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BMS 622 Exam 3 > Lecture 14: Papillomavirus, Adenovirus, Parvovirus - Chap 41, 42, 45 > Flashcards

Lecture 14: Papillomavirus, Adenovirus, Parvovirus - Chap 41, 42, 45 Flashcards

1
Q

Which virus is associated with warts and cervical cancer?

A

HPV (Human Papillomavirus)

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2
Q

What do HPV types 16 and 18 increase the risk of?

A

Cervical, anal, penile, and oropharyngeal cancers

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3
Q

How does HPV evade immune detection?

A

Hides from immune responses, allowing persistent infection

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4
Q

What cells does HPV primarily infect?

A

Epithelial cells of skin or mucous membranes

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5
Q

What are the key oncogenes in HPV that promote cell growth?

A

E6 and E7 proteins

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6
Q

How does HPV affect p53 and RB proteins?

A

Inactivates them to promote uncontrolled cell growth

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7
Q

What is the common symptom of HPV infection on the skin?

A

Benign warts

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8
Q

How is HPV commonly transmitted?

A

By direct or sexual contact, and fomites

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9
Q

Which method is used for HPV detection in clinical settings?

A

PCR genome analysis of cervical swabs

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10
Q

Which HPV types are targeted by available vaccines?

A

Types 6, 11, 16, 18, 31, 33, 45, 52, and 58

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11
Q

What virus is linked to Merkel cell carcinoma?

A

MCPyV (Merkel Cell Polyomavirus)

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12
Q

What disease does JCV cause in immunocompromised individuals?

A

Progressive multifocal leukoencephalopathy (PML)

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13
Q

How is JCV transmitted?

A

Inhalation or contact with contaminated water or saliva

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14
Q

What type of cells are affected in JCV-associated PML?

A

Astrocytes and oligodendrocytes

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15
Q

What is a distinguishing characteristic of PML lesions?

A

Demyelination with large abnormal astrocytes and oligodendrocytes

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16
Q

How is PML diagnosed in patients suspected of JCV infection?

A

PCR detection of viral DNA in cerebrospinal fluid and MRI/CT scans

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17
Q

What organ is primarily affected by BK virus in immunocompromised individuals?

A

Kidneys

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18
Q

How do polyomaviruses, such as BK virus, maintain persistent infection?

A

Establish latent infection in organs like kidneys and lungs

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19
Q

Which proteins do both HPV and polyomaviruses use to disrupt cell cycle regulation?

A

T antigen (in polyomaviruses) and E6/E7 proteins (in HPV)

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20
Q

What method is ineffective for polyomavirus control and treatment?

A

No effective mode of control is currently available

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21
Q

How does HPV tissue tropism vary by type?

A

Specific HPV types infect different tissues and determine disease manifestation

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22
Q

Which polyomavirus is commonly associated with kidney disease?

A

BK virus

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23
Q

What triggers reactivation of JCV and BK virus?

A

Immunocompromised state

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24
Q

Why are JCV infections usually asymptomatic in early life?

A

The virus remains latent and does not cause symptoms in healthy individuals

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25
Q

In which population are both HPV and polyomaviruses a significant health concern?

A

Immunocompromised individuals

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26
Q

What does CIN stand for in relation to HPV infection?

A

Cervical Intraepithelial Neoplasia

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27
Q

How do HPV infections typically resolve?

A

Slowly and often spontaneously due to immune response

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28
Q

What is the main transmission method for HPV laryngeal papillomas?

A

Passage through an infected birth canal (Types 6 and 11)

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29
Q

How is HPV distributed worldwide?

A

Ubiquitously, with no seasonal incidence

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30
Q

Why does JCV infection lead to progressive neurological symptoms?

A

Due to demyelination and damage to brain cells

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31
Q

Which two types of polyomaviruses are specifically noted for opportunistic disease?

A

JCV and BK virus

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32
Q

Why are warts common with HPV infection?

A

Caused by benign outgrowth of infected epithelial cells

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33
Q

What demographic factor increases the risk of BK virus-related kidney disease?

A

Immunosuppression (e.g., transplant patients)

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34
Q

What type of genome do papillomaviruses and polyomaviruses have?

A

DNA genome

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35
Q

How would you describe the capsid structure of papillomaviruses?

A

Small, naked capsid

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36
Q

What is the significance of a ‘naked capsid’ in virus structure?

A

Resistant to environmental stress, aids in transmission

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37
Q

Which proteins are key for HPV’s ability to manipulate the host cell cycle?

