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Haematology > Micro > Flashcards

Micro Flashcards

1
Q

structure of herpes virus

A

iscosahedral capsid
lipid envelope
~dozen virus-encoded glycoproteins

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2
Q

what is the tegument of a herp virus?

A
  • bw capsid and envelope

- location of proteins needed for infection, rep

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3
Q

which herp type is the biggest?

A

CMV

[cause its mega]

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4
Q

what is the genome of herp like?

A

large
DS DNA
150-250 kb pairs

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5
Q

where does replication of herp genome take place?

A

nucleus of host cell

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6
Q

what type of inf does herp ususally cause? what is the exception to this?

A
  • self limiting, no symptoms

- exception for immunocompromised pt, Cx and life-threatening inf

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7
Q

what kind of replication does herp have?

A

lytic

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8
Q

name the overall stages of herp infection:

A 
I. attachment and entry
II. production of IE proteins
III. E proteins
IV. L proteins
V. exit
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9
Q

what are the three herp virus types Ryan taught us? where are they hibernate/latetent?

A

EBV
CMV
HH8/KHSV

lymphocyte

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10
Q

describe the attachment and entry phase

A
  • virus attaches to heparan sulfate proteoglycans
  • nucleocapsid is released
  • migrates in on microtubule
  • goes to nucleus
  • barfs genetic material into nucleus
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11
Q

what is special about virus entry into the cell?

A
  • fuses directly with p.m. bc both lipid

- pH INdependent woman

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12
Q

word association time: intermediate-early protein

A 
Tx factors (viral)
RNAp II (host): directed to viral expression
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13
Q

word association time: early protein

A

replication/non-structural proteins
DNAp (viral)c
thymidine kinase

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14
Q

word association time: late protein

A

structural proteins

capsid, glyco proteins

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15
Q

where does packaging of new nuclear material occur?

A

nucleus of host cell

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16
Q

why is this called a cascade expression? what steps does intermediate-early drive?

A
  • because one step starts the next step

- early AND late

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17
Q

path of packaged virus’ exit from cell

A

ER –> golgi –> p.m. –> buds off in fully-enveloped

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18
Q

what is the importance of thymidine kinase?

A
  • phosphorylates a variety of NT besides thymidine

- point of drug Tx

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19
Q

what is key about latency?

A
  • all herps do it
  • entire genome maintained
  • NO VIRUSES PRODUCED
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20
Q

what genes are active in latency?

A

only the ones needed to maintain latency

:: more expressed in the lymphotrophic viruses than CNS-trophic

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21
Q

what are the three stages of latency?

A
  1. establishment
  2. maintenance
  3. reactivation
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22
Q

describe genome structure of HSV-1 or -2

A
  • unique-long (UL), unique-short (US) flanked by inverted repeat-long (IRL) and inverted repeat-short (IRS)
  • unique has single copy of each gene
  • IR are identical sequences but in opposite orientation :: have 2 copes per IR
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23
Q

describe the genome structure of EBV

A
  • multiple internal repeats
  • same direction
  • amplification
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24
Q

describe the genome structure of HCMV

A

same as HSV 2 U and 2 IR

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25
Q

when does reactivation occur?

A

when there is a lapse in immunity

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26
Q

what is the part of latency that causes Cx, sequelae, etc - the fact that you have it for life or the fact that you have recurrent infections?

A

having it for life

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27
Q

what are the three genome classes of heps? what are their top members? where are they latent?

A
  • alpha: CNS-tropic; HSV-1 and -2, varicella
  • beta: lymphotropic; CMV, HHV-6, HHV-7
  • gamma: lymphotropic; EBV, HHV-8
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28
Q

what do the beta and the gamma have inc common?

A

both lymphotropic

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29
Q

word association: Acyclovir

A 
prodrug
thymidine kinase (virus)
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30
Q

word association: Ganciclovir

A

analog

CMV

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31
Q

word association: Foscarnet

A

pyrophosphate analog

backup Tx

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32
Q

word association: Cidofovir

A

citadine analog

DNAp inhibitor

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33
Q

CMV (is/is not) highly contagious

A

is NOT

34
Q

CMV incidence is increased in what population?

A

adult
low SES: 80%
higher SES: 50%

35
Q

CMV infection occurs when?

A

low SES: 1-2 YO

higher SES: 16 YO

36
Q

what is CMV found in? so who does this put at risk?

A

saliva, urine, breast milk, semen, cervical secretions, blood/transplanted organs

neonates, day care workers, immunicomprimised pts, gay men

37
Q

how do you get CMV?

A

direct contact with secretions

38
Q

what cells does CMV infect? what does CMV look like under the microscope?

A

Bcells
Tcells
monocytes
lymphoctes

large, puffed-up cells

39
Q

what can neonatal CMV infections result in? what about adult?

A

fetuses: most asymptomatic, but can cause retardation and deafness!
adults: mono with fever

40
Q

who is esp at risk for CMV? what are the vehicles of transmission?

A

AIDS, transplant pts**

AIDS - sexytime
transplant - (+) donor gives to (-) recipient or latent in recipient is reactivated when immunosupressed for Sx

41
Q

CMV AIDS pts are esp at risk of

A

retinitis

42
Q

what commonly presents with CMV organ transplant pts?

