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Medical virology > Gammaherpesvirus > Flashcards

Gammaherpesvirus Flashcards

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USMLE® Step 1 flashcards
1
Q

What are gammaherpesviruses?

A
  • herpesvirus
  • dsDNA genome
  • infect lymphoblastoid cells and some epithelial cells
  • typically target and latently infect T and B cells
  • Epstein Barr Virus, Kaposi’s Sarcoma Virus
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2
Q

Describe EBV

A
  • most common persistent asymptomatic infection in humans
  • 90-95% of the population
  • first human tumour virus to be discovered
  • latently infects B cells
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3
Q

Name 3 diseases EBV is associated with

A
  • human cancers
  • infectious mononucleosis
  • multiple sclerosis
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4
Q

How is EBV transmitted?
What age group is most commonly affected?
What affects associated diseases?

A
  • transmitted through saliva
  • most people are infected by the age of 8 but can be older in resource-rich places
  • EBV-associated cancers are more and less prevalent in different geographical areas
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5
Q

What are some diseases associated with EBV infection?

A
  • infectious mononucleosis - chronic immune dysfunction
  • B cell disorders and cancers
  • multiple sclerosis
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6
Q

What are some cancers associated with EBV infection?

A
  • Burkitt’s lymphoma
  • nasopharyngeal carcinoma
  • Hodgkins and non-Hogkins lymphomas
  • 50% of people with these cancers have encountered EBV
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7
Q

Describe the EBV virion structure

A
  • envelope glycproteins allow entry and antigenicty
  • nucleocapsid surrounds the DNA
  • tegument proteins like all herpesviruses
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8
Q

Describe the EBV genome

A
  • linear but forms a circle in the host nucleus
  • many miRNAs are important in its latency
  • EBNA regions of RNA are involved in perturbing host innate responses
  • EBER 1-6 and LMP proteins involved in latency
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9
Q

How does EBV enter cells?

A
  • attachment protein, 4 fusion proteins and gH/gL complex important here
  • targets for neutralising Abs and vaccines
  • interacts with CD21 on epithelial and B cells
  • additionally interacts with CD35 and MHC II on B cells
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10
Q

How does EBV infect and go from primary to latent infection?

A
  • enters epithelial cells in the oro-pharynx and may replicate here
  • transcytoses through these to CD21 B cells
  • lymphoid organs such as tonsils establish pools of latently infected B cells
  • can sometimes reactivate and infect oro-pharyngeal epithelial cells and shed virus into the saliva
  • unsure of causes
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11
Q

What are the risk factors of infectious mononucleosis?

A
  • host genetics
  • increased age at initial EBV infection
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12
Q

What is infectious mononucleosis infection like?

A
  • high EBV replication in B cells in the oral cavity with up to 50% of memory B cells infected during the acute phase
  • rapid expansion of NK cells and CD8+ T cells
  • strong inflammatory response
  • fever, swollen glands for weeks
  • extreme tiredness for months
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13
Q

Describe the genome in latent EBV

A
  • transcriptionally silent and circularised
  • if the cell divides the genome is replicated with it
  • virus protein EBNA1 binds the genome and interacts with dividing chromatin to ensure this
  • 9 EBNA proteins are produced during latency but EBNA1 is the only one produced in all stages and is required for latent genome replicatin
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14
Q

What kinds of roles do EBV latent proteins play?

A
  • reduce apoptosis
  • regulate tumourgenesis pathways
  • many are required for the transformation of different B cells into latency-infected cells
  • others are involved in evading the immune response and aren’t vital for transformation
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15
Q

What are the functions of EBV latent non-coding RNAs / miRNAs?

A
  • maintain latency by targeting EBV lytic genes and modulating LMP1 expression
  • BART miRNAs target proapoptotic proteins and can inactivate TSGs
  • BHRF1 miRNAs aid in B cell transformation to latency
  • EBER1+2 contribute to the activation of innate immunity
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16
Q

What are the stages of EBV latency and how does gene expression change between them?

