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Micro unit 2 > L7 > Flashcards

L7 Flashcards

1
Q
  • Herpes Simplex Virus Type 1 (HSV-1)

- family

A

Alphaherpesviridae

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2
Q

*Herpes Simplex Virus Type 1 (HSV-1)

genome

A

dsDNA

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3
Q

*Herpes Simplex Virus Type 1 (HSV-1)

virion

A

Enveloped

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4
Q

*Herpes Simplex Virus Type 2 (HSV-2)

Family

A

Alphaherpesviridae

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5
Q

*Herpes Simplex Virus Type 2 (HSV-2)

genome

A

dsDNA

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6
Q

*Herpes Simplex Virus Type 2 (HSV-2)

virion

A

Enveloped

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7
Q

Cytomegalovirus family

A

Betaherpesviridae

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8
Q

Cytomegalovirus genome

A

dsDNA

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9
Q

Cytomegalovirus virion

A

Enveloped

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10
Q

Epstein-Barr virus

family

A

Gammaherpesviridae

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11
Q

Epstein-Barr virus

genome

A

dsDNA

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12
Q

Epstein-Barr virus

virion

A

Enveloped

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13
Q

Human Papillomavirus

family

A

Papillomaviridae

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14
Q

Human Papillomavirus

genome

A

dsDNA

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15
Q

Human Papillomavirus

virion

A

nonEnveloped

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16
Q

Alphaherpesvirus Variable

A

host range

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17
Q

Alphaherpesvirus Short

A

reproduction cycle

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18
Q

Alphaherpesvirus Rapid spread in

A

culture

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19
Q

Alphaherpesvirus Efficient destruction of

A

infected cells

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20
Q

Alphaherpesvirus Capacity to establish

A

latency in sensory ganglia

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21
Q

Alphaherpesvirus Infection

A 
HSV-1
Oral-oral, oral-genital
Nearly 2/3 adults are seropositive
HSV-2
Primarily genital-genital, oral-genital also possible
More prevalent with sexual activity
Approximately 1/5 adults are infected
Primarily infect epithelial cells in the skin or mucosa; mucosa are more susceptible
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22
Q

Alphaherpesvirus Incubation

A

HSV-1&2: 2 – 14 days, typically 4 – 5 days

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23
Q

Alphaherpesvirus Symptoms

A

Flu-like, includes localized lesions (virus spreads to neighboring cells primarily)
Only 1/3 show symptoms
Asymptomatic can still transmit
Last for 8 to 12 days

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24
Q

Alphaherpesvirus Latency

A

Stationary cells, genome circularizes and stays as an episome in the nucleus

Peripheral ganglia common site of latent infections
Triggers: sunburn, systemic infection,immune impairment,stress

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25
Q

Cell mediated immune response required

Alphaherpesvirus

A 
People unable to produce antibodies can still handle herpesvirus infections
T lymphocytes detect antigens presented by MHC class I or II proteins
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26
Q

Alphaherpesvirus Modulation of the immune response

A

Viral proteins bind antibodies and complement proteins

Counter effects of interferon

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27
Q

Alphaherpesvirus Prevention

A

Avoid contact (e.g., kissing, sex) during active herpes recurrence

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28
Q

Alphaherpesvirus treatment

A

Acyclovir can be used to limit virus replication

Will not eliminate latent infections

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29
Q

Betaherpesvirus

A

Restricted host range
Long reproductive cycle
Slow progression in cell culture

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30
Q

Betaherpesvirus Enlargement of

A

infected cells (cytomeglia)

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31
Q

Betaherpesvirus

A

Carrier cultures
Latent infection in a variety of tissues
Prototypical member: Cytomegalovirus (CMV)

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32
Q

Gammaherpesvirus key characteristics

A 
Restricted host range
Targets T & B lymphocytes
Lytic infections
Latency in lymphoid tissues
Prototypical member: Epstein-Barr virus (EBV)
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33
Q

Beta/gammaherpesvirus Disease (Cont.)

A

EBV associated carcinomas

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34
Q

Burkett’s lymphoma

Beta/gammaherpesvirus Disease (Cont.)

