Chapter 24 Flashcards

1
Q

the basic structure of herpes simplex virus

A

enveloped icosahedral with 6 different proteins and T=16 capsid, linear ds-DNA; envelope has 10 different glycoproteins; tegument between capsid and envelope with 14 glycoproteins

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2
Q

HSV genes have

A

two Unique regions: U[L] and U[S], flanked by inverted repats

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3
Q

“a” region is

A

packing signal and recombinations

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4
Q

there are about

A

84 different genes (U[L]=65 and U[S]=14)

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5
Q

recombination during replication creates

A

4 genome isomers, all being infectious

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6
Q

“b” region and “c” region has

A

4 and 1 genes, respectively

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7
Q

during infection, the HSV genome is adopted in

A

circular form

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8
Q

human herpesvirus [alpha]

A

HSV 1&2 - Labial and genital lesions

Varcella-zoster virus - Shingles and Chickenpox

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9
Q

human herpesvirus [gamma]

A

Epstein-Barr virus - mononucleosis

Human Herpesvirus 8 - Kaposi’s sarcoma

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10
Q

human herpesviruses are latent virus

A

symptomless after initial infection, and maybe reactivated

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11
Q

in HSV entry, initial attachment proteins are

A

gB & gC with initial receptor “heparan sulfate”

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12
Q

in HSV entry, the second attachment protein is

A

gD with second receptor, “nectin-1 & HVEM”

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13
Q

FUsion with PM occurs through

A

gB, gH and gL

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14
Q

during the HSV entry, tegument is released in

A

cytoplasm after envelope fusion with PM

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15
Q

capsid travels through the cytoplasm using

A

microtubule and dynein, with tegument proteins attached to the capsid

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16
Q

when the capsid is attached to nuclear envelope,

A

DNA and associated proteins are released in the nucleus. the genome is circularized. VP16 tegument protein is also released.

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17
Q

HSV transcription is done by

A

cDdRp II

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18
Q

most mRNAs are

A

unspliced

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19
Q

genes expressed in 3 temporal classes are:

A

immediate early (early gene activation), early (DNA replication, late gene activation), Late (structural proteins, regulatory proteins)

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20
Q

[Alpha] proteins are

A

ICP0, ICP4, ICP22, ICP27, ICP47

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21
Q

ICP0’s function is

A

promiscuous activator of gene transcription (viral and cellular). Acts as ubiquitin ligase (E3). Localizes to nuclear domain 10 structures

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22
Q

ICP4’s function is

A

major regulatory protein, required for all [Beta] and [Gamma] virus gene expression. Binds to viral DNA; interacts with cellular transcription factors. Regulates transcription both positvely and negatively

23
Q

ICP22’s function is

A

enhancing the expression

24
Q

ICP27’s function is

A

blcoking DNA splicing

25
Q

ICP47’s function is

A

blocking immune system

26
Q

[Alpha] genes are activated by

A

VP16 with host Oct-1 and HCF-1 on [Alpha]-gene transcription enhancer

27
Q

[Alpha]-gene transcription enhancer

A

TAATGARATT

28
Q

U[L]41 is for

A

degrading cellular mRNA and [alpha]-gene mRNA

29
Q

[Beta] proteins are

A

U[L]9, U[L]29 *ICP8, U[L]5+U[L]8+U[L]52, U[L]30, U[L]42

30
Q

U[L]9’s function is

A

binding to replication origin, Ori S,S, L and meting dsDNA

31
Q

ICP8’s function is

A

binding to ss-DNA

32
Q

U[L]5,8,52 is

A

helicase-primase complex

33
Q

U[L]30 is

A

DNA polymerase

34
Q

U[L]42 is

A

processivity factor

35
Q

rolling-circle replication occurs

A

later in the infection

36
Q

U[30] and U[L]42 complex read both

A

inner and outer strands as leading strand synthesis and lagging strand synthesis, respectively

37
Q

like leading strand synthesis,

A

U[L]30 and U[L]42 displaces 5’ part of own strand

38
Q

like lagging strand synthesis,

A

U[L]30 and U[L]42 is nicked and its 3’-end is extended by Pol U[L]30, and need helicase-primase

39
Q

[Gamma]-gene activation is made by

A

[Beta]-gene regulatory proteins or completion of replication

40
Q

[Gamma] proteins are

A

virion proteins and regulatory proteins

41
Q

Scaffolding proteins are

A

VP21, 22a, 24

42
Q

Major and secondary coat proteins are

A

VP5 and 26

43
Q

pac1 and pac2 in “a” region are

A

inserted into the immature preformed capsid

44
Q

terminase (UL6) mediates

A

packaging through portal

45
Q

insertion of progeny genome continues

A

up to next “a” region

46
Q

once complete,

A

conformational change seals capsid

47
Q

there are three models to

A

envelopment and engress of HSV

48
Q

model 1 illustrates

A

NC budding into the nuclear membrane, forming an envelope, exit as a vesicle budding, then secreted through vesicle fusion with plasma membrane

49
Q

model 2 illustrates

A

NC budding into the nuclear membrane, and exits, then enter through golgi membrane to form envelope, then secreted through vesicle fusion with plasma membrane

50
Q

model 3 illustrates

A

NC exiting through enlarged nuclear pore, forming envelope through entering in the golgi vesicle, then then secreted through vesicle fusion with plasma membrane

51
Q

virus latency occurs as

A

the virion losing most of VP16 on the way to neurons, remaining as dormant genome

52
Q

the dormant genome remains

A

as transcription factors in neurons Luman and Zhangfei bind to HCF-1, blcoking VP16 binding, consequently to prevent early-[alpha]-gene expression.

53
Q

the dormant genome requires

A

Oct-1 and HCF-1 to resurface to the skin or mucosal cells to be active