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I&I SC1 > Chronic viral infections > Flashcards

Chronic viral infections Flashcards

Lectures: -Week 2, day 3, lecture 1: Chronic viral infections - HIV-AIDS -Week 2, day 3, lecture 2: Chronic viral infections - Herpesvirus -Week 2, day 3, lecture 3: Chronic viral infections - HBV

1
Q

Which cells are primarily targeted by HIV?

A

CD4+ T-cells

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2
Q

What is the difference between HIV and AIDS?

A

HIV is the virus, AIDS is the clinical syndrome it causes

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3
Q

What is AIDS?

A

Aquired immune deficiency syndrome -> opportunistic infections arise due to the inability of coordinated immune responses due to a lack of CD4+ T-cells

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4
Q

What is the therapeutic strategy for HIV?

A

cART -> combination antiretroviral therapy

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5
Q

How many mechanistic classes of cART are available?

A

6

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6
Q

Why is antiretrovial therapy always used in combination with another type of antiretroviral therapy?

A

Retroviruses are prone to mutations -> combination of pathways prevents mutations causing resistance

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7
Q

What is the main obstacle to an HIV cure?

A

HIV latency

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8
Q

What is the entry receptor of HIV?

A

CD4 & a co-receptor, either CXCR4 or CCR5

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9
Q

What is HIV latency?

A

Cells not actively producing virus, but retaining the ability to do so because the viral genome is integrated into the host genome

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10
Q

What is the HIV viral reservoir?

A

All the latent cells, mostly CD4+ (memory) T-cells

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11
Q

When is HIV reactivated?

A

When the host cell is activated -> upregulates transcription (of virtually the whole genome) -> viral genome also activated

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12
Q

Which four factors influence HIV latency (mainly the amount of virus transcribed)? (4)

A
  1. Blocks at transcription initiation -> causes less gene expression
  2. Transcriptional read-throughs -> if the virus integrates at a transcriptinally less active site, there is less viral gene expression
  3. Transcriptional collision -> when the virus genome integrates backwards (as opposed to the host genome), RNA-polymerases bump into eachother during transcription -> less viral gene expression
  4. Integration near heterochromatin -> more densely packed nucleosomes -> lower transcriptional activity
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13
Q

How can a cell transcribe a gene containing the HIV genome, but not produce virus?

A

HIV-genes are commonly spliced out of genes

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14
Q

What is the so-called ‘shock and kill’ strategy for curing HIV?

A

Making cells visible to the host immune system by inducing the production of virus, then induce cell death or point the immune system to infected cells by immune activation

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15
Q

How can latent HIV be reactivated artificially?

A

Latency reducing agents (LRA)

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16
Q

What is the downside of using LRA’s in the shock-and-kill method?

A

LRA’s activate only part of the latent cells

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17
Q

What is the so-called ‘block and lock’ strategy for curing HIV?

A

Permantly silencing HIV transcription

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18
Q

Herpesvirus genomes are relatively [small/large], compared to other viruses

A

Herpesviruses have large genomes, encoding 70-200 proteins

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19
Q

What makes herpesviruses very stable in vivo?

A

The fact that they have a strong capsid

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20
Q

What is the portal complex in herpesviruses used for?

A

Enables injections of viral DNA into the particle, and allows DNA to leave the particle once a new host has been infected

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21
Q

Herpesviruses have a tegument. What is a tegument?

A

Structure between the capsid and the viral membrane, consisting of viral and host proteins

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22
Q

What are the structural layers of herpesvirus particles from outside to inside? (3)

A
  1. Lipid envelope, containing viral glycoproteins
  2. Tegument
  3. Capsid
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23
Q

What are the functions of the lipid envelope+glycoproteins of herpesviruses? (3)

A
  1. Attachment
  2. Cell-cell fusion
  3. Immune evasion
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24
Q

What are 4 common properties of all herpesviruses?