A

Most common childhood cancer in equatorial Africa
Tumor in jaw, eye socket, ovaries
In all cases, tumor cells have monoclonal EBV episome
Role of EBV still not understood
Spur B cell growth, mutations, or
Genes transform cells

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35
Q

Beta/gammaherpesvirus Disease

A

EBV associated carcinomas (Cont.)

Hodgkin’s lymphoma

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36
Q

Hodgkins lymphoma

A

Three types
NL – nodular sclerosing
MC – mixed cellularity
LD – lymphocyte depleted

EBV present in 60% to 90% of MC & LD tumors, 20% to 40% of NL tumors
Exact role of EBV unknown

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37
Q

Antiviral Host Response

Intrinsic

A

Block cell death

Inhibits apoptosis

38
Q

Antiviral Host Response

Innate

A

Decrease NK cell activity

Inhibit NK receptor activation

39
Q

Antiviral Host Response

Adaptive

A 
Decreased antigen presentation
Degrade MHC class I & II
Blocks MHC class II and T-cell receptor interactions
40
Q

Beta/gammaherpesvirus Disease CMV

A

Persist in hematopoietic progenitor cells and macrophages in vitro
Chronic persistent infection, not latency
Controlled by healthy, active immune system

41
Q

EBV

A

Persistence of genome in memory B cells

Virus proteins ensure B cell proliferation and EBV genome replication

42
Q

Infections are usually

Beta/gammaherpesvirus Treatment & Prevention

A

self limiting in immune competent individuals

43
Q

Beta/gammaherpesvirus Antiviral therapy

A

Recommended for disseminated CMV & EBV in immune compromised individuals
Ganciclovir, foscarnet, acyclovir:

Inhibits viral genome replication
Resistance can develop during therapy
Less effective treating EBV induced lymphoproliferation, genome replication not essential for viral gene expression

44
Q

Beta/gammaherpesvirus Antiviral therapy

A

Prophylactic or preemptive treatment, common in transplant patients

45
Q

Immunoprophylaxis

Beta/gammaherpesvirus

A

Passive transfer of antibodies for prevention of CMV infection
Transfer of EBV-specific T lymphocytes

46
Q

Human Papillomavirus family

A

Papillomaviridae

47
Q

Human Papillomavirus genome

A

circular dsDNA

48
Q

Human Papillomavirus virion

A

non-enveloped

49
Q

Human Papillomavirus Biology -Gain access through

A

abrasion of the skin

50
Q

Human Papillomavirus Biology -Establish infection in

A

basal layer

51
Q

Human Papillomavirus Biology -Cell polymerase required for

A

genome replication

52
Q

Human Papillomavirus Biology -Virus production in

A

differentiating cells

53
Q

Human Papillomavirus Biology -Non-lytic, virus released with

A

dead cell shedding

54
Q

Human Papillomavirus Disease infection

A 
direct skin-to-skin contact, fomites
Normal skin is a very strong barrier
Mucous membranes more susceptible
Virus enter body through abrasions
Virus is hardy to environmental stresses; allows transmission via fomites
55
Q

Human Papillomavirus Disease (Cont.) symptoms

A

Site of infection
Take months to manifest
Warts – raised or flat
~50% regress on their own in 2 years

56
Q

HPV disease Respiratory papillomatosis

A

Rare complication
Respired virus
Can be lethal

57
Q

HPV diseas Oncogenesis – cervical cancer

A

HPV requires actively replicating cells to replicate and produce progeny
E7 blocks retinoblastoma (Rb) protein – continued cell proliferation
E6 blocks the p53 tumor suppressor pathway
Actual path to cancer unknown
Viral transformation
Cell proliferation leading to cancerous mutation

58
Q

HPV Most treatments

A

ablative

Liquid nitrogen, surgical excision, laser, caustic chemicals
Treatments may have to be repeated

59
Q

HPV No proof that condoms

A

reduce risk

60
Q

HPV Vaccination

A

Gardasil (Merck) – protects against HPV-6, 11, 16, and 18

61
Q

Antiviral Therapy Antivirals block

A

specific steps in the virus life cycle

62
Q

Antiviral therapy Must be active against

A

virus replications, but not normal cellular function to reduce toxicity

63
Q

Antiviral therapy Exploit

A

structural, functional, and genomic information to identify targets

64
Q

Virus resistance to

A

antiviral drugs is common and requires continued development efforts

65
Q

Antivirals preventing entry Enfuvirtide – HIV

A

Blocks refolding of gp41, inhibits membrane fusion

66
Q

Antivirals preventing entry:

