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Immunology 3 > #14 Lymphotropic Herpes > Flashcards

#14 Lymphotropic Herpes Flashcards

1
Q

Characteristics of Lymphotropic HSVs

  1. Replication and latency in cells including_____ origin
  2. Persistantant infection is balance btwn _______
A

lymhoid

lytic and latent

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2
Q

γHSV—oncogenic:

A

EBV (HHV-4) and Kaposi’s Sarcoma Virks (HHV-8)

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3
Q

EBV (HHV-4) and Kaposi’s Sarcoma Virks (HHV-8) are latent in

A

Latent in B cells and Plasma cells

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4
Q

Human herpes- 6b
HHV-6b
Latent in

A

T lymphocyte

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5
Q

CMV or Cytomegalovirus what type of herpesvirus

A

β Herpes virus:

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6
Q
  1. Infected Cells

a. get very big, have inclusion bodies and characteristic OWLS eyes

A

CMV

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7
Q
  1. Disease referred to as what for CMV
A

Cytomegalic inclusion body disease, CMV disease, Inclusion body disease

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8
Q

HHV-5 (beta) is what herpes viurs

A

CMV, dsDNA, icosahedral

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9
Q

Transmission of CMV

A

secretions-semen, cervix, blood, saliva, tears, breast milk, urine and feces, blood transfusion, organ transplant, and transplacental transmission

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10
Q

CMV presentation in healthy adults

A

Asymptomatic in health adults: see mild mononucleosis or cold-like symptoms

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11
Q

What is the leading cause of congential birth defects?

A

CMV (HHV5) beta HSV

	a. mild to severe mental   retardation, deaf, death
	b. TORCH: it’s the ‘C” and is an acroynm for viruses that cause congenital birt defects
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12
Q

If you get CMV and are immunocompromised, what do we see?

A
  1. Symptomatic upon immunosuppresion

a. Chemo/organ transplant/HIV

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13
Q

CMV persistant infection we see

A

atherosclerosis/ immunosenescenes/ neuroblastoma

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14
Q

Stages of gene expression for CMV

how many genes does it express?

A

Stages of gene expression: immediate/early/ and late

—-. expresses over 750 proteins~ that’s a TON!

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15
Q

CMV Encodes own _______ machinery

A

DNA repliation

thats why it so fucking huge

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16
Q

CMV LYTIC Replication cycle

Binding/penetration happens withing ____ mins and we can see membrane fusion or endocytosis in the _______

A

30 mins

epithelial cell

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17
Q

Once CMV Enters into cytoplasm

a. Sends tegument protein ______ to nucleus for transcrtiption

A

pp65

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18
Q

What is the purpose of pp65 in CMV?

A

its a tegument protein CMV sends to nucleus for transcription

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19
Q
  1. Transcription if CMV occurs in: ______

a. immediate early transcrtipion of DNA→ early transcription→ late transcription

A

nucleus

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20
Q

For CMV:
DNA replication:
Encapsidation at :
Envelopment/release will take:

A

1-2 days
2-3 days
72-96 hours

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21
Q

Lytic CMV infected Cell

1. infected cell the nucleus is HUGE because

A

a. virus in making TOS of viral DNA

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22
Q

What ‘s special about the nucleus during the lytic cycle in CMV

A

See the nucleus bent arount the replicaiton cytosole

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23
Q

Transmission of CMV

A
  1. Direct contact w/ virus containg secreations: semen/cervicle/blood/saliva/tears/breast milk/urine/poo
    ~ Inoculation onto mucosal site
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24
Q
  1. Other routes not as common for CMV
A

blood transfussion, organ tranplants/ transplacental transmission

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25
Q

For CMV, shedding can occur:

viral excreation starts at 1 month and shedding can contineu for months to >1 yrs

A

with or without symptoms

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26
Q

Highest rate of incidents and transmission for CMV

A

trasmission via daycares~~~ big population in children under 18 monts

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27
Q

CMV dissemination

A

CMV dissemination

1. Cell associated—poorly released from infected cell	
2. Slow replication cycles
3. Lytic replication; occurs EVERYWHERE
4. Laten infectin: more in CD34+ hematopietic progenitor cells and monocytes
5. Frequency of reactivation: 1 in 10,000 of infected monocytes~ not a ton, but enough
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28
Q

Where does lytic replicaiton occur for CMV

A

everywhere

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29
Q

Location for latent infection of CMV

A

more in CD34+ hematopietic progenitor cells and monocytes

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30
Q

Innate immune response to CMV

A

Macrophage, INF and NK cells control but are insufficient to clear virus

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31
Q
  1. Humoral response to CMV:
A

no role, but may limit re-infection.

