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Renal, Hematological, and Cardiovascular Organ Systems > CMV, EBV, and KSH pp and outline > Flashcards

CMV, EBV, and KSH pp and outline Flashcards

1
Q

what are the similarities of CMV EBV and KSHV?

A
  • all are herpesviruses
  • all share a tropism for lymphocytes
  • EBV and KSHV are oncogenic viruses
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2
Q

What are the properties of a herpesvirus?

A

-linear, dsDNA (150-250 kbP)
-icosahedral capsid, enveloped, dozen glycoproteins
-DNA is replicated and viruses are assembled in the nuvleus
(the tegument is the space between the DNA core and capsid and the envelope

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3
Q

Where does replication of herpesvirues occur?

A

genome is replicated and viruses assembled in the nucleus

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4
Q

what is the general concept about herpesviruses and infections?

A

in general, herpesviruses produce self-limiting infections but life-threatening infections or cancers can occur, esp in immunocompromised hosts

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5
Q

What are the three types of herpesviruses? how many total?

A

8 total with three classifications
alphaherpesviruses
betaherpesviruses
Gammaherpesviruses

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6
Q

What are the alphaherpesvirinea and what is important about them?

A

neurotropic for latency, aggressive lytic growth
Herpes simplex virus type 1 (HSV-1)
HSV-2
Varicella-zoster virus (VZV)

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7
Q

What are the Betaherpesvirinea and what is important about them?

A

lymphotropic for latency, more insidious
Cytomegalovirus (CMV)
Human herpesvirus 6 (HHV-6)
HHV-7

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8
Q

What are the Gammaherpesvirinea and what is important about them?

A

Lymphotropic for latency, more insiduous
Epstein-Barr virus (EBV)
HHV-8 (Kaposi’s Sarcoma-associated herpesvirus; KSHV)

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9
Q

What is the general gene structure for HSV-1, EBV and HCMV?

A

-protypical genomic structures
2 unique structures (ULong and Ushort) that encode for unique viral proteins
– unique long and short sequences(code of viral proteins) are bracketed by inverted repeat sequences the genes that are specific sequences, and so found in two copies of the virus, going in the opp directionof the UL or US sequence
–EBV differnce: multiple internal repeat area all going the same direction, unknown siginficance
HCMV-identical to HSV

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10
Q

What is the lytic cycle?

A

Herpesviruses undergo lytic replication in a variety of cell types to propagate the virus

  1. Following virus attachment, penetration occurs by virus glycoprotein-mediated fusion of envelope and plasma membrane
  2. Released nucleocapsid migrates to nuclear envelope via microtubules, uncoats, and DNA enters the nucleus. Certain of the virion components act to shut off host macromolecular synthesis
  3. Programmed expression of viral genes- cascade regulation
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11
Q

What is the gen-cascade regulation?

A

a. immediate early (IE) genes are virus-specific transcription factors
i. use host RNA polymerase II
ii. stimulate transcription at virus early promoters
b. early genes are next expressed, encode many nonstructural proteins, enzymes
i. DNA replication machinery, including viral DNA polymerase
ii. thymidine kinase (tk) which phosphorylates a variety of nucleotides besides thymidine
c. late genes are also dependent on IE transcription factors plus genome replication for expression
i. encode structural proteins (capsids, glycoproteins)
ii. viral glycoproteins are incorporated into virus envelopes and also transported to infected cell surface where they can cause syncytia formation
d. virus assembly occurs in the nucleus where nucleocapsids bud first into the perinuclear space
e. virus particles migrate to the cell surface where they are released

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12
Q

Can these viruses also undergo latency? if so what is this?

A 
YES!
Occurs soon after initial infection
No virus particles are produced
Entire genome is maintained extrachromosomally
Few viral genes are expressed
3 stages
Establishment
Maintenance
Reactivation
Latency leads to life-long infection
Latency can lead to recurrent infections or sometimes cancer, but this generally requires an immunodeficiency for CMV, EBV, or KSHV
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13
Q

What are the three stages of latency?

A

Establishment
maintenance
reactivation

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14
Q

what is reactivation?

A

Reactivation generally occurs when there is a lapse in immunity and results in the production of virus particles and recurrent infection

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15
Q

What is result of latency?

A

anyone infected with a herpesvirus is infected for life and runs the risk of having recurrent infections or other sequelae (such as cancer)

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16
Q

What are the antivrials used for txment?

A

Acyclovir
Ganciclovir
Foscarnet

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17
Q

What is Acyclovir?

A

a prodrug that is activated by viral thymidine kinases, and adds a phosphate group
has low side effects
not as effective as ganciclovir

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18
Q

what is ganciclovir?

A

-a ganosine analog similar to acyclovir, the prototype which is used in HSV, VZV and EBV
anyone infected with a herpesvirus is infected for life and runs the risk of having recurrent infections or other sequelae (such as cancer)

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19
Q

What is focarnet?

