the upper epithelial layers, and the virions are shed into the environment

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13
Q

How long does the natural shedding process of the mucosa take?

A

approx. 21 days

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14
Q

What happens when the HPV virions are shed into the environment?

A

other people can get contaminated by direct contact

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15
Q

What does the HPV molecule bind to on the cell?

A

binds to heparan sulfate proteoglycan (HSPGs) on the surface of the cell

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16
Q

After the HPV molecule has bound to the cell, what happens to it?

A

it then becomes endocytosed and becomes and endosome

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17
Q

What happens after the HPV virus becomes an endosome?

A

endosome then becomes a late endosome, and the virus uncoats within this

the viral genome complex with L2 is then released

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18
Q

After being released, what does the L2-genome complex do?

A

The L2-genome complex traffics through the cytoplasms and enters the nucleus

This process takes 24hrs

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19
Q

Once the L2-genome complex has reached the nucleus, what does it do?

A

Once within the nucleus it complexes with ND10 and then the RNA transcription begins

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20
Q

What happens to a virally infected cell that starts on the basal complex?

A

Eventually the cell which starts on the basal complex will move through the various layers of the epithelium from stratum basale to stratum spinosum, to stratum granulosum and then the superficial layer

From the superficial layer, the mature cell is lost and at that point it can spread and contaminate

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21
Q

What epithelial layers does a basal cell need to move through before being shed?

A

basal complex —> stratum basal —> stratum spinosum —> stratum granulosum —> superficial layer

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22
Q

What HPV types are associated with the development of papillomas?

A

HPV 6 and 11 (low risk types)

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23
Q

What does E7 protein bind and inactivate?

A

retinoblastoma protein (pRB)

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24
Q

What does E6 protein bind to, and what does it do to it?

A

binds p53 and earmarks it for destruction by the ubiquitin pathway

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25
Q

In HPV infection, why is the apoptotic pathway for the cell lost?

A

because E7 binds and inactivates pRB, and E6 binds to and destroys p53

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26
Q

During the normal HPV life cycle, where is viral DNA maintained?

A

viral DNA is maintained episomally in the nucleus of the affected cell, a state predominantly associated with “low-risk” HPV types such as HPV 6 and 11

27
Q

How can a HPV infection cause cancer to develop?

A
  • When the apoptotic pathway is lost this allows the cell to continue to proliferate
  • These cells acquire the ability to stimulate the micro-environment to produce blood vessels (angiogenesis)
  • These cells can therefore grow unregulated, and stimulate the micro-environment to provide the nutrition to facilitate tumour growth

** proliferation—>angiogenesis—>unregulated growth—> nutrition—>tumour growth **

28
Q

In which epithelial layer do mutagenic changes occur in, in a HPV infected cell?

A

stratum spinosum
- can get the development of a cell with a malignant phenotype which can then proliferate up through the superficial stratum and be shed

29
Q

What is the basic difference between low risk and high risk HPV types?

A

Low risk HPV types don’t target tumour suppressors in the same way the high risk types do

30
Q

What are the benign kinds of oral HPV lesions?

A
  • papilloma
  • condylomata
31
Q

What is the malignant type of oral HPV lesion?

A

cancer - SCC (squamous cell carcinoma)

32
Q

What does an oral papilloma look like, and what causes it?

A
  • has finger like projections
  • benign lesions caused by low-risk HPV
  • tend to be caused by sexual contact in the mouth
33
Q

What do condylomata lesions look like and what causes them?

A
  • more flat/round than papillomas
  • tend to be multiple
  • tend to be caused by sexual contact in the mouth
34
Q

In what percentage of oral cancers does HPV play a role?

A

up to 25%

35
Q

What 2 types of head and neck cancer have a strong association with HPV?

A

tonsillar related cancers, and oropharyngeal cancers (up to 80% are HPV associated)

36
Q

Is HPV more associated with mouth cancer, or oropharyneal cancer?

A

HPV much more associated with oropharyngeal cancer than mouth cancer
For mouth cancer, smoking and alcohol are main risk factors, then HPV

37
Q

What are the risk factors for HPV?

A
  • number of sexual partners
  • weakened immune system
38
Q

What methods are used for HPV detection by a pathologist?

A
  • P16 staining
  • In-situ hybridisation (ISH)
39
Q

What is P16 staining?

