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IIH > Viral immune invasion > Flashcards

Viral immune invasion Flashcards

1
Q

Which viral infection is most likely to be overcome by a Pt, acute or chronic?

A

Acute

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2
Q

Why are chronic infections harder to fight than acute?

A

Chronic infection causes inflammation and promotes conditions for bacterial infections.

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3
Q

What is influenza?

A

A segmented RNA virus that presents as strain A, B or C with A being most severe. Causes an acute infection of the upper and lower respiratory epithelium with no period of latency.

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4
Q

What segments is influenza made up of?

A

Has 8 segments, 1-6 encode for 1 protein each whilst 7-8 encode for 2 proteins each. For the virus to be functional all 8 segments are needed to produce all 10 proteins. The segments will form the membrane antigens Haemagglutinin and Neuraminidase.

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5
Q

How does antigenic shift occur in influenza?

A

Two strains infecting one host at the same time leads to reassortment and production of a new strain.

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6
Q

Which immune cells protect against influenza?

A

CD8 T cells protect the respiratory mucosa causing pneumonitis. Neutralising Igs limit spread and protect against reinfection.

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7
Q

What can be done to reduce the incidence of influenza?

A

Annual vaccinations of those vulnerable. Only protects against current strains.

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8
Q

What is antigenic drift?

A

Accumulation of new mutations over time due to a virus with a high mutation rate that is put under selective pressure leading to adaptive changes to evade the immune system.

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9
Q

What is antigenic shift?

A

Reassortment of antigens and segments of a viral genome leading to a new strain.

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10
Q

Why does influenza have the potential for antigenic shift?

A

It is a segmented virus that has the ability to infect other organisms to humans, leading to human flu co-infecting with another species type.

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11
Q

What is the original antigen sin?

A

On primary infection, Ig and memory cells are produced. On secondary infection of a similar strain, the immune system mistakes the new strain for the old and leads to inappropriate activation of memory, producing an ineffective response.

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12
Q

What type of virus is HIV?

A

A retrovirus with RNA genome that requires reverse transcriptase to integrate the DNA in to the host genome. It remains permanently integrated to control its expression but can be latent.

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13
Q

What are the two species of HIV?

A

HIV - 1: from cross species transfer

HIV - 2: low risk of transmission and slow progression

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14
Q

What 3 genes does HIV code for?

A

gag for capsid
pol for polymerase, integrase and protease
env for envelop and receptors
The genes mediate its pathogenicity and evasion of the immune system.

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15
Q

How does HIV evade the immune response?

A

Its plastic RNA genome is continuously changing due to antigenic drift, replicating faster than the immune system can produce antibodies (7-14 days). So whilst the immune system produces Igs for the original virus, the virus has already produced a mutated strain that is resistant to the antibodies.

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16
Q

Which type of cells does HIV infect?

A

Macrophages and CD4 T cells by binding GP120 to CD4 receptors and coreceptors CCR5 and CXCR4. This binding triggers structural changes to allow the membranes to fuse and release the viral capsid into the host.

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17
Q

What enzymes are involved in infection of host cells?

A

Reverse transcriptase converts ssRNA to dsDNA.
Viral integrase ligates the provirus into the host genome.
Viral proteases produced are packaged into new viruses to allow the virus to be infectious by cleaving p55 into smaller proteins.

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18
Q

Why is a vaccine ineffective?

A

The provirus is permanently integrated into the host genome and antigenic species are continuously produce.

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19
Q

What treatments can be used to slow infection?

A

Antiviral nucleoside analogues - inihibit reverse transcriptase
Protease inhibitors - to reduce pathogenicity

20
Q

What are the 3 phases of a HIV infection?

A

1) Acute seroconversion = infection is established and proviral reservoir is produced
2) Asymptomatic infection = occurs for 7-15 years with increasing immunodeficiency
3) AIDS results as the immune cells are depleted. Susceptible to fatal infections such as TB, CMV

21
Q

What are the symptoms experienced during the acute phase?

