Viral Persistence Flashcards

1
Q

What is the decision point following acute infections?

A

Either goes into chronic infection or the immune system overcomes the virus

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2
Q

What is annelovirus?

A

A negative strand DNA virus that is in all of us and is a chronic virus but doesn’t really cause any disease

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3
Q

What is interesting about ERVs (endogenous retroviruses)?

A

They are retroviruses that have integrated themselves into our genomes, and got into the Germline at some point, about 9% of our genomes are ERVs.

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4
Q

What persistent infections occur in neuronal cells/CNS?

A

HSV-1
JC virus

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5
Q

What persistent virus infections occur in the liver?

A

HBV
HCV

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6
Q

What persistent virus infections occur in immune cells?

A

HIV-1
HTLV
HHV6
EBV

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7
Q

What are the two ways of viral genome being maintained in the cell?

A

Main way is episomal replication in the nucleus
Alternative is what retroviruses do and integrate its genome into host chromosomes

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8
Q

Why do some viruses benefit from autophagy?

A

Protect against cell death
Maintains viral reservoir
Enhance virus production

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9
Q

Why do some viruses have to combat autophagy?

A

Sequesters virus particles
Promotes latency

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10
Q

What HCV protein inactivates RIG-I signalling?

A

HCV NS3

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11
Q

What is incorporated into virions to inactivate complement?

A

CD55/CD59

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12
Q

What does EBNA-1 do?

A

Prevents processing of viral proteins therefore stops activation of T cell response

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13
Q

What happens when herpes virus goes into latent stage?

A

No viral DNA or RNA produced, no activation of immune response, dont get activation of recognition

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14
Q

What is the virus in which we know there is a largest amount of genetic difference in a single host?

A

Hepatitis C virus, one species of virus, 40% difference in its nucleotide sequence

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15
Q

Why does hepatitis C have such a large genetic difference?

A

RNA-dependent RNA polymerase has no error checking

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16
Q

What happens when a cell is infected in lytic stage with herpesvirus?

A

That cell will be destroyed, this is what causes cold sores

17
Q

Where do alphaherpes viruses establish latent infections?

A

In sensory neurones

18
Q

What are beta gene expressions?

A

Polymerases and replication enzymes

19
Q

When are LATs produced?

A

During replication, as long as virus has infected the right cell, it can go into latent stage and produce LATs

20
Q

What are most LATs?

A

Intron sequences spliced from an 8.3kb transcript

21
Q

What do LATs do?

A

Promote cell survival - (block Nfkappab, block apoptosis)
Inhibit AKT kinase, can switch off process associated with caspase 3 recruitment and activation - apoptosis

22
Q

Where does EBV establish productive infection?

A

In the oropharyngeal mucosa

23
Q

What type of virus is EBV?

A

Gammaherpesvirus

24
Q

What type of cell does EBV establish latency within?

A

B cells

25
Q

What does EBNA-1 do?

A

Required by the cell in latent states - expressed in all stages of latency

26
Q

What does EBNA-1 bind to?

A

OriP

27
Q

What are the two essential elements of OriP?

A

DS and FR

28
Q

What is DS in OriP?

A

Contains 4 low affinity binding sites for EBNA-1 and is the origin of replication

29
Q

What is FR in OriP?

A

Contains 20 copies of a 30bp sequence, each containing a high affinity site for EBNA-1

30
Q

What inhibits EBNA-1 from being degraded?

A

Has a Gly-Gly-Ala repeat at its amino terminus

31
Q

What is EBV latency I expression of?

A

EBNA-1 and LMP-2A only

32
Q

What is latency II expression of?

A

EBNA-1, LMP-1 and LMP-2

33
Q

Where is latency-I found?

A

In EBV-positive Burkitt’s lymphoma, NK-cell lymphoma and gastric cancer

34
Q

Where is EBV latency II found?

A

Hodgkin’s disease and nasopharyngeal carcinoma

35
Q

How many genes are expressed in latency III?

A

9 EBV genes

36
Q

What are the chances of getting integration into transcripitonally active v non-active sites and why?

A

Into active sites is greater as it is rarely unwound