A
  1. Large genomes encoding a large array of enzymes, allowing them to take control of their own replication within the infected cell
  2. Herpesviruses make use of compartments in the host cell
  3. Production of infectious virus is generally accompanied by lysis of the infected cell
  4. Herpesviruses employ cellular latency as a mechanism for lifelong presence in their hosts
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25
Q

Which compartments do herpesviruses use for which processes? (2)

A
  1. Nucleus: virus gene transcription, synthesis of viral DNA and nucleocapsid assembly
  2. Cytoplasm: tegument construction & envelopment
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26
Q

What are the characteristics of lytic infection by herpesviruses? (3)

A
  1. Production of virus particles
  2. Cell-cel transmission
  3. Cell death

Results in disease

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27
Q

What are the characteristics of latent infection by herpesviruses? (3)

A
  1. No virus production
  2. No cell-cell transmission
  3. No cell death

No disease

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28
Q

Which three herpesvirus families are known?

A
  1. Alphaherpesvirinae
  2. Betaherpesvirinae
  3. Gammaherpesvirinae
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29
Q

What are the characteristics of alphaherpesvirinae? (4)

A
  1. Short replication cycle
  2. Rapid spread in culture
  3. Efficient destruction of the host cell
  4. Latency: primarily in sensory ganglia
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30
Q

What are the characteristics of betaherpesvirinae? (5)

A
  1. Restricted host range
  2. Long replication cycle
  3. Slow progression in culture
  4. Infected cells become enlarged -> cytomegalia
  5. Latency in secretory glands, lymphoreticular cells & kidneys
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31
Q

What are the characteristics of gammaherpesvirinae? (2)

A
  1. Restricted host range: T- or B-cells
  2. Latency in lymphoid tissues
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32
Q

What are the latency reservoirs of alpha-, beta- and gammaherpevirinae?

A

Alpha: sensory ganglia
Beta: secretory glands, lymphoreticular cells, kidneys
Gamma: lymphoid tissues

33
Q

How many human herpesviruses are known?

A

8

34
Q

To which location is HSV-1 usually linked? How do individuals become infected?

A

HSV-1 is associated with oral herpes
Mostly acquired early in life through parents

35
Q

To which location is HSV-2 usually linked? How do individuals become infected?

A

HSV-2 is associated with genital herpes
Mostly acquired through sexual contact

36
Q

What is unique about human herpes simplex viruses?

A

Most primates only have one herpes simplex virus; there are two varietis in humans

37
Q

What is meant by the ‘shifting epidemic’ of herpes simplex viruses? What induces this shift?

A

HSV-1 shifting to genital variant. This is caused by humans tending to get infected by HSV-1 at a later age -> when they become sexually active

38
Q

Where do herpesviruses enter the body, and where do they first start replicating?

A

Breached epithelium, after which they start replicating in the basal epithelial layers

39
Q

What are cold sores?

A

Blisters filled with fluid and viral particles, caused by herpesviral replication in basal epithelial layers

40
Q

How do herpesviruses reach neural ganglia?

A

Retrograde axonal transport

41
Q

What is the preferred ganglion of HSV-1?

A

Trigeminal ganglion

42
Q

Where is the viral genome located during herpesvirus latency? In what form?

A

Located in the nucleus in a circularized form

43
Q

How does the host cell react to latent herpesvirus DNA being present in its nucleus?

A

It chromatinizes the DNA to try to shut it down

44
Q

Which gene is still expressed by herpesvirus during latency? What is the function of this gene? (3)

A

Latency associated transcript (LAT)

Non-coding transcript that:
1. Blocks apoptosis of the host cell
2. Regulates histone tails on chromatinized virus
3. Represses innate immune responses in neurons

45
Q

True of false: to give clinical symptoms of HSV-1 reactivation, a minimum of 100 neurons have to undergo virus reactivation

A

False; during HSV-1 reactivation, only one or a few neurons experience virus reactivation

46
Q

What triggers herpesvirus reactivation? How?

