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Bugs & Drugs > Viruses I > Flashcards

Viruses I Flashcards

1
Q

first virus isolated?

A

tobacco mosaic virus

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2
Q

viral characteristics

A

obligate IC parasites
no capacity for: protein synthesis, generation of E
no cell wall/nuc
DNA/RNA, NOT both
reproduce by subunit assembly (“always the same diameter”) NOT growth/division

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3
Q 
classification of viruses:
nature of genome
structure of genome
envelope
capsid symmetry
A

RNA or DNA
Single or double stranded/Segmented or non (most viruses; come in pieces: influenza, rotavirus)
present/absent
helical or cubic (icosahedral)

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4
Q

protein shell that encases the coral genome

A

capsid

polio: just genome + capsid

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5
Q

cell culture allows for?

before it was animals/plants

A

synchronized infection in cells to allow for monitoring; allowed for discovery of single-step growth curve

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6
Q

why the drop in viral titer?

A

viruses must break apart to release their genome into cells; then titer rises once machinery starts producing parts

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7
Q

8 steps of viral replication?

AEUERLAR

A 
att
entry
uncoat
early gene
replication
late gene
assembly
release
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8
Q

2 components of attachment?

reaction characteristics

A

att protein/complex
cellular receptors/co-receptors

saturable, specific, IRREV
MULTIVALENT (many different receptors/proteins) allows for high-affinity binding

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9
Q

types of receptors

A

proteins (CD4, CCR for HIV)
carbohydrates (heparin-HSV; SA-influenza)
glycolipids

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10
Q

host range

tropism

A

ability to infect a host

certain cell/tissue/organ

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11
Q

two ways of entry?

2 virus e.g. that can use both?

A

Fusion: only ENVELOPED - HIV
Receptor-mediated: BOTH
Herpes simplex, Poxviruses

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12
Q

receptor-mediated endocytosis entry viruses rely on what critical step?

A

acidification of endolysozome –> conformational change

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13
Q

Infervitide

A

prevents GP120 from folding back onto itself –> antiviral drug that prevents entry

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14
Q

for most viruses, what causes simultaneously with entry?

A

release of genome

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15
Q

poxviruses are unique in that they replicate where?

A

in cytoplasm

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16
Q

larger DNA viruses
IE genes
DE genes
late genes

A

regulatory
replication
structural proteins

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17
Q

smaller DNA viruses
larger DNA viruses
all but one DNA virus requires what?

A

uniquely dependent on host cell enzymes, polymerase
usually encode early proteins that direct cell machinery to viral genome

adeno/herpes…encode own polymerase and replication factors

host enzymes to make mRNA

POX viruses encode ALL for mRNA and DNA replication

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18
Q

positive strand RNA viruses have what in their DNA that negative-strands do not?

A

gene for polymerase
+ genome is mRNA –> polymerase production is FIRST

  • genome must first be copied to + strand; polymerase is STRUCTURAL PROTEIN
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19
Q

retroviruses have what type of genome? significance of RT? where is RT?

A

+ strand
after entry, genome copied into dsDNA via RT
RT antiviral target for HIV
structural protein

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20
Q

why aren’t retroviruses in the + strand virus category?

A

because first step isn’t translation, it’s reverse transcription

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21
Q

hepatitis B virus unique because?

A

dsDNA virus, but has a reverse transcriptase! bah!

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22
Q

the monocistronic RNA problem:

how do viruses get around this (7)?

A

host cells translate 1st open reading frame in mRNA

separate promoters for each gene (rhabdo/rabies)
mRNA splicing
translate one large polyprotein that is then cleaved into indiv proteins
segment genome, each protein on different RNA (influenza/rotavirus)
frame shifting - skip bases (pseudo-knot:allows for regulating how much of each protein to make e.g skip happens 10% of the time)
IRES

most viruses use multiple methods

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23
Q

two viruses w/ separate promoters for each gene

A

rhabdo/rabies

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24
Q

two viruses that segment genome

A

influenza/rotavirus

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25
Q

IRES

A

can replace/fxn as 7’ guanosine cap

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26
Q

critical feature of assembly of icosahedral viruses

A

scaffold proteins

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27
Q

one viral infx that is symptomatic (most are asymptomatic)

A

measels

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28
Q

purpose of causing sx as a virus after infection?

A

enhances transmission

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29
Q

examples of vertical transmx

A

Rubella or CMV
occurs in utero and requires viremia
most common during primary infx
most infx are horizontal

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30
Q

most common mech of transmit?

A 
#1 airways
#2 GI tract
GU
animal vectors
animal bites
aerosolized
needle sticks
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31
Q

respiratory virus transmx e.g.?

