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Immunity and infection > Mechanisms of viral infection and pathogenesis > Flashcards

Mechanisms of viral infection and pathogenesis Flashcards

1
Q

Factors affecting infection acquisition

A
  • Age (varicella zoster, children = chicken pox, adults = shingles)
  • Lifestyle (e.g. no. of sexual partners)
  • Lifestyle and age (e.g. Epstein Barr virus causing glandular fever in kissing teenagers
  • Immunocompromised? (Kaposi’s sarcoma in HIV patients)
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2
Q

Primary Infection?

A

First encounter with virus

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3
Q

In primary infection what can the virus do?

A

1) Stay at site of infection and replicate there
e. g. influenza, rhinovirus
2) Replicate at site of infection and spread
e. g. varicella zoster - starts in resp tract and then spreads

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4
Q

Reactivation of infection

A 
Example: varicella zoster
Replication in skin (chicken pox)
Migration (to CNS)
Latent 
Migration back to skin 
Reactivation skin (shingles)
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5
Q

Secondary infection

A

Infection with 2nd organism

e. g. following antibiotics = thrush (Candida albicans)
e. g. immunocompromised patient (HIV) bacterial/fungal infection following viral respiratory tract infection

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6
Q

Reinfection

A

Infection by the same organism

e. g. influenza (viral proteins rapidly changing)
e. g. rhinovirus (common cold)

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7
Q

Viruses that enter through respiratory tract

A

Influenza
Rhinovirus
Varicella zoster

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8
Q

Viruses that enter through faecal-oral route

A

Norovirus
Rotavirus
Hep A

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9
Q

Viruses that enter through blood

A

HIV

Hep B and C

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10
Q

Viruses that enter through bodily fluids

A

Epstein Barr Virus

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11
Q

Viruses that enter through cuts in skin

A

HPV

Molluscum contagiosum

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12
Q

Viruses that enter through sexual transmission

A

HPV
Herpes simplex virus
HIV

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13
Q

Viruses that enter through animal bites

A

Rabies

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14
Q

Viruses that enter through insect bites

A 
Haemorrhagic fever 
Lassa fever (Adrena virus)
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15
Q

Examples of Acute disease

A

Rabies
Rhinovirus
Influenza
Rotavirus

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16
Q

Examples of chronic virus

A

Hep B

Hep C

17
Q

Pathogenesis is determined by

A 
Nature of virus (influenza vs herpes)
Site of entry
Tissue tropism 
Cell damage caused
Ability of immune system to clear virus
18
Q

7 ways of evading the immune responses

A

1) Perinatal infection - infect when immune response isn’t optimum (e.g. herpes simplex in babies)
2) Vertical transmission: foetus unable to mount protective response (e.g. rubella and parvovirus)
3) Latency (they do not replicate and only make a few viral proteins (e.g. Varicella zoster lies latent in nerve ganglia where immune system cannot reach it)
4) Down regulate and hinder antigen presentation (MHC class 1)- e.g. (cytomegalovirus)
5) Replicating in WBCs (CMV, HIV|)
6) Changing viral proteins- takes time to generate adaptive response (e.g. Influenza, Herpes simplex virus)
7) Decoy particles (e.g. Hep B virus produces decoy particles which diverts the immune response

19
Q

Why do some viruses cause cancer?

A

Viruses can infect cells which do not replicate (they do not have cell machinery to replicate)
So viruses have to transform cells in order to start replicating
E.g. HPV, Hep B, Hep C
These transformed cells cause cancer

20
Q

Human Papillomavirus (HPV) structure

A

Non enveloped
double stranded
DNA

21
Q

High Risk HPV

A

Strains 16, 18, 35, 45

22
Q

How does HPV infect cells?

A

Infects epithelial cells
Infects basal layers of cells (only layer dividing) and then migrates to cell nucleus
Then behind to copy its own DNA

23
Q

How many open reading frames does the viral genome of HPV encode?

A

8 open reading frames
Early genes - E1-7
Late genes - L1-L2 (code for structural proteins)

24
Q

What does E2 do?

A

Before integration:
-Downregulates E6 and E7 expression (these are cancer causing genes)
After integration:
- When integrated, viral genome splits E2 in half = cannot regulate transcription anymore
-This allows increased transcription of E6 and E7

25
Q

What does E6 do?

A

Before integration
-It inhibits p53 tumour suppressor activity (normally p53 causes apoptosis of cell’s DNA if its is damaged or infected)
After integration
-Increased expression
-Transforms cells
-Epithelial cells no longer leave cell cycle
-Also activates telomerase

26
Q

What is telomerase?

A

Telomerase stabilises telomere length and stops erosion
Telomere ends regulates how many times a cell can divide
They shorten each time DNA replicates

27
Q

What does E7 do?

A

Before integration
-It inhibits retinoblastoma (RB1) tumour suppressor - binds to RbB1 and inactivates it = stops tumour suppression
After integration
-Increased expression
-Increased inactivation of RB1
-Transforms cells
-Epithelial cells no longer leave cell cycle

28
Q

Zika virus

A

Family: flaviridae family
Enveloped
Short stranded RNA
Positive sense: can produce proteins straight away
Transmission of virus is via mosquitos
Causes microcephaly when pregnant women get virus (increased risk in 1st trimester)

Immunity and infection (4 decks)

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