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Virology > Virology Pathogenesis and Lab Diagnosis > Flashcards

Virology Pathogenesis and Lab Diagnosis Flashcards

1
Q

What is pathogenesis?

A

Disease process occurring as result of interaction of host and infectious organism.

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2
Q

What factors the nature of a disease? Severity of a disease?

A

Tropism determines nature, while viral and host factors determine severity.

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3
Q

What are the two types of viral infections?

A
  1. Permissive: Productive infectious virions produced

2. Nonpermissive/Abortive: Virus cannot attach and enter. May enter but infection does not result

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4
Q

What are the 3 types of permissive infection?

A
  1. Lytic (acute)
  2. Persistent (chronic, latent, recurrent, transforming)
  3. Slow
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5
Q

What happens in abortive infections?

A

Mature virions are not produced. Does not proceed through all steps of replication cycle.

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6
Q

What are acute/lytic infections?

A

Rapid onset followed by clearance. Often self-limiting

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7
Q

What is persistent infection?

A

Linger and not readily cleared by immune system. Host cell survives, harboring the virus. Onset may be acute.

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8
Q

What is chronic infection?

A

Can be lifelong; continuous producting and shedding of virions. e.g. Hep B and Hep C

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9
Q

What is latent infection?

A

Intermittent viral replication and shedding with long periods of dormancy when virus is not replicating.

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10
Q

How does the virus spread throughout body upon reactivation?

A

Viruses spread from sensory ganglion down axon to periphery where virus replicates in local epithelial cells, where lesion forms.

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11
Q

What is an example of latent infection and its triggers?

A

Herpes simplex and varicella-zoster activated by UV light, stress, fever, nerve injury, or immunosuppression.

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12
Q

What is recurrent infection?

A

Virus cleared by immune system but returns short time later. (2 infections within 6 mos or 3 infection within 1 yr)

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13
Q

What is transforming infection?

A

Virus cause loss of control by cell, usu overexpression of growth factors: uncontrolled growth and division. Could lead to tumor formation.

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14
Q

What is slow infection?

A

Poorly understood. Require an accumulation of viral material that often takes many years.

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15
Q

What are 5 cytopathic effects (cell killed)?

A
  1. Inclusion bodies: accumulation of virions
  2. Synctium formation: fusion with neighbor cells
  3. Stopping cellular processes: Block protein/DNA synthesis
  4. Lysis: Loss of membrane integrity
  5. Apoptosis: programmed cell death
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16
Q

Which of the cytopathic effects is a “quiet” process that does not illicit inflammatory response?

A

Apoptosis: mitochondria cease to function and cell destroys own DNA.

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17
Q

What are 3 non-cytopathic effects (damage without killing the cell)?

A
  1. Altered shape: Cells no longer attach to each other and become rounded.
  2. Detachment from substrate: Alteration of shape & disruption of cytoskeletal matrix.
  3. Transformation: Changes of growth
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18
Q

What factors resulting from transformation may contribute to tumor/cancer development?

A

Loss of contact inhibition and decreased requirement for growth factors.

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19
Q

What are the basic steps in viral pathogenesis?

A
  1. Entry into host
  2. Immune evasion
  3. Entry into cells and primary replication
  4. Spread within host
  5. Cell injury and clinical illness
  6. Shedding
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20
Q

What are the two most common points of entry for viruses? Other portals of entry?

A

Most common: respiratory tract and GI tract

Others: conjunctiva, urogenital tract, and areas of injury or penetration.

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21
Q

What is tissue tropism?

A

For establishment of viral infection, must be in limited range of permissive cells to be infected.

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22
Q

What is immune evasion?

A

Mechanism to avoid detection and destruction. May involve alterations to virions or manipulation of host cell components.

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23
Q

What are 4 mechanisms of immune evasion?

A
  1. Inhibiting antigen presentation
  2. Antigenic variation
  3. Molecular mimicry
  4. Immune privileged sites
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24
Q

How does detection avoidance by inhibiting antigen presentation work?

A

Expression of MHC class I molecules are down regulated so host cells cannot present the viral antigens to T cells to activate specific immune response.

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25
Q

What is antigenic variation?

