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Viral Pathogenesis And Infection > Molecular Biology And Human Herpes 1 > Flashcards

Molecular Biology And Human Herpes 1 Flashcards

1
Q

How are herpesviruses transmitted?

A

Via intimate contact with body fluids

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2
Q

What is the herpes virus structure?

A

Linear ds DNA genome

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3
Q

What are alpha herpesviruses?

A

Herpes simplex virus types 1 and 2, and varicella-zoster virus

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4
Q

What are characteristics of alpha herpesviruses?

A

Short replicative cycle, broad host range, characteristically establish latent infection in sensory nerve ganglia

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5
Q

What are beta herpes viruses?

A

Cytomegalovirus, human herpesviruses 6 and 7

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6
Q

What are characteristics of beta herpesviruses?

A

Long replicative cycle, restricted host range
Establish latent infection in secretory glands or reticuloendothelial system and the kidneys

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7
Q

What are gamma herpesviruses?

A

Epstein-Barr virus and human herpes viruses 8

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8
Q

What are characteristics of gamma herpes viruses?

A

Very restricted host range
Latent infection in lymhoid cells
Lytic infection in specific epithelial

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9
Q

What is the HSV1 genome?

A

Segmented linear genome, unique long and short covalently attached molecules

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10
Q

How many different genome rearrangements can HSV-1 genome have?

A

Both segments (long and short) can be inverted, resulting in 4 different genome rearrangement possibilities
(P, IL, IS, or ILS)

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11
Q

How many different glycoproteins of HSV-1 are there?

A

12
(B, C, D, E, G, H, I, J, K, L, M and N)

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12
Q

What is overview of HSV-1 life cycle entry?

A

Virus particles encounters a cell, glycans on surface allow lots of things to weakly assocaited, low affinity reactions before virus bumps into primary receptor and initiates high affinity
Then get fusion and glycoprotein D undergoes structural change to induce membrane fusion then release of capsid into cytoplasm

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13
Q

What happens in HSV-1 following fusion?

A

Capsid is released to cytoplasm with some attached tegument proteins
VP16 separates and translocates to the nucleus
Capsid travels to the cell nucleus using microtubukes
Linear DNA enters the nucleus

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14
Q

What happens in HSV-1 immediate early transcription?

A

VP16 enters the nucleus with HCF-1 and Oct-1
Transcription of alpha genes
ICP0
ICP4
ICP22
ICP27

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15
Q

What does ICP0, 4, 22 and 27 do?

A

0 - potent transactivator of gene expression
4 - positive regulation of intermediate and late genes
22 - regulates expression of 0
27 - negatively regulates alpha genes and upregualted late genes

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16
Q

What happens in HSV-1 early transcription?

A

Alpha genes participate in transcription of beta genes
Genes work cooperatively to induce transcription of late gamma genes
True-late genes down-regualte beta gamma genes progressively expressed, gene transcription

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17
Q

What happens in HSV-1 encapsulation?

A

Mature, DNa containing capsids exit nucleus
Glycoproteins traverse form ER thorugh Golgi to the cell surface
Capsid acquire elements of tegument en route to exosome machinery
Mature particle buds from exosome

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18
Q

What stimulates alpha gene expression?

A

VP16

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19
Q

What is the negative feedback loop of alpha beta and gamma genes?

A

Alpha genes stimulate beta genes
Alpha and beta genes simulate gamma gene trasncpriton
Gamma genes downregulate beta genes
Gamma and beta genes downregulate alpha genes

20
Q

What is lysis event of HSV-1 induced by?

A

Caspase 8 activation

21
Q

What cell type does HSV-1 primarily infect?

A

Epithelial cells
But can invade and replicate in CNS, establishing latent infection in dorsal root ganglia

22
Q

What are the key features of HCMV life cycle?

A

Oropharyngeal cavity is seeded and lungs become infected
Innate effector recruitment
Imamate immune cell infection
Primary dissemination
Viral replication to high titre
Secondary dissemination
Viral replication in salivary gland, mammary glands, kidneys etc.
HCMV infected bodily secretions

23
Q

What is the prevalence of HCMV in adult populations?

A

Is roughly 70%

24
Q

How is HCMV transmitted?

A

Via urine, saliva, blood, tears, semen, breast milk, transplanted organs and blood transfusions

25
Q

How can HCMV enter?

A

Tries to enter via fibroblast - get pH independent plasma membrane fusion
Epithelial cells - similar receptors bit endosome uptake - Endocytosis
Myeloid cells - macropinocytosis

26
Q

How does innate immune system detect cytosolic dsDNA?

A

CGAS detects dsDNA
CGAS catalyses synthesis of cGAMP
cGAMP activates mediator of IRF3 activation (MITA)
MITA activates IRF3 leading to transcription of type 1 IFNs

27
Q

Why is MITA important in HCMV

A

Important has HCMV will inhibit it , number of proteins act on this pathway to disrupt expression of type 1 interferons

28
Q

What does UL82 do in HCMV?

A

Inhibitors MITA

29
Q

What does HCMV latently infect?

A

CD33+/CD34+ cells in the bone marrow and differentiated CD14+ monocytes in the peripheral blood

30
Q

How does HCMV reactivate?

A

Occurs when HCMV-infected cells enter the tissue, cells differentiate into macrophages or dendritic cells
Spread of locally-reactivated HCMV infection is prevented

31
Q

What is reactivation of HCMV mostly assocaited with?

A

Pneumonitis

32
Q

What is the seroprevalence of EBV?

A

80-90%

33
Q

Where does EBV replicate?

A

In epithelial cells of the pro-pharynx

34
Q

Where does EBV establish latent infection?

A

In dividing populations of B cells

35
Q

How does EBV entry occur?

A

Not just one mechanism
Have clusters of glycoproteins that cna bind different ligands to infected either a B cell (CD21/MHC2) or epithelial cell (integrins)

36
Q

What is primarily involved in initiating fusion of EBV?

A

GHGL

37
Q

What does primary infection with EBV lead to?

A

Infectious mononucleosis

38
Q

What does chronic infection of B cells from EBV lead to??

A

Burkitt’s lymphoma
Nasopharyngeal carcinoma
Primary effusion lymphoma

39
Q

What type of burkitt’s lymphoma is EBV assocaited with?

A

Endemic BL

40
Q

What is the likely cellular origin of EBV assocaited burkitt’s lymphoma?

A

B cells of the germinal centre

41
Q

What is EBV-associated nasopharyngeal carcinoma?

A

Rare type of cancer affecting the throat connecting the back of the nose to the back of the mouth

42
Q

What does the development of nasopharyngeal carcinoma involve?

A

Early exposure to environmental factors
Early exposure to high risk EBV subtypes
Hereditarily genetic predisposition
EBV-induced genetic destabilisation in NP cells

43
Q

What is NPC genetic predisposition?

A

More common in men
Increased prevalence in south-eastern Asia and southern china

44
Q

What is PEL?

A

EBV assocaited primary effusion lymphoma
Is a rare B cell lymphoma

45
Q

Where is PEL usually found?

A

In body cavities

46
Q

What is an effusion?

A

An abnormal collection of fluid in hollow spaces or between tissues of the body

Viral Pathogenesis And Infection (16 decks)

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