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HPV
HPV infection and tumourigenesis
| Question | Answer |
|---|---|
| Overview | Infect a wide range of species Infect number of different tissue stypes Number of different groups - Alpha group causes mucosal and cutaneous lesions in humans and primates. Beta group cutaneous lesions in humans |
| Overview prt2. | 200 HPV types 40 infect anogenital region - most prevalent group of STIs after Chlamydia Incidence of HPV associated cancers higher in males however cervical cancer most prevalent of cancers between men and women (23,000 cases in UK) |
| Head and Neck Cancer | Oropharynx - 35% HPV positive, 90% HPV-16 Oral cavity - 25-40% HPV positive, 70% HPV-16 Larynx c- 25% HPV positive |
| Head and Neck Cancer Epidemiology | 650,000 new cases of head and neck cancer per year worldwide approx 50% mortality within 5 years of diagnosis tobacco/alcohol account for 75-80% of cases HPV-positive HNSCC different from HPV-negative Tend to be younger age group, treatment better |
| Recurrent respiratory papillomatosis | low risk anogenital types 6 and 11 benign disease, maligancy in 3-4% |
| Juvenile RRP | contracted through passage of birth canal lesions apparent in 1-4 years old larynx very rare requires surgery to clear airways (sometimes weekly) |
| High Risk HPV | Infection always precedes tumourigenesis persistent infection is a pre-requisite High risk HPV is the cause of cervical cancer 500,000 new cases a year worldwide |
| High Risk HPV | serotypes 16 and 18 - significantly higher chance of progression to cancer the longer infection persists Infections highest 16-25 year olds, symptoms appear years after initial infection |
| HPV-16 Genome: E6 E7 | Cell cycle control, apoptosis inhibiton, cell structuring and signalling (early genes) |
| E1 | Episomal replication (early/intermediate) |
| E2 | replicational and transcriptional modulation (early) |
| E4 | cell restructuring G2 arrest (intermediate) |
| E5 | Cell signalling immune modulation (intermediate) |
| L2 | Minor capsid (late) |
| L1 | Major capsid (late) |
| Life Cycle | Infects through cuts on skin, access basal layer of cells. HPV replicates within basal layer leading to persistence in dividing cells As dividing cells migrate towards surface of skin, virus changes gene expression. Early - intermediate - late |
| Life Cycle 2 | Leading to formation of viral capsids and virion assembly - infected cell reaches dead squamous layer, virus is released |
| Infection vs cancer | Infection - extrachromosomal circular episome, divides when cell divides. benign growth or wart Cancer - integration of HPV DNA into a host chromosome, deregulated expression of E6 and E7, interacts with cellular regulatory proteins - malignant tumour |
| Co-factors in progression (borderline risks) | early age of first sex high number of sexual partners poor hygiene |
| Co-factors in progression (borderline protective factors) | circumcision condom use |
| Co-factors in progression | genetic susceptibility viral factors viral integration |
| Co-factors in progression (invasive cancer) | oral contraceptives use IV drug use HIV + other STIs smoking |
| Detecting HPV | Pap smear Liquid based cytology, both non-specific and not very sensitive HPV RNA testing for E6 and E7 now available - much higher specificity and sensitivity |
Created by:
teemo616
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