A

Viruses change or remove surface proteins so antibodies will no longer recognize the virus.

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26
Q

What is molecular mimicry?

A

Viruses express a protein on its surface very similar to host protein.

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27
Q

What is immune privileged sites?

A

Points of entry for some viruses with little immune protection e.g. eye or brain

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28
Q

What are 4 mechanisms of viral spread?

A
  1. Local spread: epithelial surfaces
  2. Subepithelial invasion and lymphatic spread
  3. Viremia: virus in blood
  4. Teratogenic: fetus infection
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29
Q

What is local spread of virus?

A

Movement of fluid and mucus in respiratory tract enables spread to surrounding epithelial cells near site of entry e.g. influenza virus. May have short incubation period unless basal layer is infected e.g. papillomavirus

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30
Q

What is subepithelial invasion and lymphatic spread?

A

Virus traverses epithelium into lymphatic capillary and virus enters a lymph node where it can either be engulfed by macrophage or escape into blood stream.

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31
Q

What is viremia?

A

Most effective vehicle for spread of virus: bloodstream. Dissemination beyond primary site and systemic infection involving multiple organs

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32
Q

What are teratogenic organisms?

A

Cross the placenta and infect the fetus. e.g. TORCH organism

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33
Q

What are TORCH organisms?

A 
T- Toxoplasmosis
O- other (syphilis, HBV, coxsackie virus, EBV, VZV, and human parvovirus)
R- Rubella
C- Cytomegalovirus
H- Herpes Simplex Virus
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34
Q

What is shedding?

A

Release of virus into the environment, not to be confused with spread of disease.

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35
Q

What are the 3 critical processes of a host reaction to viral infection?

A
  1. Recognition (of the pathogen)
  2. Amplification (of the immune response)
  3. Control (of the infection)
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36
Q

What are innate (nonspecific) defenses?

A
  1. Interferons & Cytokines
  2. Complement (alternative & lectin pathways)
  3. Natural Killer cells (NK cells)
  4. Phagocytes (macrophages, neutrophils)
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37
Q

What are adaptive (specific) defenses?

A
  1. B cell activation (antibody production)
  2. T-helper cells (Th cells)
  3. Cytotoxic T cells (CTL cells)
  4. Memory cells
  5. Complement (classical pathway)
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38
Q

What are the 3 important steps that follow in response to viral infection?

A
  1. Destruction of infected cells
  2. Production of interferon
  3. Neutralization of viruses
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39
Q

Where are interferons produced and what triggers their production?

A

Produced by host cells and triggered by the presence of dsRNA (dsRNA & ssRNA viruses).

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40
Q

How do interferons work?

A

Do not directly kill the virus, but stimulate natural viral defense mechanism. Specific to host but not on virus

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41
Q

What are the 3 types of interferons and where are they secreted from?

A

1&2. IFN-alpha & IFN-beta: (cytokines) secreted by cells that are infected BY the virus.
3. IFN-gamma: (immune interferon bc it modulates immune response) secreted by variety of cells of immune system.

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42
Q

How does helper T cells work?

A

Activates B cells to divide and differentiate into antibody-secreting plasma cells.

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43
Q

How do antibodies function?

A

Produced to specific viral antigens, functions to physically neutralize virus infectivity by binding to virion and preventing it from binding to host cell and gaining entry.

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44
Q

What are the 6 approaches to prevention and control of viral disease?

A
  1. Quarantine
  2. Hygiene & sanitation
  3. Vector control (mosquitos)
  4. Change of lifestyle
  5. Immunization
  6. Antiviral chemotherapy
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45
Q

What is quarantine?

A

The segregation of EXPOSED but STILL HEALTHY individuals.

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46
Q

What are the two types of immunization?

A

Passive and Active immunization

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47
Q

What is passive immunization?

A

Administration of ANTIBODY, used as short-term protection (antibodies quickly degrade). E.g. Toxin/venom, needlestick injury, varicella exposure during birth, rabies.

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48
Q

What is active immunization?

A

Administration of an ANTIGEN (vaccine) to induce an immune response.

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49
Q

What is herd immunity vs. individual immunization?