a. involves neutralizint antiBs directed agains surface antigens such as gB, gH, pp65, pUL-128

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32
Q
  1. Cell mediated immune response to CMV:
A

keey CTLs will kill CMV infected cells

a. up to 10% of all CD8 T cells in body are directed against CMV (huge %!!!)
b. cytotoxic T cells are main players in fight CMV
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33
Q

main players to fight CMV

A

cytotoxit T cells

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34
Q

can host immune reponse completely take care of CMV

A
  1. Immune response can’t completely control CMV

Reinfection by different CMV variants occurs: high degree of intra-host genomic variability

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35
Q

Symptoms of CMV in healthy adults

A

mild disease and unappareant
a. see fever, fatigue, sore throat, headache for 2-3 weeks w/ slightly elevated ALT
slight increase in lymphotyces and swollen lymphnodes

36
Q

Mononucleuosis

a. Heterophile anitB is negative

37
Q

Key diagnostics for CMV

serology

A

Serology: IgM not reliable–t IgG will indicate recent or distant past infection
IgG avidity increase w/ time and helps distinguish btwn recent and past infectin

38
Q

See owls eye incluction body

A

CMV

ds DNA linear, icosohedral herpesvirus with tegument

39
Q

genome for CMV

A

ds DNA linear, icosohedral herpesvirus with tegument

40
Q

TX of CMV

A 
Ganciclovir (IV or valganciclovir)
 Foscarnet (IV)
 Cidofovir (IV)
 CMV does NOT encode a thymidine kinase: acyclovir is less effective 
Anit-CMV IgG products given in parallel
41
Q

structual mimic of pyrophosphate will inhibit pyrophosphate binding site on viral DNA polym.

42
Q

synthetic 2’deoxycytidine analogue… doesn’t need phosphorylation and ≠viral DNA polymerase

43
Q

a. synthetic 2’deoxyguanosine analogue that’s activated by viral kinase
b. inhibits viral DNA polymerase

A

Ganciclovir

44
Q

Congeinital CMV: common congenital infection

1. 1 in 150 babies infected with CMV at birth and 1 in 750 have birth defects (1st semester = worse outcome)
2. Only 14% women have heard of CMV: key to educate women in childbearing age to decrease exposure
45
Q
  1. Perinatal infectinon of CMV: at time of birth from
A

ervical secreations/transmission via milk an IG no clincal signs

46
Q

Symptoms of congenital infection (CMV)

A

(poor outcome)
Petichial lesions/ small size/hepatoslenomegaly/jaundice
Permanent symptoms: hearing loss/ vision loss/mild-severe MR/Muskuloskeletal abnormatiles

47
Q

(poor outcome)
Petichial lesions/ small size/hepatoslenomegaly/jaundice
Permanent symptoms: hearing loss/ vision loss/mild-severe MR/Muskuloskeletal abnormatiles

A

congenical CMV infection

48
Q

CMV in immunosuppressed pts

A

Life threating: for transplant pts/ on immunosuppresants/undergoing chemo of HIV pts
Transplant pts: solid organ or hematopoietic stem cell
a. at risk for pneumonia/ fever/hepititis/ encephalitis/retinitis/ neuropathy
b. CMV donor and recepient status is evaluated

49
Q

HIV with CMV

A

a.see retinits (rare if on HAART) or fever/esophatigis/ gastritis/colitis

50
Q

βHHV:

A

human herpes virus 6b

51
Q

Roseola virus:

A

Herpesverdia
HHV6b
ds DNA linear, icosohedral

52
Q

Herpesverdia
HHV6b
ds DNA linear, icosohedral

A

roseolavirus

53
Q

Roseolavirus:
viral genome can integrate into host chromosome: implications in transmission—INTEGRATES into host which is surprising bc this

A

a HUGE virus

54
Q

Diseaes: in children for roseolaviurs (HHV6)

1.____ of children over 2 are seropositive

55
Q

Roseola HHV6b symptoms:

A

have high fever~ 4 days, irritable, maliase and lympadenopathy
Rash occurs in 10% of kids 12-24 hours after fever breaks
no sequele and common cause of admittance to ER for pts

56
Q

have high fever~ 4 days, irritable, maliase and lympadenopathy
Rash occurs in 10% of kids 12-24 hours after fever breaks
no sequele and common cause of admittance to ER for pts

A

Roseola HHV6b

57
Q

see a kid tht was really sick… kinda got better then had really bad rasah!

