Viruses and Cancer (7.2) Flashcards

1
Q

When in mitosis can cells enter G0 and what happens when they do?

A

Between the M and G1 phase, here cells do not divide and remain neutral.

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2
Q

What is an oncogene and how does it form?

What is an oncovirus?

A

Oncogene: Genetic material that carries the ability to induce cancer.
Oncovirus: a virus that can cause cancer

It’s a sequence of DNA that’s been altered/mutated from its original form the ‘Proto-oncogene’

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3
Q

How is HPV classified, transmitted and tested for?

A

Classified based on high or low risk

Transmitted through direct contact with infected skin

Tested on

  • males: with a visual exam
  • females: with a visual exam and detection through smears
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4
Q

Describe the basic structure of HPV, how omg is its incubation period?

A

Double stranded DNA virus, non enveloped and has a capsid. It’s incubation period is 3-4 months

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5
Q

What often occurs on the skin in an HPV infection and how can it be treated?

A

A condyloma (raised growth resembling a ‘cauliflower’ wart) typically in the genial region. Can be treated with meds but preferably treated with surgical or laser methods

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6
Q

What happens if HPV goes on untreated?

*List 3 things

A
  1. Transmission will continue occurring (amongst sexual partners and newborns)
  2. May cause cervical cancer
  3. Condyloma may block openings to anus, vagina and urethra
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7
Q

How can malignancy form when infected with HPV?

What are some treatment options for genital cancers?

A

The HP virus persists in the squamous cell, integrating its viral DNA into the host’s inducing chronic infection - causing dysplasia and malignancy

Genital cancers can be treated with radiation and/or chemotherapy and removal of the entire diseased organ (in extreme cases)

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8
Q

What does CIN stand for?

A

Cervical intraepithelial neoplasia

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9
Q

What is meant by the term grader and what is its significance?

A

The degree of differentiation of the neoplasm

Low grade: well differentiated and resembles parent tissue, slow growth

High grade: poorly differentiated and doesn’t resemble normal tissue, likely it will grow more quickly

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10
Q

What is meant by the term grader and what is its significance?

A

The degree of differentiation of the neoplasm

Low grade: well differentiated and resembles parent tissue, slow growth

High grade: poorly differentiated and doesn’t resemble normal tissue, likely it will grow more quickly

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11
Q

Describe the CIN grading, which grades are higher risk? How does this affect prognosis?

A

LOW RISK: CIN 1 - dysplasia involves ~1/2 thickness of epithelium. The prognosis of a micro invasion is good and treatment can be relatively conservative!

HIGH RISK:
CIN 2 - abnormal changes in ~2/3 of epithelia layer
CIN 3 - affects >2/3 of layer
The prognosis becomes more serious if the invasion is deeper as it becomes more likely that the spread will increase dramatically

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12
Q

How is the management of HPV patients decided?

A

Based on their CIN grade

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13
Q

Name three factors associated with an increased incidence of CIN

A
  1. Infection with trichomonas vaginalis
  2. Early age of first sexual encounter
  3. Many different sexual partners
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14
Q

Describe what other component of HPV makes a difference in terms of the likelihood of malignancy

A

The type of HPV, types…

Low risk: 6-11: associated with benign warts

High risk:
16,18: mainly found in CIN 2 and 3
16: commonest in squamous cell carcinoma
18: more associated with adenocarcinoma

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15
Q

What makes HPV type 16 and 18 such high risk?

A

Their mechanism of action: They encode E6 and E7 proteins:

E6: binds and blocks p53
E7: also has an anti-apoptotic effect through mutations in the p53 protein by interfering with G1

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16
Q

Describe the three main ways that HPV can integrate

A
  1. Linear virus: integrates into a tumour suppressor gene (i.e p53), so once it has been integrated into the DNA the host expresses oncogenes and produces a nonfunctional protein which doesn’t suppress neoplastic activity
  2. Enhanced expression of oncogenes
  3. If the DNA also integrates into areas where it might cause intrachromosomal rearrangement - leading to altered expression of genes involved and cellular instability
17
Q

How does HPV mainly interfere with the cell cycle?

A

Alters the cell cycle checkpoints so there is continual unregulated and unsuppressed cell growth, eventually leading to a malignancy

18
Q

What is the significance of p53?

A

It’s a tumour suppressor that normally promotes apoptosis of genetically damaged cells and plays a key role as the cell transitions from G0-G1-S phase

19
Q

What is the significance of hybridization?

A

A process that determines whether there is the presence of high risk viruses

20
Q

What is entailed in a visual examination of the cervix?

A
  1. Dilute acedic acid solution is put onto the cervix, damaged cells will turn a slightly whiter colour and through visual inspection the degree of cervical change can be observed
21
Q

How is cervical neoplasia prevented?

A

Vaccinating young women against an HPV infection (a vaccine has been developed that protects against 4 of the most common HPV strains, including those linked to cancer)

22
Q

Other than HPV, what other factor can cause carcinoma of the cervix?

A

Tobacco smoking

23
Q

Other than cervical, what other types of cancers are HPV related? In which population are they most common?

A

Oral cancers, most common in 40-50 yr old heterosexual men

24
Q

What are the two types of herpes viruses and which types of herpes do they cause?

A

HSV1 - oral herpes

HSV2 - genital herpes

25
Q

How is herpes transmitted and tested?

A

Transmission: contact (sexually or with herpes sore), mother-child

Tested: visual exam, blood test

26
Q

Are genital herpes associated with cervical cancer?

A

There has been some studies suggesting a correlation between persistent HSV2 infections but not enough evidence

27
Q

What happens once the herpes virus enters the body?

A
  1. Fuses to the cell membrane
  2. Initial attachment leads to a cascade of reactions involving viral and host cell proteins - leading to penetration of the viral nucleic capsid
  3. Nucleic capsid then transported to nuclear membrane
  4. Viral DNA released and new viruses are assembled
  5. New virions use the nuclear membrane as an envelope and exit the cell
28
Q

Describe the appearance of herpes

How long is the virus’s incubation period?

A
  1. First clear fluid-filled blisters form as HSV kills the epithelia
  2. Blisters may burst releasing a large number of virus particles and leaving behind soft wet ulcers. Ulceration can also lead to secondary infections
  3. A new layer of skin may form (so the surface appears normal) but the virus remain dormant in the body and may migrate

The incubation period is ~5 days

29
Q

When can latent herpes become reactivated and where do they tend to remain dormant?

A

Can remain dormant in the ganglia of nerve cells so emotional or physical stress or being sick can trigger its reactivation

30
Q

What disease is the Epstein Barr virus commonly associated with?

A

Burkitt’s lymphoma

31
Q

Name two general antiviral treatments, what is one treatment specific to herpes?

A
  1. Antiviral medications (to shorten and prevent outbreaks)
  2. Daily suppressive therapy for chronic herpes can reduce transmission and frequency of outbreaks

The antiviral agent Acyclovir can reduce the number of herpes lesions and reduce the risk of transmission (sexually or childbirth)

32
Q

Name four DNA viruses and two RNA viruses that are capable of causing human cancers

A

DNA viruses: Epstein-Barr, HPV, Hep B, human herpes

RNA viruses: human T lymphotrophic virus type 1, Hep c

33
Q

What class of viruses are DNA viruses?

A

Double or single stranded