Amantadine & rimantadine – influenza

A

Blocks influenzaion channel (M2) preventing nucleocapsid releaseat the end of the cellentry process

67
Q

Nucleoside analogs →

A

chain terminators

68
Q

Acyclovir (treatment of herpesvirus infections)

A

First antiviral approved for clinical use
Key hurdles for antiviral success
Specificity depends on virus thymadine kinase (TK)
Bioavailability
Most effectiveagainst HSV-1& HSV-2, lesseffective for EBV & VZV,even less effective for CMV

69
Q

Acyclovir

A

like nucleoside inhibitors for herpesvirus infections

70
Q

Ganciclovir

A

effective against CMV, more toxic due to interference with cellular kinases

71
Q

Valganciclovir

A

activity similar to acyclovir, improved oral bioavailability

72
Q

Foscarnet (herpesvirus treatment)

A

Prevents viral polymerase activity
IV administration
Toxic

73
Q

Antivirals preventing genome replication

A

Nucleoside inhibitor of RNA viruses

74
Q

Antivirals preventing genome replication ribavirin (many mechanisms)

A

Triphosphate form inhibits polymerases
Monophosphate form inhibits inosine monophosphate dehydrogenase lowering GTP in cell
Impairs capping of mRNA

75
Q

Antivirals Preventing Viral Proteases

Maturation of progeny viruses often requires

A

cleavage of virus polypeptide

76
Q

Antivirals Preventing Viral Proteases Immature progeny are not

A

infectious

77
Q

Antivirals Preventing Viral Proteases - Example: ritonavir (treatment of HIV)

A

Blocks cleavage of Gag-Pol polypeptide
“Boosts” activity of other protease inhibitors because it also blocks the action of cellular proteases that act on other viral protease inhibitors

78
Q

Antiviral Challenges - Bioavailability

A

Absorption into the body
Transport to site of viral infection
Intake by cell
Therapeutic window (half-life)

79
Q

Antiviral Challenges - Specificity

A

Targets the virus activities exclusivelyor with great preference

80
Q

Antiviral Challenges - Toxicity

A

Low impact on patient

81
Q

Natural antivirals Interferons

A

Fortuitous discovery by Isaacs & Lindenmann
Noted that cultured cells infected with one virus were resistant to infection by a second virus
Effect was transferable to uninfected cells
Identified proteins responsible for the effect

82
Q

Interferons Mechanism of action

A

not well understood

More effective against RNA viruses than DNA viruses

83
Q

Vaccines Term vaccination started

A

with Dr. Edward Jenner in 1801 with a publication of his findings for smallpox vaccination

84
Q

Vaccines founding

A

Milkmaids who had cowpox, could not under variolation (skin inoculation with smallpox)
Performed experiment in 1796 on young man demonstrating cowpox infection (vaccine virus) was protective against smallpox infection
Vaccination became the preferred method because it was much less severe

85
Q

Active immunization –

A

administering all or part of a pathogenic agent to induce antibodies or cell-mediated immunity

86
Q

Passive immunization –

A

administration of exogenously produced antibodies

87
Q

Vaccines - Two forms:

A

live, attenuated; killed

88
Q

Vaccines Reversion –

A

possible complication with live, attenuated vaccines

89
Q

Vaccine-acquired paralytic poliomyelitis (VAPP)

A

1:1,000,000 to 3,000,000 of vaccinations
Local epidemics where used
Because rate of polio is so low in the US, only the killed vaccine is used

90
Q

Vaccines utilizing B cell and T cell immunity including

A

secretory IgA

Influenza, polio, oral typhoid

91
Q

Vaccine considerations

A

Age
Young children & the elderly
Weaker immune systems
May not be able to respond to live, attenuated vaccines

Special populations
Immunocompromised persons may have greater need of vaccination or be counter-indicated for vaccination
Complications – for example, smallpox vaccine for persons with eczema

Micro unit 2 (12 decks)

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