A

Measles
also can enter via conjunctiva
doesn’t actually cause infx in lung

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32
Q

humidity/temp/envelop and virus survival

A

low humidity up survival
lower temp enhances
non-enveloped can survive better on surfaces

33
Q

tx for viral diarrhea?

A

hydration

not many antivirals avail

34
Q

2 e.g. of fecal-oral transmx viruses that don’t cause diarrhea

A

enterovirus

polio

35
Q

characteristics of fecal-oral transmx viruses?

A

large amts shed in feces
highly-resistant; survive long time in env
heat/protease/alcohol resistant
require bleach to kill
organic matter in feces protects (from bleach e.g.)
hand washing may not kill but can remove from hands

36
Q

characteristics of viruses transmx by close contact? one e.g. of virus transmitted by fomites?

A

most are labile or shed in low amts
kissing/sex
fomites can transmit (HPV)
route of many PERSISTENT viruses

37
Q

key property of viruses transmitted by insect vector?

A

must be able to replicate in both vertebrate host and insect

38
Q

animal vector transmission chars?

A

emergent infections

highly lethal b/c humans aren’t natural host

39
Q

transmission via direct injection

A

viremia required

40
Q 
define:
productive infection
permissive cell
abortive infection
non-permissive cell
A

infectious virus is produced
supports complete real cycle
non-productive; no infectious virus produced
doesn’t support replication and produces infectious virus

41
Q

localized infection

A

virus stays at site of entry (herpes; HPV; respiratory pathogens)
CAN STILL dev systemic sx e.g. influenza, while only in lungs

42
Q

disseminated infection
primary v. secondary viremia:
persistance/titer/sx/detection in BS

A

first time in blood: primary viremia (localized replication in epithelial cells; spreads to lymphatics; transient and low titer/doesn’t persist)

Secondary: higher titer, more sustained, target tissues now infected (liver/brain), now have sx (chance inc w/higher titer and duration of secondary viremia) can now detect virus in BS

PROCESS TAKES 10d-2wks

43
Q

patterns of infx: acute v persistent

A

acute: acquired, defenses respond, virus cleared
persistent: acquired, defenses respond, defenses don’t clear, host infected for life/long time

44
Q

2 types of persistent infx?
e.g. of each (2:5)
what virus exhibits both types?

A

chronic: presence of isolatable infectious virus 6 mo after initial infection (Hep B/C) –> pts are infectious at all times
latent: virus cycles btwn infectious(shed/isolatable) and when no virus can be detected (Herpes, adeno, papilloma, papova, paro); reactivated into “lytic” cycle; during latent stage, only can detect circular genome

HIV

45
Q

what is the unique feature of acquisition of latent infectious viruses? one e.g.?

A

initial infection is asymptomatic

e.g. genital herpes

46
Q

mechanisms of direct damage?
which is the major mech?
how does this occur (3)?

A 
host shutoff (of gene expr; viruses cherry-pick genes)
inhibition of host translation

alter phosphorylation of initiation proteins
proteolytic cleavage of init factors
digestion of mRNA

47
Q

inhibition of host gene expression (3)

A

block RNA pol (pol II)
interfere w/splicing of mRNA
interfere w/transport of mRNA to cytoplasm

the above will kill the cell

48
Q

interfering w/cell cycle (3)

A

shutoff halts cell cycle
DNA viruses push S phase than stops it before replication –> incr expression of proteins used in replication (cells make for viruses to use)

common to cancer-causing viruses

49
Q

def: infection results in changes in cell shape

A

cytopathic effect
rounding/detachment
development of inclusion bodies (e.g. Negri body: rabies, HCMV, RSV)

50
Q

syncycium formation plays what role in infection?

A

allows for viral spread in presence of neutralizing antibodies

51
Q

primary v immortilized v transformed cells

A

limited lifespan then enter senescence

mutant primary cells that overcome senescence; grow continuously; do not cause tumors in animals

mutant immortalized cells that lost anchorage independence and form tumors in animals

52
Q

acute (one e.g.) v. chronic (one e.g.) cancer viruses

A

carry genes that drive the transformation process (and thus have short incubation period); polyclonal tumors; multiple tumors can arise at the same time; HHV8 Kaposi’s

do not carry directly transforming oncogene but makes cells more likely to acquire new mutations bc of frequent division; immortalize cells; require additional mutations to cause cancer; long incubation; monoclonal tumors; HPV cervical cancer

53
Q 
viruses and their assoc cancer: HTLV
HHV8
EBV
HepC/B
Merkel
HCMV
A 
adult T-cell leukemia
Kaposi's, lymphoma, Castlmans
cervical, anogenital, skin, H/N
lymphoma, nasopharyngeal, GI
hepatocellular
merkel cell
gliomas, GI
54
Q

risk factors for infection

A

age
hormones (pregnancy e.g. HepE)
nutrition (immune fxn)
fever

55
Q

infection chain of events

A

epithelial cells –> TLR’s recognize –> IFN-1 (via nFkB) –> adjacent cells –> rig-1/MDA5 recognize viral RNA’s and induce IFN –> cytokines attract NP’s –> PMNs infiltrate and cytokine release to attract T-cells –> APCs pick up and tax to nodes –> T/B cells activated –> antibodies

56
Q

single most important defense mech we have?