A

Herd immunity prevents spread of viral disease AMONG individuals, individual immunization prevents spread of viral disease INSIDE a host.

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50
Q

What is a vaccine?

A

Any preparation intended for active immunological prophylaxis.

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51
Q

What is the difference btwn live attenuated and inactivated vaccines?

A

Live viruses are non-virulent organisms that possess growth characteristic that prevents wild-type, disease causing replication.
Inactivated include killed organisms or just parts of the organisms.

52
Q

How are live attenuated vaccines generated?

A

Direct genetic manipulation or by some type of selective pressure e.g. temp.

53
Q

What is the advantage of live attenuated vaccines?

A
  1. Cells are alive, so organism can multiply & emulate actual infection (virtually identical)–> stronger immunological response.
  2. Can induce humoral & cell-mediated protection.
  3. Usu effective w one dose
54
Q

What are the drawbacks of live attenuated vaccines?

A
  1. Cells are alive and multiplies, cannot give to immunocompromised individuals.
  2. May cause inflammatory response (revert to pathogenic wild-type strain)
  3. Antibodies can eliminate the organism–> reduced immunity
  4. Fragile: killed by heat and light
55
Q

What are 6 examples of live viral vaccines?

A

Influenza (intranasal), measles, mumps, rubella, varicella, adenovirus

56
Q

How are viruses inactivated for vaccine use?

A

Inactivated by heat or chemical treatment (formalin or formaldehyde)

57
Q

What is the advantage of using inactivated vaccines?

A

Can be given to immunocompromised individuals

58
Q

What are the drawbacks of using inactivated vaccines?

A

Because organism is dead or fractionated, more antigen required (multiple doses or boosters)

59
Q

What is a killed whole cell vaccine?

A

A vaccine that uses dead bacteria or viruses e.g. viral: rabies, hepatitis A

60
Q

What are two types of fractional vaccine?

A
  1. Protein-based vaccine in which only part of the organism are used
  2. Polysaccharide-based vaccine: only bacterial, no viral
61
Q

What are the two types of protein-based fractional vaccines?

A
  1. Subunit: single or multiple antigenic proteins, usu surface protein e.g. influenza
  2. Toxoid: Inactivated toxin (no viral vaccines)
62
Q

What is recombinant/hybrid vaccine?

A

Genetically engineered: insert vaccine antigen in an organism that is not pathogenic to humans (yeast, virus, bacteria).

63
Q

What is the objective of hybrid virus?

A

To produce safe virus that will express and present viral proteins to the immune system e.g. viral HBV and HPV

64
Q

What is an example of a recombinant-live attenuated viral vaccine?

A

Rotavirus

65
Q

What is an example of an inactivated fractional viral vaccine?

A

Influenza (shot)

66
Q

What is an example of recombinant-fractional viral vaccine?

A

Hep B

67
Q

What is an example of a hybrid viral vaccine?

A

Human papilloma Virus (human/bovine)

68
Q

What is an example of an inactivated whole organism viral vaccine?

A

Polio

69
Q

What is the basic strategy of antiviral chemotherapy? Why is this problematic?

A

Inhibit viral replication, problematic due to viruses’ intracellular location and parasitic characteristic.

70
Q

All current antivirals are __________.

A

Virustatic (inhibit growth and development, not destroy)

71
Q

To be a successful antiviral agent, the drug must have these 3 characteristics.

A
  1. Target viral function/structure unique to virus (host structure less susceptible.)
  2. Interfere with cellular function to inhibit replication
  3. Kill only virus-infected cells
72
Q

What are the limitations of antiviral drugs?

A

Number of antiviral drugs very small, and its activity is limited to only a specific family of viruses.

73
Q

What the 3 reasons for antiviral limitations?

A
  1. Difficulty in obtaining selective toxicity
  2. Drugs are ineffective
  3. Emergence of drug-resistant strains
74
Q

What is selective toxicity and why is it so difficult to obtain?

A

Ability to target processes specific to the virus, but difficult to obtain bc viral replication is so intimately tied to normal cell activities.

75
Q

The most selective drugs are activated by what aspect of the virus?

A

Virus-encoded product within the infected cell.

