Viral Pathogenesis Flashcards

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1
Q

modes of transmission

A

direct contact, injection, transplantation, fecal oral (+/- envelope important)

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2
Q

how often are we exposed to pathogen

A

constantly; they are everywhere though they vary based on living conditions

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3
Q

reasons viruses continue to persist in population

A

health, nutrition, genetic makeup, age, immune status

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4
Q

what is an outbreak

A

introduction of a virus into a new location which originates from a common source

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5
Q

how is the identification of the source of an outbreak so important

A

to stop the outbreak

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6
Q

what is an epidemic

A

introduction of a new strain of virus to an immunological naive population which occurs over a LARGER geographical area

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7
Q

what is a pandemic

A

worldwide epidemic

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8
Q

are a majority of viral disease symptomatic

A

no but those that target essential tissues/organs –> serious disease

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9
Q

symptoms and severity of viral diseases depend on what

A
  • Patient’s ability to prevent/resolve infection
  • Virulence and target tissue
  • Ability to repair damage
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10
Q

what are some mechanisms of viral pathogenesis

A
  • Circumvent protective barriers
  • Evade immune control
  • Kill cells or trigger destructive immune and inflammatory response (control infection)
  • Possibly transform cells
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11
Q

what are some inherent barriers for host defenses

A

– Skin
– Mucous
– Ciliated epithelium
– Low pH

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12
Q

what are some induced barriers for host defenses

A

– Fever
– Low pH
– Humoral and cellular components

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13
Q

what are some non specific host defenses

A

– Interferon
– Complement
– Other cytokines

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14
Q

what are some specific host defenses

A

– Antibody production

– Specific immune system

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15
Q

when does transcription of interferons occur?

A

transcription only occurs after exposure to an inducer – viral infection, dsRNA – RNA viruses best

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16
Q

what do viruses do to our immune responses

A

it suppresses them

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17
Q

what can immune response to viral infection cause

A

tissue injury

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18
Q

example of immune response to viral infection causing tissue injury: what can circulating immune complexes lead to?

A

deposits —> arthritis

aka CMV

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19
Q

in dengue, what is the mechanism in which tissue injury happens?

A

hemorhagic shock syndrome: fixation of complement by circulating immune complexes 􏰁–> release of products via complement cascade 􏰁–> sudden increase in vascular permeability, shock, death

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20
Q

basic steps of viral disease

A
  • Acquisition
  • Initiation of infection at the primary site
  • Incubation period (amplification, spread to secondary site maybe)
  • Replication in target tissues
  • Immune responses (limit AND contribute)
  • Transmission
  • Resolution or persistent infection
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21
Q

can viruses cause more than one disease

A

yeah

22
Q

what is it called for viruses to lose their virulence

A

attenuation

23
Q

result of viruses encoding their virulence factors

A

– Promoting replication, transmission
– Access and binding to target tissue
– Escape of immune system

24
Q

outcomes of viral infection

A

1) Abortive - Failed “attempts”: no virus multiplication
2) Lytic - Cell death
3) Persisting - Infection without cell death, selection of ideal target cell subsets (Chronic – nonlytic, productive)
4) Latent-recurrent infection - Presence of virus without virus production but with potential for reactivation

25
Q

difference between replication of virus during acute infection and during chronic infection via continuous productive infection

A

both of them after virus infects host cell –> entry and uncoating –> gene expression –> assembly and release (they have antigens for B and T cell recognition)

but in chronic a variant strand of the virus (one that was not killed) will begin the process all over again and produce variant antigens for B and T cell recognition

26
Q

how is latency established

A
  • modulation of viral gene expressions
  • viral subversion of cellular apoptotic pathway
  • avoidance of clearance by the immune system
  • selection of cell subsets ideal for long-term maintenance of the viral genome
27
Q

when does persistence occur in viral infections

A

when the cell is not killed - could be chronic, latent, recurrent, immortalizing, transforming

28
Q

what are determinants on if a virus will be lytic or persistent

A
  • access to target tissue
  • stability
  • ability to cross barriers, establish viremia, and spread
29
Q

viruses apply a lot of avoidance strategies to persist. what are some of these strategies?

A
  • viruses can alter / interfere with the processing of viral peptides by professional APCs
  • can downregulate co-stimulatory and/or MHC molecules (required for T cell signaling, expansion)
  • inhibit the differentiation of AP conventional dendritic cells, infect effector T and B cells directly

all of these are just ways in which the infected host’s innate or adoptive immune system is suppressed

30
Q

what does the susceptibility of host cell to virus depend on?

A

presence of receptor for virus attachment

31
Q

during what basic steps of viral disease does one see the prodrome phase?

A
  • It could just be during acquisition

- Or it could be in acquisition, primary and/or secondary site replication

32
Q

during what basic steps of viral disease does one see the symptoms of disease

A

at the sites of replication or at the target tissue

33
Q

outcome and severity of viral infection can be due to what factors?

A
  • virus strain, inoculum size

- health of host host response system (immune response helps determines severity, duration)

34
Q

what does the target tissue of a virus determine

A

the predominant disease

35
Q

most common site of viral infections and disease

A

oral and respiratory tract (upper and lower)

with primary infections spreading to other sites

36
Q

how do oral and respiratory tract viral infections spread

A

respiratory droplets, contact, food, water, saliva

37
Q

example of a respiratory tract viral infection

A

influenza

38
Q

mechanism in which influenza occurs

A

aerosol inoculation of virus –> replication in respiratory tract –> desquamation of mucus secreting and ciliated cells –> influenza syndrome

39
Q

desquamation of mucus secreting and ciliated cells can lead to what?

A

secondary bacterial infection (pneumonia), primary viral pneumonia, CNS muscle involvement

40
Q

what other things add to the desquamation of mucus secreting and ciliated cells that lead to influenza

A

antibody, interferon induction, T cell responses

though antibody and T cell responses do lead to future protection

41
Q

what are consequences of GI tract viral infection

A

no symptoms –> gastroenteritis, vomiting, diarrhea

Generally self limiting

42
Q

what promotes GI tract viral infections

A

poor hygiene

43
Q

GI tract viral infections has more significant effect in what population

A

infants

44
Q

example of a GI tract viral infection

A

rotavirus

45
Q

transmission of rotavirus

A

fecal matter especially in day care settings (respiratory possible)

46
Q

who is at a risk for GI tract viral infections

A

Infants

47
Q

how do you control rotavirus

A

hand washing and isolation

live vaccines

48
Q

effects of rotavirus

A

from asymptomatic –> viral disease

49
Q

what is rotavirus resistant to

A

environmental and gastrointestinal conditions

50
Q

virus induced skin diseases

A

exanthems and hemorrhagic fevers

51
Q

major classifications of viral rashes

A
  • macules (flat colored spots)
  • papules (slightly raised areas from immune response)
  • nodules (larger raised areas of the skin)
  • vesicular lesions (blisters likely to contain virus)
52
Q

what do hemorrhagic fevers infect

A

endothelial cell lining of the of the vasculature, possibly compromising the structure of the blood vessel