A
  • immunohistochemical staining looking for P16 protein, a protein downstream of p53 and retinoblastoma gene
  • HPV caused increase in P16 expression because of these genes being targeted
  • P16 used as surrogate marker but isn’t very specific
40
Q

What is in-situ hybridisation (ISH)?

A
  • looks for HPV RNA or DNA within the cells
  • looking for dark brown staining within the epithelial cells, either the cytoplasm or the nucleus
41
Q

What is more favoured, P16 staining or ISH

A

ISH

42
Q

What are the 3 HPV vaccinations?

A
  • quadrivalent Gardasil (6, 11 (LR), 16, 18 (HR))
  • bivalent Cervarix (16, 18 (HR))
  • nonvalent Gardasil (16, 18, 31, 33, 45, 52, 58 (larger range of HR))
43
Q

How many doses are given of the HPV vaccines?

A

2, with the second dose 6-12 months after the first

44
Q

In the UK, who can get the HPV vaccination?

A
  • girls and boys ages 11 and 12 (from Sept 2019)
  • individuals aged 13 to 26 if they haven’t already been vaccinated
  • MSM up to 45 yo, from sexual health clinics in England (from Apr 2018)
45
Q

What is the significance of HPV of cancer treatment outcome?

A

HPV positive tumours have been found to respond better to treatment than HPV negative tumours

46
Q

Why is it important to know if mouth/oropharyngeal cancer is HPV associated?

A

In oropharyngeal cancer especially, if HPV positive, slightly different treatment dose and multimodal therapies which involve induction chemotherapy, radiochemotherapy

47
Q

What is Epstein-Barr Virus (EBV)?

A

A type of herpes virus

48
Q

What is EBV associated with?

A
  • mononucleosis
  • lymphoma
  • nose and throat cancers
49
Q

How is EBV transmitted?

A

by contact with saliva, sexual contact, blood transfusion, and organ transplantation

50
Q

How many people worldwide will be infected with EBV in their lifetime?

A

> 90%, and most do not develop any symptoms

51
Q

What herpes subfamily does EBV belong to?

A

the gamma subfamily, which is split into 2 - lymphocryptovirus and rhadinovirus

52
Q

What does EBV infect?

A

latently infects B-lymphocytes

53
Q

What are the symptoms of infectious mononucleosis?

A
  • systemically unwell
  • enlargement of tonsillar bed
  • cervical lymphadenopathy

causes glandular fever

54
Q

What is Burkitt’s lymphoma?

A

the cancer associated with EBV
- a B-cell lymphoma, affects the nasal region and can cause significant tumours to develop

55
Q

What areas can EBV directly impact?

A

Can directly impact on the nasopharynx, on the pharyngeal epithelium and cause a tumour called nasopharyngeal carcinoma
- more common in african sub-continent than europe

56
Q

Why can HIV lead to cancer?

A

infection with HIV weakens the immune system and makes the body less able to fight off other infections that cause cancer

57
Q

What cancers does HIV increase the risk of?

A
  • Kaposi sarcoma
  • lymphomas (inc. both non-Hodgkin lymphoma and Hodgkin disease)
  • cancers of the cervix, anus, lung, liver, and throat
58
Q

What are some oral symptoms of HIV?

A
  • candidiasis
  • hairy leukoplakia
  • accelerated periodontal disease
  • Kaposis’s sarcoma
  • salivary gland disease
  • oral ulcers
59
Q

What can cause Kaposi sarcoma?

A

Kaposi sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus-8 (HHV-8)

60
Q

How is KSHV most commonly spread?

A

most commonly spread through saliva, can also be spread through organ or bone marrow transplantation, and possible blood transfusion

61
Q

How can people with HIV lower their risk of KSHV-related complications?

A

by using antiretroviral therapy

62
Q

What is Kaposi’s sarcoma?

A

a rare type of cancer that affects the skin, mouth and occasionally the internal organs

63
Q

In the UK, what percentage of Kaposi’s sarcoma cases are caused by both HHV-8 AND HIV infection?

A

94%

the remaining 6% are caused by HHV-8 with no HIV present

64
Q

What are the first symptoms of Kaposi’s sarcoma?

A

usually red, purple, or brown patches, plaques, or nodules on the skin
(the abnormal growth of small blood vessels just below the skin gives the lesions their purplish hue)

BDS Module 4 (65 decks)

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