infectious agents and head and neck cancer viruses

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what are the 3 important viruses that cause oral cancer etc
HPV, HIV, EBV
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What kind of cancer does the high risk HPV cause? how does this virus spread
cervical, anal, oropharyngeal, vaginal, vulvar, penile cancers. the virus spreads through direct sexual contact
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how is HPV described ( as it target mucosa ...it is called ...) what kind of DNA does HPV have ?
epitheliotrophic, it has double stranded DNA
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What virus group does HPV belong to? what is HR HPV associated with - what carcinogens
papovavirus- small, non enveloped DNA viruses of a symmetrical icosahedral shape. 16,18,31,33,35,39,45,52
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what kind of cells get infected by HPV
undifferentiated proliferative basal cells which are capable of dividing
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what viral proteins are expressed at a low level
E1,E2,E6,E7
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what could E6 and E7 do
disturb the normal terminal differentiation by stimulating cellular proliferation and DNA synthesis
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where do L1&L2 accumulate
in the mature epithelial cells
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how can HPV infection result in latency and malignant transformations
through interactions of viral E6 and E7 proteins with p53 and pRB. E6 binds p53 and marks for destruction. E7 binds and inactivates a human tumour suppressor gene product, the retinoblastoma protein pRB
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What is the state associated with low risk HPV such as HPV6 and HPV 11
during the normal HPV life cycle, viral DNA is maintained episomally in the nucleus of the affected cell
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what are the genes of HPV 16
E1,E2,E4,E5,E6,E7 and L1,L2
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What is the sequence of invasion of the HPV
after initial binding to herapan sulfate proteoglycan and furin cleavage, the virus is transferred to a receptor on the cell surface. Virus enters the cell via an endocytic pathway and within 4h localises in the early endosome,. by 12h,
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continued
the virus uncoats within the late endosome and the viral genome complexed with L2 is released. the L2 genome complex traffics through the cytoplasm, perhaps via microtubules and enters the nucleus by 24 hrs. after nuclear entry the complex co localiz
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continued 2
with ND10 and RNA transcription begins
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what are the risk factors for HPV
number of sexual partners and weakened immune systems
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how is HPV detected
p16 and In-situ hybridisation
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what are the two vaccines for HPV and for what HPV in particular is each vaccine
Gardasil (HPV 6,11,16,18) Cervarix (16,18)
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why do HR HPV positive tumours respond better to multimodal therapies compared to HPV -ve tumours
the compromised pathways still retain some function. precedes of wild type p53 in combination with low levels of Bcl-2/bCL-xL and EGFR which are features of HPV +ve tumour in non smokers, may enhance this treatment advantage
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what is EBV and how is it transmitted
a type of herpes virus, transmitted by contact with saliva, sexual contact, blood transfusions and organ transplantation
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EBV belongs to what herpes subfamily? and what is it split into
gamma. split into lymphocryptovirus and rhadinovirus.
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what does EBV infect
B lymphocytes
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what does HIV do and what does it increase the risk of
weakens the immune system and makes the body less able to fight off other infections that cause cancer. HIV increases the risk kaposi sarcoma, lymphomas, also cancers of the cervix , anus, lung , liver and throat
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how is HIV transmitted
via blood and through sexual contact and share needles
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what other condition cases kaposi sarcoma
kaposi sarcoma associated herpes virus - known as human herpesvirus 8
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how is human herpes 8 spread
saliva but it can also be spread through organ or bone marrow transplantation (and blood transfusion )
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what is kaposi sarcoma and what are the 1st symptoms
rare type of cancer that affects the skin, mouth and occasionally the internal organs. symptoms: red, purple, brown patches, plaque or nodules on the skin
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give the differences between high risk and Low risk HPV
HIGH: encodes E6 products. binding and degradation of p53, specific PDZ- domain proteins . inhibition of apoptosis and of interferon response and of keratinocyte differentiation. bypass of growth arrest following DNA damage . telomerase activation
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low risk:
no E6 products , weaker binding (no degradation ) of p53, no binding of PDZ domain proteins. no activation of telomerase activation and no activation of c-myc activation. weaker inhibition of interferon response and normal growth arrest following DNA
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Card 2

Front

What kind of cancer does the high risk HPV cause? how does this virus spread

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cervical, anal, oropharyngeal, vaginal, vulvar, penile cancers. the virus spreads through direct sexual contact

Card 3

Front

how is HPV described ( as it target mucosa ...it is called ...) what kind of DNA does HPV have ?

Back

Preview of the front of card 3

Card 4

Front

What virus group does HPV belong to? what is HR HPV associated with - what carcinogens

Back

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Card 5

Front

what kind of cells get infected by HPV

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