A

interferon

e.g. most infectious of common cold just before you have sx

57
Q

antimicrobial peptides e.g.

A

made by host cells
alpha/beta cathelecidines
pores in bact
bind to viruses that block attachmt; can also disrupt envelope

58
Q

interferon!

3 critical unregulated genes

A

Type I a/B
binds to cell surface and induces 300 different genes
spp specific, not virus specific (e.g. mouse IF doesn’t do squat in humans)

59
Q

IFN mechanisms (3)

A

PKR: phosphorylates eIF2a –> cells can’t initiate any protein synth
Ribonuclease L: nuclease specifically digests mRNA (both cell and viral)
MXA: binds influenza virus polymerase and prevents fxn

these are made and then SIT THERE in an inactive conformation

60
Q

signals to activate the 3 death proteins:

A

PKR via binding to dsRNA
RNAse L via ds RNA and 2’5’oligoadenylate (2asynthase activated by dsRNA)
(dsRNA present at high levels in virus infected cells)

61
Q

viruses fight interferon with?

A

interferon!

  • secrete soluble IF receptor decoy (binds to IF in system)
  • block phosphorylation and thus signal transduction
  • proteolytically digest signal messengers in pathway to shut down IF response
  • sequestering proteins that bind messengers
  • turn on SOX proteins that naturally damper IF response
62
Q

how does antibody block viruses?

A

can bind and neutralize via blocking attachment or uncoating

ab binding to infected cell and suppress gene expression

opsonization–>phagocytosis

Fc mediated complement activation

63
Q

antibody enhancement

e.g.?

A

non-neutralizing abs bind to virus –> Fc exposed –> cells w/Fc receptors take up virus that would otherwise be non-permissive cell –> dengue hemorrhagic fever

MP’s secrete tons of TNF-a –> vascular leakage –> hemorrhage

a concern for HIV-related vaccination

64
Q

interesting fact about vaccines?

A

don’t prevent infection; just sx (except HPV)

65
Q

viral immune evasion

A

cytokine interference via blockage of antiviral proteins activated by IF, decoy receptors, immunosupprx cytokine analog encoded by virus, produce peptides that cannot be digested to then be presented (EBV)

66
Q

most common way to damper immune system?

A

interference w antigen presentation: block transport into ER, loading onto MHC, trap MHC in ER, downreg expression of MHC proteins (reduce transcription/induce endocytosis of cell surface proteins)

67
Q

other viral mechanisms to interfere w immune sys

A

virus has Fc receptor
encode proteins that bind complement
down reg of co-stim molecules
induce apoptosis of T’s (HIV gp120 can kill T’s)
immune exhaustion
escape variants (mutates so sys can’t see it –> HIV/HepB –> causes viral titer to keep going up and down bc mutant variants escape)

68
Q

which virus has a rapid mutation rate?

A

HIV

69
Q

e.g. of type 1 hypersensitivity response

A

respiratory viral infections can exacerbate asthma

70
Q

ADCC is seen in what?

A

type II

Fc portions of antibody binds to Fc receptors on NK/MP/PMNs

71
Q

leading cause of infectious blindness in the US?

A

Herpes

72
Q

herpes simplex keratits in an example of what type hypersesitivity?

A

type IV

73
Q 
Name the virus:
enveloped/icosahedral
naked/helical
naked/isosahedral
enceloped/helical
A

herpes
tobacco mosaic
adenovirus
measles

74
Q

direct fusion entry 2 e.g.?
receptor-mediated endocytosis 2 e.g.?
both routes 1 e.g.?

A

herpes/HIV (fusion protein –> pore)
influenza/rotavirus (phagolysosomes –> acidification and release)
herpes simplex

75
Q

requires lysosomal proteases to cleave capsid to allow for passage into cell?

A

rotavirus

76
Q

the tactic of “ribosomal frame shifting” is used to make which key viral protein?

A

reverse transcriptase

77
Q

Picornaviruses solve the monocistronic mRNA problem by which strategy?

A

IRES

78
Q

what’s funky about polio and coxackie virus and their portal of entry?

A

enter via GI but don’t cause GI sx

79
Q

name two viruses that can enter via inhalation of urine/feces?

A

hantavirus and lassa fever

Bugs & Drugs (15 decks)

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