76
Q

Give 2 reasons why antiviral drugs are ineffective.

A
  1. Many cycles of viral replication and virus has spread in the body even before the symptoms become noticeable.
  2. Some viruses become latent.
77
Q

What accounts for the emergence of drug-resistant strains?

A

Rapid mutations

78
Q

What is IFN-alpha, how is it taken, and how does it work?

A

It is the only interferon used in antiviral therapy. Taken by injection. Do not act directly on the virus, but induce genes in host cells to produce proteins for viral replication interference.

79
Q

What are the 2 forms of IFN-alpha currently in use for antiviral therapy?

A
  1. IFN-alpha 2a (HepC, AIDS-related Kaposi’s Sarcoma)

2. IFN-alpha 2b (Chronic Hep B or Hep C)

80
Q

What are “pegylated forms” of IFN-alpha?

A

Polyethylene glycol added to IFN-alpha: increase 1/2 life (protection from proteases).
Less required injections and greater patient compliance.

81
Q

What are the two forms of pegylated INF-alpha currently in use?

A
  1. Pegintereferon-alpha 2a: Hep C

2. Pegintereferon-alpha 2b: Chronic Hep C

82
Q

What is the only monoclonal antibody therapy approved for viral infection (passive)? What is it used to treat?

A

Palivizumab. Used to treat RSV (respiratory synctial virus.

83
Q

What are nucleoside/nucleotide Inhibitors of viral DNA polymerase?

A

Class of antiviral drugs that include nucleoside & nucleotide analogs with modifications to the base and/or sugar.

84
Q

How do nucleoside/nucleotide inhibitors of viral DNA polymerase function?

A

Work as antimetabolites. Similar to natural nucleotides, it’s incorporated into growing DNA strands. BUT lacks 3’ -OH group so that next deoxynucleotide cannot form 5’-3’ phosphodiester bond to extend chain–> strand termination

85
Q

Why are drugs in the nucleoside/nucleotide inhibitor class considered “prodrugs”?

A

Drug must be activated by phosphorylation (by host or virus’ kinase enzyme).

86
Q

How does nucleoside/nucleotide inhibitor class show selective toxicitiy?

A

Selectively inhibit by binding more strongly to the viral replication enzyme than host enzyme. And it is more prevalent in infected cells bc it displays rapid DNA synthesis.

87
Q

Majority of the nucleoside/nucleotide inhibitors are 1.________(nucleoside or nucleotide). But 2.____ is the only 3._____ inhibitor.

A
  1. Nucleoside
  2. Cidofovir
  3. Nucleotide
88
Q

Name 9 nucleoside inhibitors.

A

Acyclovir, Adelfovir, Ganciclovir, Famciclovir, Penciclovir, Ribavirin, Trifluridine, Valacyclovir, and Valganciclovir

89
Q

What is Acyclovir used to treat?

A

Herpes Simplex Virus (HSV): genitalis, labialis, encephalitis, keratitis, belphritis
VZV: chicken pox, herpes zoster

90
Q

What is Adefovir used to treat?

A

Chronic HBV (Hep B)

91
Q

What is Ganciclovir used to treat?

A

CMV in AIDS

Propylaxis for BMT and organ transplant

92
Q

What is Famciclovir used to treat?

A

Herpes zoster

93
Q

What is Penciclovir used to treat?

A

Herpes labialis

94
Q

What is Ribavirin used to treat?

A

RSV and Hep C

95
Q

What is Trifluridine used to treat?

A

HSV keratitis and HSV keratoconjunctivitis

96
Q

What is Valacyclovir used to treat?

A

HSV genitalis and labialis

VZV herpes zoster

97
Q

What is Valganciclovir used to treat?

A

CMV retinitis

98
Q

What is Cidofovir used to treat?

A

ONLY nucleotide inhibitor, treats AIDS-related CMV retinitis

99
Q

What are non-nucleoside inhibitors of viral DNA polymerase? How do they work?

A

Analogs of pyrophosphate. Selectively inhibit DNA polymerases by binding to pyrophosphate-binding site (rather than substrate-binding) of DNA polymerase wo requiring further modification.

100
Q

How do non-nucleoside inhibitors work specifically?