A

Foscarnet is approved for CMV retinitis treatment in AIDS patients
a. Pyrophosphate analog that inhibits DNA polymerase, but does not require phosphorylation for activity

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20
Q

what is cidofovir?

A

Cidofovir is a deoxycytidine analog

a. Competitive inhibitor of CMV (and HSV) DNA polymerase, but does not require viral kinase action for activity
b. approved for CMV retinitis treatment in AIDS patients

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21
Q

Anti-herpetic drugs cannot cure herpes infections nor treat cancers caused by EBV or KSHV– why is this?

A

Antivirals inhibit virus replication to limit infection. Viruses are not replicating during latency, hence the genomes are not affected and remain. Oncogenesis is also the result of latency, not acute infection.

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22
Q

How contagious is cytomegalovirus?

A

not very

  • Still, early infection and adult rates up to 80% in lower socioeconomic settings
  • In higher socioeconomic settings, typically acquired after age 16 and about 50% rate in adults
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23
Q

How is CMV transmitted?

A
  • Sexually transmitted

- direct contact with secretions (saliva, urine, breast mild, semen, cervical secretions, blood) not by aerosol

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24
Q

What are the most at risk pts?

A

Neonates
–In utero infection, 1% of US births
–90% of infections are asymptomatic, but can result in deafness and mental retardation
Day care workers
Pregnant workers
Gay men
Immunocompromised, especially transplant patients
–AIDS patients are susceptible to retinitis, colitis, and pneumonia

25
Q

Where is the primary replication of CMV occur?

A

Epithelial cells adn then spreads to lymphoid tissue

-latent in B and T cells, monocytes and lymphocytes where is causes large puffed up cells

26
Q

What are the symptoms of CMV?

A
  • Neonatal infections can occur in utero; most are asymptomatic, but can result in retardation and deafness
  • Childhood infections are mostly asymptomatic
  • Adult infections may result in mononucleosis with fever
27
Q

What are the main things about immuoncopromised hosts and their risk to CMV?

A
  1. Most organ transplant patients get CMV infection with pneumonitis representing the most life-threatening aspect
    a. Can result from infection by CMV+ donor or by reactivation of CMV+ recipient
    b. Prophylactic treatment with CMV Ig and ganciclovir looks promising in limiting complications
    c. When you think transplant patient, think CMV!
  2. AIDS patients are prone to CMV retinitis, colitis, and pneumonitis
28
Q

How can you diagnosis CMV?

A
  1. ELISA or PCR detection
  2. Shell vial assay in which indirect immunofluorescence is used to detect an immediate early protein after 24 h of cell culture infection
  3. Detection of large lymphoctyes
29
Q

Will most transplant pts develop CMV and should somptoms?

A

Most transplant patients will develop CMV infection, but not all infections will lead to disease symptoms

30
Q

How can an infection by CMV occur?

A

Infection can occur by receipt of CMV+ organ or by reactivation of CMV+ recipient

31
Q

What is the most severe out come from CMV in transplant pts?

A

is pneumonia about 1-4 months after transplant (preceded by fever)

32
Q

How can CMV be treated in transplant pts?

A

Selective prophylaxis with CMV Ig and ganciclovir

33
Q

What should ou think when you think about a transplant pt?

A

CMV!!!!

34
Q

How prevalent is EBV infection?

A

VERY!!!
Greater than 90% of US population is seropositive for EBV
Early infection in lower socioeconomic settings, mostly asymptomatic
Teen and young adult infections in higher settings, can result in infectious mononucleosis

35
Q

Is EBV infection symptomatic if so what can it cause?

A

infectious mononucleosis in adult populations

36
Q

What can EBV cause in immunocompromised pts?

A

oral hairy leukoplakia
can by txed by acutx to clean up the area, but will return when txment stopped
-Productive infection of tongue epithelial cells
-Rarely seen except in AIDS patients

37
Q

What does EBV cause in post transplant pts?

A

posttransplant lymphoproliferative diseases

a. Uncontrolled proliferation of B cells due to their transformation by EBV and the absence of CTLs to control them
b. Highest risk is in seronegative transplant recipients in the first year
c. Treatment: stop immunosuppression
i. Must monitor for rejection
ii. ACV not useful because the infection is latent, virus is not replicating

38
Q

What neoplasms are associated with EBV?

A

Burkitt’s lymphoma and nasopharyngeal, carcinoma, mixed cellular hodgkins lymphoma

39
Q

What is the pathogensis of EBV?

A
  • Spread through saliva
  • Incubation period is several weeks (4-7)
  • Initial replication in oropharyngeal epithelium, spread to lymphocytes and then liver and spleen
  • EBV remains latent in throat epithelia and B cells,
  • there can be oral shedding for weeks
40
Q

What are the smyptoms of EBV?

A
  • most are asycmptomatic
  • Infectious mononucleosis
    a. Sore throat, fever for one to two weeks, malaise, lymphadenopathy
    b. Recovery is uneventful
41
Q

How can you diagnose EBV?