A

roseolavirus

58
Q

Roseola can reactiate in SCT receptients and relpicates:

A

inside CD4+ T cells and site of latency

59
Q

Where is the site of replication and latency for Roseolavirus

A

inside CD4+ cells

60
Q

1st seen in Burkitt lymphoma in 64~~~ cancer causing virus
Seropositiveity: see over 95% are seropositive by 20yrs old
. 90% EBV +ve exhibit intermittent shedding w/out symptoms
Asymptomatic infections are common

A

EBV (HHV4) general

61
Q

Genreal on EBV

A

HHV-4 (gamma)
ds DNA linear, icosohedral
yes to tegment and env

62
Q

Transmission of EBV

A

saliva and blood

63
Q

Infection path of EBV

A

Infect cells in blood stream (B-cells) and disseminate throughout body, Bind to epithelial cells intially and then go to B-cells which rapidly proliferate (primary mono) causing formation heterophile antibodies and activation of atypical downey T-Cells to control infection (cause mono symptoms), infection may also produce latency leading to reactivation and spread of virus or cancer

64
Q

Disease caused by EBV

A

infectious mononucleossis
Post Transplant Lymphoproliferative Disorder (PTLD) and see low survivial
Lymphomas~~ B, T, and NK cell

65
Q

Possible outcomes of infection of EBV:

A

replicate in B cells or epithelial cells
~~~latent infection in memory B cells and limits whre it infects the body
Stimulate and immortalize B cells

66
Q

When first infected with EBV it will infect what cell tyep

A

B cells and then latently in memory B cells

67
Q

EBV:

slow replication, limited host range,bind epithelial cells of pharynx or ____and have early, and late gene expression,

68
Q

EBV encodies its own______machinery to replicate DNA and make new viral particles—

A

DNA replication

69
Q

With EBV, reactivation of latently infected activated B-cells Latency _____- result of viral antigens in memory B cells cause cancers and

70
Q

Latency type_____-result of viral antigens in proliferating B cells cause infectious mono, and post-transplant lymphoproliferative disease

71
Q

type causes mono and PTLD

72
Q

________ is the ONLY time you get mononucleossis (Lat III!!!)

A

Primary infection

73
Q

see atypical T or ‘DOWNEY “ cells and Heterophile antiB (good diagnostics for mono d/t EBV)

A

EBV at Lat III

74
Q

Humoral response to EBV

A

see neutralizing antiB which has no effect on virus SHED but good for antiB diagnostics

75
Q

Cell mediated reponse to EBV

A

CD8 +T lymphs and NK cells—lysis of EBV infected cells

a. see loss of T cell fnx resulting in B cell proliferative diseaes
b. Mono results from rapid proliferation of atypical T cells—Downy cells

76
Q
  1. EBV diesae: overactive immune response: infectious mononucleosis and EBV mediated _______ imortalization and lack of effective immune control (PTLD)
77
Q

lack of effective immune control in EBV can lead to

78
Q

During Cell mediated response to EBV: see loss of T cell fnx resulting in

A

B cell proliferative diseaes

79
Q

EBV-mediated B cell proliferative disease

	a. immunosuppresive therapy activates infection and seen in 1-33% of organ transplants
	b. w/in first year after transplant and arises in donor B cells or reactivation in recepient
	c. low risk if graft contains donor T cells—if there are already T cells that work against EBV
A

Post Transplant Lymphoproliferatieve disorder

80
Q

EBV mononucleosis test

A

a. test for heterophile antiB by agglutination of animal RBCs!!! Key.. animal blood will agglutinate from the heterophile antiBs

81
Q

Lab test for PTLD

A

flourescent int situ hybridization to EBER RNA in neoplastic cells and NAT PCR

82
Q

Burkitts lymphoma

	a. B cell lymphoma of jaw and face seen in kids in africa
	b. associated wth chromosomal translocation btwn chr 8 and 14
	c. IgG promoter-myc prot-oncogene
A

General on Burkits

83
Q
  1. Burkitts lymphoma
    B cell lymphoma of jaw and face seen in kids in africa associated wth chromosomal translocation btwn chr
    IgG promoter-myc prot-oncogene
84
Q

EBV DNA in epithelial tumor cells and seen in china/alaska/E. Africa

A

Nasopharyngeal epithelial carcinoma:

85
Q

Disease: assocaited with KS, primary effusion lymhoma (PEL) and muticentric casteman disease (MCD)

A

Kaposis sarcoma

HHV8 (gamma)

86
Q

Kaposis Sarcoma: general

A

HHV-8
gamma Herpes virus
dsDNA

87
Q

Kaposis Replication in what cells:

A

CD19+ periperal B cells, endothelial cells, monocytes and epithelial cells

Immunology 3 (20 decks)

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