A

pneumonia 1-4 mo after Sx, preceded by fever

43
Q

how do you diagnose CMV?

A

ELISA
PCR
Shell assay (24h)

44
Q

what is the Rx of choice for CMV?

A

Ganciclovir

45
Q

what are side effects of Ganciclovir?

A

neutropenia

GI bleeding

46
Q

EBV infection occurs when?

A

low SES: early age

higher SES: adolescence, early adult hood (when people start kissing)

47
Q

hoe much of the adult population has ENV Ab?

A

90-95%

48
Q

what can EBV cause in immunnocomp pts?

A

oral hairy leukoplakia (on tongue)

mostly AIDS pts

49
Q

what can you Tx oral hairy leukoplakia with? but what happens when you stop Tx?

A

acyclovir

comes back

50
Q

oral hairy leukoplakia is caused by active/latent EBV

A

active

51
Q

what is PTLD?

A

post-transplant lymphoproliferative disease from EBV

52
Q

EBV is assoc with what diseases?

A

PTLD
nasopharyngeal carcinoma
Burkitt’s lymphoma

53
Q

what is the incubation time for EBV? what is its path through the body?

A

7 wks

oropharyngeal epithelium –> lymphocytes –> liver –> spleen

54
Q

where is EBV latent?

A

throat epithelium

B-cells

55
Q

how long is EBV “shed”? where is it shed from?

A

sheds for weeks

oral shedding

56
Q

symptoms for EBV

A

mostly asymptomatic

infectious mononucleosis

57
Q

diagnosing EBV

A
  • 50% atypical, large lymphocytes
    lobulated nuclei
  • antigenic markers
  • heterophile Ab aka Monospot Test
58
Q

what is notable about the microscopic presentation of EBV?

A

the cells that are fat are Tcells responding to the infected Bcells

59
Q

what are the antigenic markers for EBV? what do they mean?

A

EBNA, VCA
primary infection: anti-VCA IgM (+)
primary infection: anti-VCA IgG (+), anti-EBNA (-)
past/resolved inf: anti-VCA IgG (+), anti-EBNA IgG (+)

60
Q

what is a (+) result in the Monospot Test? what does it rule in or out?

A

sign: agglutination of sheep RBC
(+): def EBV mono
(-): could be EBV or CMV mono

61
Q

what is the mechanism in PTLD? how do you treat it?

A

Bcells proliferating without CTLs to control them

Tx by stopping immunosupression

62
Q

what Rx is not useful in PTLD? why?

A

Ancyclovir

bc virus latent

63
Q

what is Burkitt’s Lymphoma? where does it present anatomically and geographically? what populations?

A
  • neoplasm of Bcells
  • affects jaw
  • central Africa, new Guniea
  • young children
64
Q

what 3 things is Burkitt’s assoc with?

A
  1. early EBV inf
  2. activation of C-MYC: under Ig promoter :: overexpression
  3. malaria: supresses typical immune response
65
Q

Burkitt’s lymphoma can/can’t be cured if caught early.

A

can

80% cure rate

66
Q

is Burkitt’s always assoc with EBV?

A

no, bc only 20% of pts have EBV assoc outside of Africa

67
Q

where is the assoc bw nasopharyngeal Cx and EBV highest? why?

A

southern China

due to high salt diet from the fishies they eat

68
Q

is nasopharyngeal Cx survivable? how does it present?

A

lump in neck

nope, at best 60% live past 10y

69
Q

what are other disease assoc with EBV that aren’t confirmed, but suspected?

A

Hodgkin’s Lymphoma

MS

70
Q

what does HHV-8 “cause”? why the air quotes?

A

it “causes” Kaposi’s Sarcoma

air quotes bc it is “necessary but not sufficient” to cause KS (95% of tumors KS +, 80% seropositive)

71
Q

what pt pop is KS common in?

A

AIDS

72
Q

where do the KS tumors occur? what cell does it infect?

A

lining of lymphatic system

Bcell

73
Q

what are the types of KS? what is the immune-loss mechanism?

A
  1. Classical: Mediterranean; no sex // being old

2. AIDS: umm….gays; sex // AIDS

74
Q

HHV-8 is present/not present in what secretions?

A

not in vag and jizz
in spit
:: get from rimming

75
Q

what is the incubation period of HHV-8 before you get KS?

A

10 years

76
Q

symptoms of HHV-8

A

95% asymptomatic

still can be mild when symptomatic

77
Q

Tx in AIDS pts for HHV-8?

A
  • symptomatic
  • treat tumor (resection, chemo)
  • treat HIV
  • can’t spf treat virus
78
Q

what are the Bcell abnormalities linked to HHV-8 that we need to know exist?

A

Primary Effusion Lymphoma

Multicentric Castleman’s Disease

79
Q

why can’t antivirals cure herp or treat the assoc Cx?

A

they inhibit virus replication when virus is active :: can’t work when latent
and Cx is caused from latency NOT the infection

80
Q

EBV v. CMV

A

both: cause mono, have latency, post-transplant disorders,
CMV: sex transmitted, congenital presentation, ALWAYS heterophile/Monospot (-)
EBV: oncogenic

Haematology (5 decks)

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