A
  • latency III has lots of gene expression - EBNAs, EBERs, LMPs, BARTs and BHFR1s
  • latency II has less expression - BARTs, EBER1+2 and LMPs
  • latency I has the fewest genex expressed - EBNA1, EBER1+2 and BERT miRNAs
17
Q

What kind of EBV latency is seen in cancer?

A
  • different latency states associated with different cancers
  • gastric carnionoma with II
  • burkitts lymphoma with I
  • differences are made more complicated by differences in miRNA expression
18
Q

What mutations are seen in Burkitt’s lymphoma?

A
  • chromosomal translocations resulting in c-myc oncogene activation
  • can occur due to EBV among other mechanisms
19
Q

What is Burkitt’s lymphoma?

A
  • non-Hodgkin’s B cell lympoma
  • tumours seen in EBV latency
  • EBV proteins can prevent apoptosis of cells with c-myc overexpression
20
Q

What is nasopharangeal carcinoma?

A
  • epithelial tumour associated with EBV latency
  • EBV almost always present in malignant cells
21
Q

How is it thought thta EBV causes nasopharangeal cancer?

A
  • infection of epithelial cells in the lab doesn’t immortalise them
  • those with CDK/cyclin mutations can be immortalised
  • cells may already need specific mutations prior to infection for EBV to cause cancer
  • confirmed by the fact that EBV is usually found in high grade tumours not early staged ones
22
Q

What is multiple sclerosis?

A
  • chronic inflammatory and neurodegenerative CNS disease
  • risk factors include genetics, obesity, smoking and EBV
23
Q

What is some evidence of EBV association with multiple sclerosis ?

A
  • increased MS risk in those with history of infectious mononucleosis
  • decreased risk in seronegative people
  • increased levels of EBV-specific antibodies in those with MS
  • molecular mimcry between EBNA1 and CNS antigens
24
Q

Describe the potential role of molecular mimicry in the relationship between EBV infection and MS

A
  • antibodies from the CSF of MS patients recognise CNS proteins and EBNA1
  • they have cross-reactivity that can
  • immunisation of mive with EBNA1 peptides increased inflammation in the CNS
  • only seen in 25% of MS patients so may be other cross-reactive antibodies
25
Q

What factors hinder the development of an EBV vaccine?

A
  • no appropriate animal model
  • where to administer, how to administer, what to target?
25
Q

Are there any EBV vaccines in clinical trials?

A
  • 2 in phase 1
  • mRNA vaccine that targets glycoproteins on the virus particle
  • nanoparticle vaccine that targets surface protein gp350 on the virus and on virus infected cells
26
Q

What is Kaposi’s sarcoma virus?

A
  • gamme herpesvirus
  • causes all Kaposi’s sarcomas
27
Q

What cell types does KSHV infect?

A

many including B cells, epithelial cells, endothelial cells and DCs

28
Q

What is Kaposi’s sarcoma?

A
  • endothelial lineage tumours
  • highly aggressive in immunosuppressed/AIDS
  • KSHV latency in B cells and endothelial cells
29
Q

What forms of Kaposi’s sarcoma virus are there?

A
  • AIDS related
  • latrogenic - severity is correlated with amount of immunosuppression given after transplants
  • endemic - negative for HIV
  • classic/sporadic
30
Q

What diseases can Kaposi’s sarcoma virus cause?

A
  • Kaposi’s sarcoma
  • B cell lymphomas
  • lymphoproliferative disorders
31
Q

What kinds of treatments are used for KSHV diseases>

A
  • bolstering the immune system ie using ART in HIV
  • KS tumours can reoccur after chemotherapy
32
Q

Does EBV replicate in the epithelial cells it initially transcytoses through?

A
  • not sure
  • but much harder to establish infection through apical surfaces than basal in the lab
  • points towards infection of epithelial cells coming after B cell infection

Medical virology (15 decks)

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