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L2 HPV Flashcards

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1
Q

What is the structure of HPV, and how does it differ from enveloped viruses?

A

HPV is a small, non-enveloped virus with a circular dsDNA genome and icosahedral capsid, making it more environmentally stable than enveloped viruses.

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2
Q

What proteins form the HPV capsid, and how is it structured?

A

The HPV capsid consists of 72 pentamers made of L1 proteins, forming an icosahedral shell; L2 proteins assist genome packaging.

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3
Q

What type of cells does HPV primarily infect?

A

HPV infects squamous epithelial cells, especially in the anogenital region and oropharynx.

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4
Q

What is the lifecycle of HPV from attachment to release?

A

The lifecycle includes attachment, entry, uncoating, early gene expression (E1–E7), genome replication, late gene expression (L1/L2), assembly, and release.

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5
Q

What marks the initiation of HPV replication in host cells?

A

Attachment to basal epithelial cells via heparan sulfate proteoglycans initiates replication.

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6
Q

What is the function of E1 and E2 proteins in the HPV lifecycle?

A

E1 and E2 are essential for viral genome replication; E1 is a helicase, and E2 helps recruit host polymerases.

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7
Q

What is the role of the E4 protein in HPV infection?

A

E4 assists in genome amplification and aids viral egress by disrupting cytoskeletal structures.

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8
Q

What role does E5 play in immune evasion by HPV?

A

E5 downregulates MHC I expression, helping the virus evade cytotoxic T-cell recognition.

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9
Q

What is the role of E6 and E7 in HPV pathogenesis?

A

E6 binds p53 to promote degradation, and E7 inactivates pRb, both driving cell cycle progression.

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10
Q

How do E6 and E7 contribute to oncogenesis and genomic instability?

A

By inactivating tumor suppressors, E6 and E7 induce genomic instability and unregulated proliferation.

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11
Q

What mechanisms do E6 and E7 use to promote unregulated cell growth?

A

E6 inhibits apoptosis via p53 degradation; E7 promotes S-phase entry by binding and degrading pRb.

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12
Q

How does HPV maintain its genome during latency?

A

HPV persists as an episome in basal cells with minimal gene expression during latency.

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13
Q

How does persistent HPV infection lead to cancer?

A

Persistent infection, especially with high-risk types, may lead to DNA integration, promoting oncogenesis.

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14
Q

What happens when the HPV genome integrates into the host genome?

A

Integration disrupts viral E2 control, leading to upregulation of E6 and E7 and increased cancer risk.

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15
Q

What does the long control region (LCR) in the HPV genome do?

A

The LCR contains promoters, enhancers, and origin of replication, regulating viral gene expression.

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16
Q

What characterizes low-risk vs. high-risk HPV types?

A

Low-risk types (e.g., 6, 11) cause warts; high-risk types (e.g., 16, 18) are associated with cancer.

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17
Q

Which HPV types are considered high-risk and why?

A

High-risk types are carcinogenic because they persist longer and produce oncogenic proteins.

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18
Q

Which HPV types are responsible for most cervical cancers?

A

HPV 16, 18, and 33 account for about 75% of cervical cancer cases.

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19
Q

What types of cancers can high-risk HPV cause?

A

Besides cervical cancer, high-risk HPV causes anal, penile, vulvar, vaginal, and oropharyngeal cancers.

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20
Q

What benign conditions are caused by low-risk HPV?

A

Low-risk types like 6 and 11 cause genital warts and respiratory papillomatosis.

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21
Q

What clinical manifestations are associated with HPV?

A

HPV can cause asymptomatic infections, genital warts, or precancerous lesions.

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22
Q

What are high-grade squamous intraepithelial lesions (HSIL)?

A

HSIL are advanced precancerous lesions requiring close follow-up or treatment.

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23
Q

What is cervical intraepithelial neoplasia grade 3 (CIN3) and how long can it persist?

A

CIN3 is severe dysplasia that may persist up to 10 years and progress if untreated.

