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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
IRES
can replace/fxn as 7' guanosine cap
26
critical feature of assembly of icosahedral viruses
scaffold proteins
27
one viral infx that is symptomatic (most are asymptomatic)
measels
28
purpose of causing sx as a virus after infection?
enhances transmission
29
examples of vertical transmx
Rubella or CMV occurs in utero and requires viremia most common during primary infx most infx are horizontal
30
most common mech of transmit?
``` #1 airways #2 GI tract GU animal vectors animal bites aerosolized needle sticks ```
31
respiratory virus transmx e.g.?
Measles also can enter via conjunctiva doesn't actually cause infx in lung
32
humidity/temp/envelop and virus survival
low humidity up survival lower temp enhances non-enveloped can survive better on surfaces
33
tx for viral diarrhea?
hydration | not many antivirals avail
34
2 e.g. of fecal-oral transmx viruses that don't cause diarrhea
enterovirus | polio
35
characteristics of fecal-oral transmx viruses?
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
characteristics of viruses transmx by close contact? one e.g. of virus transmitted by fomites?
most are labile or shed in low amts kissing/sex fomites can transmit (HPV) route of many PERSISTENT viruses
37
key property of viruses transmitted by insect vector?
must be able to replicate in both vertebrate host and insect
38
animal vector transmission chars?
emergent infections | highly lethal b/c humans aren't natural host
39
transmission via direct injection
viremia required
40
``` define: productive infection permissive cell abortive infection non-permissive cell ```
infectious virus is produced supports complete real cycle non-productive; no infectious virus produced doesn't support replication and produces infectious virus
41
localized infection
virus stays at site of entry (herpes; HPV; respiratory pathogens) CAN STILL dev systemic sx e.g. influenza, while only in lungs
42
disseminated infection primary v. secondary viremia: persistance/titer/sx/detection in BS
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
patterns of infx: acute v persistent
acute: acquired, defenses respond, virus cleared persistent: acquired, defenses respond, defenses don't clear, host infected for life/long time
44
2 types of persistent infx? e.g. of each (2:5) what virus exhibits both types?
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
what is the unique feature of acquisition of latent infectious viruses? one e.g.?
initial infection is asymptomatic | e.g. genital herpes
46
mechanisms of direct damage? which is the major mech? how does this occur (3)?
``` 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
inhibition of host gene expression (3)
block RNA pol (pol II) interfere w/splicing of mRNA interfere w/transport of mRNA to cytoplasm the above will kill the cell
48
interfering w/cell cycle (3)
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
def: infection results in changes in cell shape
cytopathic effect rounding/detachment development of inclusion bodies (e.g. Negri body: rabies, HCMV, RSV)
50
syncycium formation plays what role in infection?
allows for viral spread in presence of neutralizing antibodies
51
primary v immortilized v transformed cells
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
acute (one e.g.) v. chronic (one e.g.) cancer viruses
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
``` viruses and their assoc cancer: HTLV HHV8 EBV HepC/B Merkel HCMV ```
``` adult T-cell leukemia Kaposi's, lymphoma, Castlmans cervical, anogenital, skin, H/N lymphoma, nasopharyngeal, GI hepatocellular merkel cell gliomas, GI ```
54
risk factors for infection
age hormones (pregnancy e.g. HepE) nutrition (immune fxn) fever
55
infection chain of events
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
single most important defense mech we have?
interferon | e.g. most infectious of common cold just before you have sx
57
antimicrobial peptides e.g.
made by host cells alpha/beta cathelecidines pores in bact bind to viruses that block attachmt; can also disrupt envelope
58
interferon! | 3 critical unregulated genes
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
IFN mechanisms (3)
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
signals to activate the 3 death proteins:
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
viruses fight interferon with?
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
how does antibody block viruses?
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
antibody enhancement | e.g.?
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
interesting fact about vaccines?
don't prevent infection; just sx (except HPV)
65
viral immune evasion
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
most common way to damper immune system?
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
other viral mechanisms to interfere w immune sys
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
which virus has a rapid mutation rate?
HIV
69
e.g. of type 1 hypersensitivity response
respiratory viral infections can exacerbate asthma
70
ADCC is seen in what?
type II | Fc portions of antibody binds to Fc receptors on NK/MP/PMNs
71
leading cause of infectious blindness in the US?
Herpes
72
herpes simplex keratits in an example of what type hypersesitivity?
type IV
73
``` Name the virus: enveloped/icosahedral naked/helical naked/isosahedral enceloped/helical ```
herpes tobacco mosaic adenovirus measles
74
direct fusion entry 2 e.g.? receptor-mediated endocytosis 2 e.g.? both routes 1 e.g.?
herpes/HIV (fusion protein --> pore) influenza/rotavirus (phagolysosomes --> acidification and release) herpes simplex
75
requires lysosomal proteases to cleave capsid to allow for passage into cell?
rotavirus
76
the tactic of "ribosomal frame shifting" is used to make which key viral protein?
reverse transcriptase
77
Picornaviruses solve the monocistronic mRNA problem by which strategy?
IRES
78
what's funky about polio and coxackie virus and their portal of entry?
enter via GI but don't cause GI sx
79
name two viruses that can enter via inhalation of urine/feces?
hantavirus and lassa fever

Bugs & Drugs (15 decks)

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