#14 herpes viruses Flashcards

1
Q

what type of virus is herpesviridae?

A

persistant virus - it is latent

  • will have spurts of no detectable virus
  • will reactivate and produce viral shedding
  • sometimes can be shed without any symptoms
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2
Q

what are ways viruses can passively evade the host defence?

A
  • infect non replicating cells
  • infect cells that dont express MHC i.e. Neurons
  • target sanctuary sites i.e. eye
  • target immune cells

-spread by cell fusion: syncytia

be transported via free passage through the skin or mucosal layer i.e. organ transplant or needle

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3
Q

what are active evasion mechanisms used by viruses

A
  • limiting viral gene expression
  • non-cytopathic infection
  • block immune defences
  • block apoptosis
  • generate immunosuppressive and anergic epitopes
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4
Q

what is a characteristic of latent infection

A
  • having long periods of low or undetectable virus or disease
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5
Q
herpesviridae - 
what type of genome 
enveloped?
how big is genome
cytopathic?
A
dsDNA linear 
enveloped
large genome 150kB
cytopathic infection 
latent infection
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6
Q

when will herpesviridae reactivate

A

after immunosuppression or stress

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7
Q

what viruses are in alphaherpesviruses

where do they infect?

A
  • HSV1 and HSV1
  • Varciella Zoster virus VZV
  • they infect neurons
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8
Q

what viruses are in betaherpesviruses

where do they infect?

A

Cytomegalovirus (CMV)
Human herpesvirus 6 (HHV-6)
Roseola infantum (red cheeks)

they infect monocytes and on secretory tissue

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9
Q

what viruses are in gammaherpesviruses

where do they infect?

A

Epstein Barr virus EBV
Kaposi sarcoma virus HHV-8

they infect lymphocytes
b-cells for EBV

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10
Q

are any genes made from herpesviruses during latency?

A

minimal gene expression during latency - however LATS are made during latency
i.e. EBNA-1 to 6 for EBV

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11
Q

when are the early and late genes for herpesviridae made in relation to viral DNA replication

A

early genes including regulatory genes are made before the viral DNA replication

late genes include the capsid and envelope which are only made after viral DNA replication

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12
Q

name an early gene produced for HSV

A

HSV thymidine kinase

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13
Q

how does the viral genome of herpesviridae persist in the cell

A
  • it exists as a circular episome
  • present in the nucleus
  • ## there are two forms of the episome - replicating and non-replicating (latent genome)
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14
Q

explain EBV replication during latent stage

A
  • EBV infects B-cells
  • every time the B-cell divides the latent EBV will replicate too
  • EBV Ori-P will be used to replicate the episome in latent infection
    EBNA-1 will bind to Ori-P
  • the circular genome will be replicated
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15
Q

explain EBV replication during lytic stage

A
  • promotor used will be Ori-Lyt
  • replication will occur via rolling circle
  • the linear DNA will be replicated
  • new virus particles are made
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16
Q

how does EBV seperate the lytic and latent replication of virus?

A

it uses two promoters

  • Ori-P for latent infection
  • Ori-Lyt for lytic infection
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17
Q

what does HSV in the CNS cause

A

herpes simplex encephalitis

18
Q

how is herpes simplex encephalitis diagnosed

A

PCR of CSF fluid

19
Q

how does primary infection of HSV work

A
  • virus replicates on skin
  • gains access to sensory nerves
  • travels via retrograde transport to nerve body
  • latent genomes in nerve (T-cells keep it in check)
  • virus usually doesnt transfer on to the brain
20
Q

how does HSV re-occur?

A
  • travels via axonal transport

- cause cold sores on same spot it initially infected

21
Q

what is expressed in a latent infected cell of hsv?

A
  • genome is present
  • no structural genes
  • some LAT mRNA
    (no LAT proteins)
22
Q

what family is varciella zoster virus

A

herpesviridae

23
Q

what does VZV cause

A
  • initial infection is chicken pox

- can resurface as Zoster (shingles)

24
Q

explain the infection process of VZV

and how it goes latent

A
  • infection of conjunctiva or mucosa of RT
  • viral replication in regional LNs
  • primary viremia
  • further replication in liver and spleen
  • secondary viremia
  • infection of skin causing vesicular rash (chickenpox)
  • it will gain access to the sensory nerves and lay dormant in the nerves - can spread throughout the ganglion
  • will resurface as shingles across a whole dermatome (commonly associated with immune deficit)
25
Q

how do you treat VZV

A

antiviral chemotherapy
or
passive immunisation with Zoster immunoglobulin

26
Q

what type of vaccine is the chickenpox vaccine

A

live attenuated

27
Q

what type of virus is EBV

A

-herpesviridae

28
Q

what does EBV cause

A

glandular fever

infectious mononucleosis

29
Q

how is ebv aquired

A

direct contact of oropharynx with infected saliva

30
Q

what is a characteristic sign of EBV infection

A

swollen lymph nodes

31
Q

where is productive infection of EBV made?

where is latent infection?

A

in the nasopharynx and salivary glands - virus is produced here

latent infection is in B-cells - virus does not replicate here it is just the site of latency

32
Q

what percentage of people are infected with EBV

A

90%

33
Q

explain the process of EBV infection

A
  • Primary site infection is the oropharyngeal cavity (URT)
  • Initial infection is lytic in the epithelial cells - there is expression of full complement of viral genes
  • It then Spreads to B cells as they come to defend
  • generates widespread immune response (e.g. CTL response) – results in swelling of the lymph nodes.

B-cells become the reservoir for latent infection

  • Episome is maintained by Ori-P and EBNA-1 viral protein in b-cells! (non-productive replication)
34
Q

are there any genes expressed in latent EBV infection? what are they

A

limited no. of genes expressed

EBNA 1 to 6 are expressed

LMP 1 & 2

35
Q

what is the job of EBNA1 in EBV infection

A
  • used in latent stage in b-cells
  • needed to replicate the episome in non-lytic phase
  • will bind to the Ori-P region and drive replication in dividing b-cells

needed for viral replication in latency

36
Q

what are the 3 types of EBV infection with in b-cells and what diseases to they result in

A
  • Type I: has all 9 latent Antigens, will result in lymphoproliferative disease
  • Type II: has 3 latent antigens, will result in Hodgkin’s lymphoma
  • Type III: only the EBNA-1 antigen, results in Burkitt’s
37
Q

tumorogenesis is associated with what virus in herpesviridae?

A

EBV

38
Q

what family in CMV

A

herpesviridae

39
Q

who is at particular risk of CMV?

A

newborn babies - it is the leading cause of still birth

CMV infection can cause deafness, blindness, microencephaly

also a major cause of death in bone marrow transplant patients

40
Q

what can reactivate CMV in adults?

A

immunosuppression i.e. AIDS