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24
Q

What type of lesions can high-risk HPV cause?

A

High-risk types can cause dysplasia, carcinoma in situ, and invasive cancers.

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25
What is dysplasia and how is it linked to HPV?
Dysplasia is abnormal epithelial growth often caused by persistent HPV infection.
26
What changes occur during the progression from dysplasia to cervical cancer?
Dysplasia may evolve into carcinoma in situ and invasive cancer over time.
27
How does HPV lead to invasive cancer?
Oncogenic types persist and integrate into the genome, disrupting regulation.
28
What cancers besides cervical are linked to HPV?
HPV is linked to anal, vulvar, vaginal, penile, and oropharyngeal cancers.
29
What is the relationship between HPV and anal, penile, vulvar, and oropharyngeal cancers?
HPV causes most anal and oropharyngeal cancers and is implicated in others.
30
How does HPV affect men?
Men can develop warts and HPV-associated anal and throat cancers.
31
What is the impact of HPV on pregnancy?
HPV is not known to affect pregnancy outcomes significantly but awareness is important.
32
What is the global incidence of cervical cancer?
Over 600,000 cervical cancer cases are reported annually worldwide.
33
What percentage of cervical cancer cases are attributed to HPV?
High-risk HPV is found in over 99% of cervical cancers.
34
What are the co-factors that increase the risk of HPV-related cervical cancer?
Smoking, immunosuppression, hormonal factors, and coinfections increase risk.
35
What lifestyle factors increase cervical cancer risk alongside HPV?
Early sexual activity, many partners, smoking, and oral contraceptive use are risk factors.
36
What environmental and personal factors influence HPV persistence and progression?
Immune suppression, smoking, and multiple infections worsen HPV outcomes.
37
What factors affect an individual's response to HPV vaccination?
Immune status, health conditions, and awareness can impact vaccine response.
38
What psychological effects can an HPV diagnosis have?
Diagnosis may cause anxiety, stigma, and fear about cancer or fertility.
39
How does HPV transmission occur, and how does it vary with sexual behavior?
HPV spreads via skin-to-skin and mucosal contact; risk increases with exposure.
40
What demographics are at highest risk for HPV acquisition?
Sexually active adolescents and young adults have highest acquisition rates.
41
What are the main challenges in HPV epidemiology and transmission data?
Limited data on per-contact transmission and variable behavior complicates studies.
42
How does HPV evade the immune system?
HPV evades detection by limiting antigen presentation and gene expression.
43
What is the role of the immune system in clearing HPV infections?
Most HPV infections are cleared by the immune system within 1–2 years.
44
How is HPV infection typically manifested in young adults?
Infections are usually asymptomatic and self-limiting in young people.
45
What are viral loads and how do they relate to HPV severity?
Viral loads measure HPV DNA quantity and correlate with disease progression.
46
How does HPV affect cancer treatment outcomes?
HPV-positive cancers may respond differently to therapy due to unique biology.
47
What is the purpose of HPV screening programs?
Screening detects precancerous changes to enable early intervention.
48
What does a positive HR-HPV test indicate?
A positive HR-HPV test shows infection with types that can cause cancer.
49
What are the benefits of early HPV detection?
Early detection allows treatment before progression to cancer.
50
What is a recommended frequency for cervical cancer screening?
Screening is recommended every 3–5 years for women aged 25–64, depending on risk.
51
How effective are HPV vaccines?
Vaccines are over 90% effective at preventing infections with target types.
52
How do HPV vaccines work?
Vaccines use virus-like particles to induce neutralizing antibody responses.
53
What is the impact of HPV vaccination on cervical lesion rates?
Vaccination leads to major declines in precancerous cervical lesions.
54
What percentage efficacy do vaccines show for high-risk HPV types?
Most show >90% efficacy against HPV 16/18; cross-protection may occur.
55
What is the ideal age for HPV vaccination and why?
Preteens (ages 9–14) are vaccinated before sexual exposure for maximum protection.
56
What are the goals of HPV vaccination programs?
The goal is to reduce HPV infection and associated cancers.
57
What is the overall aim of global HPV vaccination efforts?