A

E6 and E7 proteins

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38
Q

What role does the T antigen play in polyomaviruses?

A

Inactivates p53 and RB to promote cell growth

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39
Q

How does the HPV genome influence its tissue tropism?

A

Specific HPV types target different epithelial tissues

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40
Q

Where does HPV persist in the body during infection?

A

Basal layer of skin or mucous membranes

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41
Q

What is the genome type of polyomaviruses like JCV and BK?

A

DNA genome

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42
Q

What is a key feature of the HPV genome in terms of immune evasion?

A

Remains hidden from immune system

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43
Q

How does JCV affect the brain in immunocompromised patients?

A

Causes demyelination by damaging brain cells

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44
Q

What is the structure of HPV genome?

A

Double-stranded circular DNA genome

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45
Q

What HPV protein binds origin and helps increase transcription?

A

E1 protein

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46
Q

Which HPV protein helps with the release of virions?

A

E4 protein

47
Q

Which protein is responsible for EGFR activation in HPV?

A

E5 protein

48
Q

What are the structural capsid proteins in HPV?

A

L1 and L2

49
Q

Describe the genome structure of adenovirus.

A

Linear double-stranded DNA

50
Q

What unique feature does adenovirus capsid have?

A

Icosahedral capsid with fibers at vertices

51
Q

What genome structure does parvovirus have?

A

Single-stranded linear DNA

52
Q

What key function does HPV’s E6 protein serve in oncogenesis?

A

Binds p53, activates telomerase, suppresses apoptosis

53
Q

How does E7 protein promote cancer in HPV?

A

Binds to p105RB, promoting cell cycle progression

54
Q

What proteins in polyomavirus help regulate early and late gene transcription?

A

Large T antigen

55
Q

Which polyomavirus protein is a major capsid and attachment protein?

A

VP1

56
Q

What is the main disease mechanism in parvovirus B19 infection?

A

Infects erythroid precursor cells, causing lytic infection

57
Q

What does CIN1 represent in HPV infection?

A

Mild changes affecting 1/3 of cervical layer

58
Q

Describe CIN2 in HPV infection.

A

Moderate changes affecting 2/3 of cervical layer

59
Q

What is CIN3 in HPV pathology?

A

Severe changes affecting full cervical layer, not yet cancer

60
Q

What is progressive multifocal leukoencephalopathy (PML)?

A

A JCV-caused demyelinating disease in immunocompromised individuals

61
Q

What condition can adenovirus cause in crowded environments like camps?

A

Pharyngoconjunctival fever

62
Q

How is HPV typically transmitted?

A

Direct and sexual contact, birth canal for types 6 and 11

63
Q

How is adenovirus transmitted?

A

Respiratory droplets, fecal-oral route, contaminated surfaces

64
Q

What age group is most at risk for parvovirus B19?

A

Children in elementary school

65
Q

Which demographic is at risk for severe B19 complications?

A

Non-immune pregnant women and those with chronic anemia

66
Q

Who is at risk for PML with JCV reactivation?

A

Immunocompromised patients

67
Q

What age group is often affected by adenovirus in crowded settings?

A

Children under 14

68
Q

What diagnostic test is commonly used for HPV?

A

PCR genome analysis

69
Q

How is PML diagnosed in suspected JCV infection?

A

PCR on cerebrospinal fluid, MRI or CT for lesions

70
Q

What diagnostic method is used for adenovirus typing?

A

PCR of respiratory or fecal samples

71
Q

How is parvovirus B19 infection confirmed?

A

PCR or IgM antibody test

72
Q

What vaccine protects against multiple HPV types?

A

Gardasil 9

73
Q

What HPV types are included in Gardasil 9?

A

Types 6, 11, 16, 18, 31, 33, 45, 52, 58

74
Q

Is there a vaccine for adenovirus?

A

Yes, for military use covering types 4 and 7

75
Q

How is parvovirus B19 infection typically controlled?

A

No specific treatment; managed with supportive care

76
Q

What type of immune response is crucial for clearing parvovirus B19?

A

Antibody response

77
Q

What is a control method for adenovirus in shared environments?

A

Good hygiene and disinfection of contaminated surfaces

78
Q

How would you describe the virus structure of Parvovirus?

A

naked icoshedsral capsid
single stranded (+ or - sense) dna genome

79
Q

What is the genome type of Papillomaviruses (HPV)?

A

Double-stranded circular DNA

80
Q

What structural proteins form the capsid of HPV?

A

L1 and L2 proteins

81
Q

How does HPV primarily achieve cell transformation?

