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D&D, BL Unit III > Feb 24 2014- Viruses > Flashcards

Feb 24 2014- Viruses Flashcards

1
Q

What is a virus?

A

Submicroscopic, infectious, obligate, intracellular parasites

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2
Q

What are virions?

A

Proteins produced with self assembly that can spread themselves to new hosts

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3
Q

Advantage of viral dsDNA?

A

Easily transcribed into mRNA’s by host’s Pol II

[ex. herpes, adenovirus]

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4
Q

First step in viral gap-DNA or ssDNA transcription?

A

Reverse-transcriptase regenerating the gap / making ss into ds
[ex. gap DNA = hep B, ssDNA = parvovirus]

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5
Q

Cells have no independent RNA polymerase (to make RNA genome). So all virus genomes have ____.

A

RDRP, RNA-dependent RNA polymerase

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6
Q

Retroviruses contain what kind of viral genome?

A

(+) ssRNA that are “ribosome-ready” with DNA intermixed

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7
Q

What do (-) and (+) ssRNA genome viruses have to do first before they can replicate?

A

Use RDRP to create the missing (+) or (-) strand; then transcription can begin

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8
Q

What do you use a plaque assay for?

A

To quantify infectivity of a virus

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9
Q

What is CPE and what does it indicate?

A

CPE = CytoPathic Effect ; evidence of viral replication

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10
Q

Do all viruses have CPE?

A

No - bc it’s difficult to culture some viruses on medium

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11
Q

Function of capsids?

A

(helical or icosahedral) They protect the genome and serve as a genome delivery service

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12
Q

What is a capsomer?

A

The surface structures seen in e- micrograph of virus

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13
Q

What is a virus envelope?

A

A host-cell-derived lipid bilayer

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14
Q

What are viral spikes?

A

Virus-derived membrane glycoproteins (w/in the viral envelope)

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15
Q

What do Ab’s often recognize on the surface of a virus?

A

The “spikes” w/in the viral envelope

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16
Q

What is the shape of a rabies capsid?

A

Bullet-shaped; helical capsid

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17
Q

What is the shape of an adenovirus capsid?

A

Complex capsid; many-faced icosahedral

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18
Q

What kind of growth curve do viruses have?

A

Single-step “burst” growth

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19
Q

What happens during the latent period in a viral infection?

A

The virus is replicating inside cells; won’t see it in the host supernatant

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20
Q

What allows for close proximity btwn host cell and attaching virus?

A

Electrostatic binding (then prot-prot interactions take over for actual attachment)

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21
Q

How do viruses gain access to many different tissue cell types?

A

They use one or more receptors, or combo prot-carb receptors

22
Q

What are the co-receptors HIV uses to access a cell?

A

gp41 and gp120

23
Q

What is the difference in entry for enveloped vs naked viruses?

A 
Enveloped = fusion
Naked = endocytosis (clathrin and caveolin-dependent)
24
Q

Strategies that maintain the compact viral genome?

A

Alternative splicing, nested RNAs, ambisence coding

IRES elements, leaky scanning for AUG,

25
Q

How are helical capsids created?

A

They are created contemporaneously with the new viral genome

26
Q

How are icosahedral capsids created?

A

The capsid is created around the already-made viral genome OR the genome is inserted into a pre-formed capsid

27
Q

What are Negri Bodies?

A

Cytoplasmic inclusions

Evidence of infection (esp. rabies!)

28
Q

Where do most viruses infect?

A

At a mucosal membrane (GI, nasal, resp system)

29
Q

What is the incubation period?

A

The time from viral infection to Sx onset

30
Q

Who is at highest risk for viral infection?

A

Infants, elderly, pregnant women, immunocompromised

31
Q

Local vs Systemic Infection

A 
Local = in and out same pathway (Ap to Ap)
Systemic = excreted anywhere (Ap, BL, sides)
32
Q

What are the Ab’s in a local infection?

A

Mostly IgM and and IgA

33
Q

Koplik Spots?

A

White plaque on gums during measles infections

34
Q

What is subacute sclerosing panencephalitis?

A

Untreated measles that migrated to the brain

35
Q

Talk to me about RSV

A

Respiratory Synctial Virus

Babies resp. infection that predisposes to perm. lung damage

36
Q

Indirect damage by viral infection?

A

Taking over the host genome replication mechanisms

37
Q

Direct damage by viral infection?

A

Membrane damage causing cells to stick together

38
Q

What do you look for when determining CPE?

A

cell lysis, nuclear shrinking, changes in the membrane, inclusion bodies

39
Q

What is syncytia?

A

Cell fusion

40
Q

What is pyknosis?

A

Nuclear shrinking

41
Q

What are some Intracellular Restriction Factors? What do they do?

A

APOBEC, TRIM5

They are protective against some classes of viruses

42
Q

What does APOBEC do?

A

Binds HIV, disallows infection

43
Q

Why does APOBEC not work?

A

HIV contains the Vif protein, which targets and degrades APOBEC

44
Q

What does TRIM5 do?

A

Recognizes viral capsids

45
Q

What does INF do?

A

It is secreted to the neighbors of sick cells and won’t allow viral replication in neighbors

46
Q

Type I vs Type II INF?

How are type I/II controlled?

A

Type I = INFα,β ; ISRE controlled

Type II = INFγ ; GAS-element controlled

47
Q

What does PKR do?

A

Protein Kinase R decreases viral translation

48
Q

What does OAS do?

A

Oligoadenylate Synthetase activates the degraders of mRNA

49
Q

Which TLRs are important in viral infection?

A

TLR 3, 7, 9

50
Q

Humoral vs Innate response?

A

Humoral is necc for virion recognition

Innate is a cell-mediated response

D&D, BL Unit III (10 decks)

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