A

After binding, blocks the cleavage of pyrophosphate moiety from deoxynucleotide triphosphates. Halts DNA chain.

101
Q

What is an example of a non-nucleoside inhibitor and what is it used to treat?

A

Foscarnet. Treats AIDS-related CMV

102
Q

What is the objective of nucleoside/nucleotide reverse transcriptase inhibitors (NRTI/NtRTI)?

A

Designed to inhibit reverse transcriptase enzyme that makes DNA out of RNA.

103
Q

What are NRTI/NtRTI?

A

Also prodrugs and analogs of naturally occurring deoxynucleotides used in synthesis of DNA.
Terminate chain elongation in same way.

104
Q

What are NRTI/NtRTI used to treat and why?

A

Because they inhibit reverse transcriptase enzyme, used to treat either HIV or HBV.

105
Q

What is 7 drugs are in the NRTI/NtRTI class of drugs?

A

Abacavir, Emtricitabine, Entecavir, Lamivudine, Telvudine, Tenofovir, Zidovudine

106
Q

Which drugs in the NRTI/NtRTI class are used to treat only HIV?

A

Abacavir, Emtricitabine, Tenofovir, Zidovudine

107
Q

Which drugs in the NRTI/NtRTI class are used to treat only HBV?

A

Entecavir and Telbivudine

108
Q

Which drugs in the NRTI/NtRTI class are used to treat both HIV and HBV?

A

Lamivudine (HIV; HIV+HBV coinfections)

109
Q

How do non-nucleoside reverse transcriptase inhibitors (NNRTI) function?

A

Act by binding to catalytic site on reverse transcriptase enzyme.
Does NOT require phosphorylation and does NOT compete with nucleoside triphosphate substrates.

110
Q

Why do NNRTIs work effectively in combination with nucleoside/nucleotide inhibitors/analogs?

A

Mechanism of action is different and so requires different mechanisms of resistance.

111
Q

What are two NNRTI drugs and what are they used to treat?

A

Efavirenz and Etravirine, both used to treat HIV

112
Q

How do protease inhibitors function?

A

Inhibit maturation steps of HIV by targeting aspartyl protease enzyme

113
Q

What is the significance of aspartyl protease enzymes?

A

Essential for cleaving polyprotein gag-pol into indiidual proteins, which are required for infectivity upon entry into nxt host cell.

114
Q

What are 3 problems associated with protease inhibitors?

A

Stability, solubility, and bioavailability.

115
Q

What are 4 drugs in the protease inhibitor class?

A

Atazanavir, Darunavir, Fosamprenavir, Lopinavir: all used to treat HIV

116
Q

What are Entry/Fusion inhibitors?

A

Drugs that interfere with the binding, fusion, and entry of the virion.

117
Q

What are 2 entry/fusion inhibitor drugs?

A

Docosanol (1st FDA-approved OTC antiviral) and Maraviroc: both used to treat HIV

118
Q

What are integrase inhibitors?

A

Block action of integrase (enzyme that aids in integration of viral genetic material into genome of target cell)

119
Q

Name an integrase inhibitor drug

A

Raltegravir (used for HIV and currently only one for salvage therapy)

120
Q

What are neuraminidase inhibitors?

A

Drugs that prevent the neuraminidase enzyme from cleaving the sialic acid residues on host cell membrane–> virions cluster at cell surface and cannot be released

121
Q

What is neuraminidase?

A

Viral enzyme, which cleaves sialic acid from hemagglutinin to release the virion from host cell.

122
Q

What are two neuraminidase inhibitor drugs? What are they used to treat?

A

Oseltamivir and Zanamivir: both used to treat Influenzavirus A AND B

123
Q

How do ion channel blockers work?

A

Act by targeting/blocking M2 protein, which prevents ion channel from forming and virus cannot uncoat once inside the cell.

124
Q

How does M2 proteins normally function?

A

Forms a channel to allow influx of H ions to reduce pH and allow uncoating. Missing in influenzavirus B strains.

125
Q

What are two drugs in the ion channel blockers class?

A

Amantadine and Rimantadine: both used to treat Influenzavirus A but not B

Virology (3 decks)

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