A
  1. Diagnosis is based on symptoms and presence of at least 50% atypical, large lymphocytes with lobulated nuclei
    a. Large lymphocytes are T-cells responding to the infection, not the infected B-cells
  2. Important antigenic markers
  3. Diagnosis can also include looking for heterophile antibodies (Monospot test)
42
Q

What is important about antigenic markers in EBV?

A
  1. Important antigenic markers
    a. EBNA – EBV nuclear antigens arise early in primary infection
    i. EBNA 1 maintains genome replication in dividing B-cells
    ii. Conversion to anti-EBNA IgG indicates resolution of primary infection
    b. VCA viral capsid antigen
    i. Anti-VCA IgM indicates primary infection
    ii. Anti-VCA IgG without anti-EBNA indicates primary infection
    iii. Anti-VCA IgG and anti-EBNA IgG indicates past infection
    c. EA early antigen is detected in cells that do not produce virus
43
Q

What does a monosport test should?

A
  1. Diagnosis can also include looking for heterophile antibodies (Monospot test)
    a. These antibodies agglutinate sheep red blood cells
    b. Not present in all patients, origin not understood
    c. If present, will distinguish EBV mono from CMV mono
44
Q

What is the treatment for EBV?

A
  1. Treatment is supportive for mono; withhold athletes due to possible inflammation of spleen
  2. Treatment of oral leukoplakia is with acyclovir
45
Q

What is Burkitt’s Lymphoma?

A

a. Neoplasm of B-cells that affects bones of the jaw
b. Endemic in central Africa and New Guinea
c. Associated with three factors
i. Early EBV infection leading to latency
ii. Activation of c-myc
iii. Malaria
d. Early detection allows cure rate of 80%
e. Outside of Africa, only 20% of BL patients have EBV genomes in tumor

46
Q

What is Nasopharyngeal carcinoma?

A

a. Neoplasm of epithelial cells
b. Association with EBV is worldwide
c. High frequency in southern China: high salt diet likely cofactor
d. Initial presentation is painless lump in the neck
e. At best, only 60% of patients survive ten years
100% associated with EBV!!!

47
Q

What else is EBV linked too and why?

A

Hodgkins’ lymphoma
Multiple sclerosis
B/c disease that develop later in life and so could have some interactions..

48
Q

Compare and contrast CMV and EBV

A

Both can cause mono and are latent in B cells. Both can cause post-transplant complications, but presentation is different. CMV is sexually-transmitted and a source of congenital infections. CMV is always heterophile antibody negative. EBV is a known oncogenic virus.

49
Q

How closly related to kaposi’s sarcoma is KSHV?

A
  • Necessary but not sufficient to cause Kaposi’s sarcoma (KS)
  • DNA can be amplified from B-cells of classical KS and AIDS KS patients
  • > 80% seropositivity among KS patients, essentially 0% among US blood donors
50
Q

what types of abnormalites are associated with KSHV?

A

B-cell and endothelial latency tropism

  1. KS tumors occur in the lining of the lymphatic system
  2. The lymphatic channels fill with blood cells, hence the bluish, bruised appearance of lesions
51
Q

What is the transmittion of KSHV?

A

Sexually-transmitted among gays (through saliva?)

in Mediterranean populations and sub-Saharan Africa (NOT sexually transmitted in these cases.. )

52
Q

What is unique about KSHV being sexually transmitted?

A

In US, most KS patients are AIDS patients

  1. Sexually-transmitted, but virus is absent from semen and vaginal secretions
  2. Virus is present in saliva; exactly how sexually transmitted is not understood
53
Q

How long is the time to onset of KS after investion?

A
  • In the past, 50% of AIDS patients would develop KS within 10 years of diagnosis
  • -Now, 95% of infections are asymptomatic, can be mild when symptomatic
  • -Tumor-specific treatment or target HIV, but not HHV-8
54
Q

What must the infection also accompany for disease symptoms to occur?

A

Infection must be accompanied by loss of immune system for disease symptoms

a. Old age in classical forms
b. AIDS in gay populations

55
Q

What can HHV-8 also cause?

A

other B cell abnormalities

  • Primary effusion lymphoma
  • multicentric Castleman’s Disease
56
Q

What is primary effusion lymphoma?

A

a. Non-Hodgkin s B-cell lymphoma
b. Commonly found in body cavities
c. Mean survival time 2-6 months
d. KSHV found in virtually all tumors of HIV+ patients

57
Q

What is castleman’s disease?

A

a. Lymph node tumors, not strictly a cancer

b. KSHV found in virtually all tumors of HIV+ patients

58
Q

What do you do when symptomatic for HHV-8?

A

When symptomatic, treatment in AIDS patients is tumor-specific (resection, chemotherapy) or targets HIV, but not HHV-8

Renal, Hematological, and Cardiovascular Organ Systems (9 decks)

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