A

Fever, flu-like symptoms and rash

22
Q

How is the virus controlled during the acute phase?

A

Ig and CD8 T cells neutralise the high level of viraemia to a stable level. But it still leads to a rapid decline in CD4 T cells.

23
Q

What is the multidrug combination used to reduce symptoms and delay immunodeficiency? Why is a combination used?

A

HAART: (reverse transcriptase inhibitors)
2 NRTIs + 1 NNTRI (nucleoside and non -nucleoside)
or
2 NRTIs + 1 protease inhibitor
Combination is used to help reduce development of resistance.

24
Q

What type of virus is herpes?

A

A group of dsDNA viruses that cause lifelong infection due to LATENCY. Only serious in immunocompromised Pts.

25
Q

What type of immune response does the herpes virus evoke?

A

CD4 and CD8 T cell response

26
Q

What is used to control the cell during latency?

A

siRNA - latency associated transcripts or proteins

27
Q

What are the types of herpes virus?

A

HHV1-3 are the Herpes SIMPLEX virus
HHV4 = EMV
HHV5 = CMV

28
Q

What does a herpes simplex virus cause?

A

HSV infects neurones and are reactive to stress factors.
HSV1 and 2 causes cold sores or genital sores
VZV (HSV3) is the viral infection of chicken pots leading to fluid filled blistered rash.

29
Q

What happens if VZV is reactivated after a phase of latency? Who is most at risk?

A

Shingles.

Elderly as immune system decreases so reactivation is likely or those who do not experience an immune boost

30
Q

What reduces susceptibility to reactivation?

A

Continuous exposure provides an immune boost. Only virus to now have a vaccination.

31
Q

What happens if a patient who has never had chicken pox is exposed to shingles?

A

They can only develop chicken Pots from VZV.

32
Q

What is EBV? What cells does it infect?

A

Epstein Barr virus infects B cells causing mild lympoma.

33
Q

How is EBV controlled and how is this different for immuncompromised Pts?

A

Normally T cells can destroy the infected B cells before lymphoma is established but in immunocompromised the development of B cell lymphoma is common.

34
Q

How does EBV present?

A

Asymptomatic in children (most are infected)

Glandular fever after puberty

35
Q

Where does EBV remain latent?

A

In B cells or epithelial cells of the throat.

36
Q

What is CMV?

A

Cytomegalovirus is an asymptomatic infection with a large tropism for many cell types, infecting lungs, liver, endothelium, myeloid etc.

37
Q

What immune response does it evoke?

A

It induces a CD4 and CD8 T cell response to suppress its reactivation.

38
Q

Why is CMV an immunodominant virus?

A

10-20% of all immune cells become CMV specific and it contiuously reactivates the immune system to keep it suppressed.

39
Q

Under what conditions will EBV be reactivated and how will this present?

A

When the T cell response is insufficient e.g. age, HIV, immunosuppressants. Infects a wide range of cell types resulting in a range of diseases with a high mortality rate e.g. pneumonitis, colitis, hepatitis

40
Q

What is a poxivirus?

A

A group of viruses with a stable genome and low mutation rates that rapidly adapts to a host. It causes skin lesions or disseminating rash. e.g. Smallpox

41
Q

What type of virus is the vaccinia virus?

A

A dsDNA poxivirus

42
Q

How is vaccinia virus inhibited exogenously?

A

Via PKR from HeLa cells to inhibit its E3L and K3L genes

43
Q

How does the vaccinia virus mutate and overcome PKR?

A

It replicates its K3L gene to form a tandem repeat until one eventually mutates by chance to increase the potency of the gene and block the PKR pathway. The 1 base change produces a better enzyme so the tandem repeat collapses to remove any unwanted proteins and overcoming PKR.

44
Q

Where does the mutation process and the collapse take place?

A

Within the squeeze box of the virus.

45
Q

What is PKR?

A

Protein Kinase R is involved in immunity against poxiviruses.

IIH (19 decks)

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