A

Stress

Stress causes the host cell to change histone tails, loosening the viral DNA, allowing transcription

47
Q

True or false: HSV-1 can only be transmitted through cold sores

A

False; ther is quite a lot of asymptomatic shedding of the virus

48
Q

Which trigeminal branch is most often infected by HSV-1? What are the second and third?

A
  1. N. mandibularis (N. V3)
  2. N. maxillaris (N. V2)
  3. N. ophthalmicus (N. V1)
49
Q

How do herpesviruses end up infecting the opthalmic branch of the n. trigeminus?

A

Self-inoculation via the hands

50
Q

What happens when HSV-1 infects the central nervous system?

A

Encephalitis (rare)

51
Q

To which disease is HSV-infection of the CNS associated?

A

Alzheimer’s disease

52
Q

Which hepatitisviruses can cause chronic infections?

A

Hepatitis B virus (HBV)
Hepatitis C virus (HCV)

53
Q

What is the DNA type of hepatitis B?

A

Circular DNA, partially double stranded

54
Q

What is the DNA type of hepatitis C?

A

+-RNA

55
Q

What type of hepatitis can only exist with HBV?

A

Hepatitis D virus

56
Q

How can HBV be transmitted? (3)

A
  1. Blood-blood contact
  2. Contaminated needles
  3. Vertical transmission
57
Q

When is the chance of chronic HBV the largest?

A

When infected at young age (often after birth) -> 90% are chronically infected

58
Q

How many patients become chronically infected with HBV when infected at adult age?

A

10%

59
Q

How can HCV be transmitted?

A
  1. Blood-bloodcontact
  2. Contaminated needles
  3. Sexual contact
60
Q

How many HCV patients become chronically infected?

A

70%

61
Q

Vaccines are available for the following hepatitis viruses:

A

Hepatitis A, Hepatitis B

62
Q

What are the target cells of hepatitis B?

A

Hepatocytes

63
Q

What are the target cells of hepatitis C?

A

Hepatocytes

64
Q

What are the two possible therapies for HBV? (2)

A
  1. Immune modulationL PEG-IFNα
  2. Viral replication inhibitors: entecavir, tenefovir
65
Q

What are the possible therapies for HCV? (2)

A
  1. PEG-IFNα + ribavirin
  2. Direct acting antivirals
66
Q

What is the pattern of serum HBV DNA after infection?

A

Steep increase in serum HBV DNA, after which a period of fluctuation occurs

67
Q

What is the pattern of serum HCV RNA after infection?

A

Steep increase with continuous replication and high viral loads -> stays high

68
Q

What is fibrosis?

A

Accumulation of connective tissue in the liver

69
Q

Why does HCC have a high mortality rate?

A

Relatively asymptomatic and therefore often detected at a late stage of disease progression

70
Q

Why are viral hepatitis studies & drug development for HCV difficult? (2)

A
  1. No in vitro models
  2. No in vivo models
71
Q

What are the most important mechanisms by which HCV therapies work? (2)

A
  1. Protease inhibitors
  2. Polymerase inhibitors
72
Q

What is the baltimore virus classification of HBV?

A

Group VII

73
Q

What is the entry receptor of HBV? What is this receptor used for?

A

NTCP
Bile acid receptor

74
Q

How does HBV enable chronicity?

A

Formation of cccDNA that remains behind in the cell
This can reactivate viral replication

75
Q

How do nucleoside/nucleotide analogues against HBV work?

A

They cause chain termination, preventing effective viral replication

76
Q

What are the two compounds used to treat HBV? (2)

A
  1. Tenefovir
  2. Entecavir
77
Q

What are the two mechanisms by which HBV can lead to hepatocellular carcinoma?

A
  1. Viral effect -> integration of virus in host DNA, interfering with tumorsuppressor genes/oncogenes
  2. Continuous immunological assault on hepatocytes
78
Q
A

I&I SC1 (20 decks)

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