A

Through E6 and E7 proteins binding to p53 and p105RB

82
Q

Describe the lifecycle of HPV in keratinocytes.

A

HPV infects basal cells, persists in basal layer, replicates in differentiating keratinocytes, releases virions in the outer layers

83
Q

What diseases are associated with high-risk HPV types like HPV-16 and HPV-18?

A

Cervical cancer, other anogenital cancers

84
Q

How does HPV evade the immune response?

A

Persistence in the basal layer, hiding from immune detection

85
Q

Describe the typical presentation of common warts caused by HPV.

A

Flesh-colored, scaly papules, often on hands and feet

86
Q

What is the main diagnostic test for identifying HPV infections?

A

PCR for HPV typing, Pap smear for cellular changes

87
Q

What vaccines are available for HPV prevention?

A

Gardasil (covers types 6, 11, 16, 18) and Gardasil 9 (covers 9 types)

88
Q

What is the structure of Adenovirus?

A

Non-enveloped, icosadeltahedral capsid with fibers

89
Q

What genome type is found in Adenoviruses?

A

Linear double-stranded DNA

90
Q

How do Adenovirus fibers contribute to infection?

A

Act as viral attachment proteins for host cell entry

91
Q

Describe the Adenovirus lifecycle.

A

1) Entry via receptor-mediated endocytosis, 2) DNA replication in nucleus, 3) Assembly and release by cell lysis

92
Q

Which infections are commonly caused by Adenoviruses?

A

Respiratory infections, conjunctivitis, gastroenteritis

93
Q

How does Adenovirus spread among hosts?

A

Aerosols, direct contact, fecal-oral route, and contaminated surfaces

94
Q

What age group is most commonly affected by Adenovirus infections?

A

Children under 14 years, especially in crowded areas

95
Q

Which diagnostic method is commonly used for Adenovirus infections?

A

PCR for viral DNA, cell culture for isolation

96
Q

How is Adenovirus controlled in high-risk settings like military camps?

A

Live oral vaccines for serotypes 4 and 7 are used for military personnel

97
Q

What type of genome does Parvovirus B19 have?

A

Single-stranded linear DNA

98
Q

Why does Parvovirus B19 need mitotically active cells for replication?

A

It lacks polymerase and relies on host cell division machinery

99
Q

Describe the lifecycle of Parvovirus B19.

A

1) Infects erythroid precursor cells, 2) Replicates in nucleus, 3) Released by cell lysis

100
Q

What condition is associated with Parvovirus B19 infection in children?

A

Erythema infectiosum (Fifth disease) with ‘slapped-cheek’ rash

101
Q

Which populations are at increased risk of severe disease with Parvovirus B19 infection?

A

Immunocompromised individuals, pregnant women, individuals with chronic anemia

102
Q

How is Parvovirus B19 primarily transmitted?

A

Respiratory droplets and oral secretions

103
Q

What are the clinical symptoms of Parvovirus B19 in adults?

A

Joint pain (arthralgia), fatigue, mild flu-like symptoms

104
Q

How can Parvovirus B19 infection be diagnosed?

A

Serology for IgM antibodies, PCR for viral DNA

105
Q

Why is quarantine not effective in preventing Parvovirus B19 spread?

A

Contagious period precedes symptom onset

106
Q

What is the biphasic nature of Parvovirus B19 disease?

A

Initial viremia with flu-like symptoms, followed by immune response causing rash and joint pain

107
Q

Describe the main prevention strategy for HPV transmission.

A

Vaccination, safe sexual practices, and screening programs

108
Q

What treatment is recommended for Parvovirus B19 in immunocompromised patients?

A

IV-IgG therapy to boost antibody response

109
Q

How does Parvovirus B19 infection affect pregnancy?

A

Risk of fetal anemia and hydrops fetalis

110
Q

What role do HPV E6 and E7 proteins play in oncogenesis?

A

E6 binds p53, preventing apoptosis; E7 binds p105RB, promoting cell cycle progression

111
Q

In what form does HPV persist in infected cells?

A

As episomal DNA in the nucleus of basal epithelial cells

112
Q

How does Adenovirus evade immune detection during infection?

A

Encodes proteins that inhibit MHC I presentation and TNF-α response

113
Q

What environmental factors make Adenovirus highly transmissible?

A

Resistance to drying, detergents, and gastrointestinal conditions

114
Q

How is Parvovirus B19’s lack of polymerase significant in its replication?

A

It must infect dividing cells to replicate, often affecting erythroid precursor cells

BMS 622 Exam 3 (12 decks)

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