Global vaccination aims to reduce disparities and cancer rates worldwide.
58
What is the expected impact of routine HPV vaccination?
Widespread vaccination decreases infections and cancer incidence long-term.
59
What is the projected effect of implementing HPV primary screening in the UK?
HPV primary screening could reduce UK cervical cancer rates by 19% by 2032.
60
How does HPV vaccination affect future generations?
Immunized individuals reduce virus circulation, protecting unvaccinated people.
61
What is herd immunity and how does it relate to HPV?
Herd immunity helps reduce population-level transmission of HPV.
62
What are the primary preventive strategies against HPV-related diseases?
Key strategies include vaccination, screening, and sexual health education.
63
What personal steps can help prevent HPV infection?
Vaccination, condom use, and routine screening lower personal risk.
64
What practical steps improve adherence to cervical screening?
Reminders, accessibility, and patient education improve screening rates.
65
What are the public health benefits of cervical screening programs?
Screening reduces incidence and mortality by detecting early disease.
66
What preventative policies help reduce cervical cancer incidence?
Vaccination and organized screening programs prevent cervical cancer.
67
What is one major challenge to achieving global HPV prevention?
Misinformation, stigma, and access barriers challenge prevention.
68
Which countries face the greatest disparities in cervical cancer outcomes?
Low- and middle-income countries face greater mortality due to limited screening.
69
What are the key components of successful HPV public health strategies?
Public health relies on vaccination, education, and screening access.
70
What role do public health campaigns play in HPV prevention?
Campaigns raise awareness, fight misinformation, and encourage screening.
71
What is the role of school-based HPV vaccination programs?
School-based programs reach adolescents before sexual debut.
72
What role do community outreach programs have in HPV prevention?
Outreach improves access to vaccines and screenings in vulnerable communities.
73
What role do community health workers play in combating HPV?
Health workers educate, support, and link people to services.
74
What role does community education play in HPV awareness?
Education increases knowledge and supports behavior change.
75
How can health education reduce HPV transmission and stigma?
Accurate information helps dispel myths and encourage prevention.
76
What educational topics about HPV are important for adolescents?
Adolescents need education on HPV risks and the value of vaccination.
77
What are effective strategies to improve HPV vaccination rates?
Outreach, reminders, and accessible services improve vaccine uptake.
78
What educational approach can reduce HPV misinformation?
Addressing myths through trusted education improves vaccination.
79
What health education strategies enhance HPV knowledge and behavior change?
Tailored education fosters informed decisions and behavior change.
80
What is the role of social media in HPV vaccine campaigns?
Social media spreads accurate information and counters vaccine myths.
81
What are some common misconceptions about HPV?
Misconceptions include that HPV only affects women or only causes cervical cancer.
82
What is the significance of HPV-related public health surveillance?
Surveillance tracks HPV types, vaccine impact, and informs policies.
83
What is the role of health systems in managing HPV burden?
Health systems implement vaccination, screening, and education efforts.
84
What successful approach reduces HPV-related health disparities?
Community-targeted efforts reduce disparities in access and outcomes.
85
What steps are involved in the HPV replication cycle?
Replication includes attachment, entry, uncoating, replication, assembly, and release.
86
What is the significance of HPV's non-enveloped nature?
Non-enveloped HPV is more resistant to drying and disinfection.
87
How does HPV achieve persistent infection?
Episomal latency with limited expression enables long-term persistence.
88
What is the impact of HPV vaccination on public health overall?
Vaccination reduces HPV-related disease burden at population scale.
89
How can individuals help reduce HPV transmission at a population level?
Vaccinated individuals contribute to lower community transmission.
90
What are the implications of persistent HPV for reproductive health?
Persistent infection can impair reproductive health and increase cancer risk
91

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