Mechanisms of viral infection and pathogenesis Flashcards
(28 cards)
Factors affecting infection acquisition
- 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)
Primary Infection?
First encounter with virus
In primary infection what can the virus do?
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
Reactivation of infection
Example: varicella zoster Replication in skin (chicken pox) Migration (to CNS) Latent Migration back to skin Reactivation skin (shingles)
Secondary infection
Infection with 2nd organism
e. g. following antibiotics = thrush (Candida albicans)
e. g. immunocompromised patient (HIV) bacterial/fungal infection following viral respiratory tract infection
Reinfection
Infection by the same organism
e. g. influenza (viral proteins rapidly changing)
e. g. rhinovirus (common cold)
Viruses that enter through respiratory tract
Influenza
Rhinovirus
Varicella zoster
Viruses that enter through faecal-oral route
Norovirus
Rotavirus
Hep A
Viruses that enter through blood
HIV
Hep B and C
Viruses that enter through bodily fluids
Epstein Barr Virus
Viruses that enter through cuts in skin
HPV
Molluscum contagiosum
Viruses that enter through sexual transmission
HPV
Herpes simplex virus
HIV
Viruses that enter through animal bites
Rabies
Viruses that enter through insect bites
Haemorrhagic fever Lassa fever (Adrena virus)
Examples of Acute disease
Rabies
Rhinovirus
Influenza
Rotavirus
Examples of chronic virus
Hep B
Hep C
Pathogenesis is determined by
Nature of virus (influenza vs herpes) Site of entry Tissue tropism Cell damage caused Ability of immune system to clear virus
7 ways of evading the immune responses
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
Why do some viruses cause cancer?
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
Human Papillomavirus (HPV) structure
Non enveloped
double stranded
DNA
High Risk HPV
Strains 16, 18, 35, 45
How does HPV infect cells?
Infects epithelial cells
Infects basal layers of cells (only layer dividing) and then migrates to cell nucleus
Then behind to copy its own DNA
How many open reading frames does the viral genome of HPV encode?
8 open reading frames
Early genes - E1-7
Late genes - L1-L2 (code for structural proteins)
What does E2 do?
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
