Mechanism of Viral Infections Flashcards
Understand the impact of a virus’ life cycle on the disease process
- viruses opt to keep their host alive long enough for abundant reproduction and transmission onto next host before host mortality
- clinical latency
- acute, chronic, persistant infections in relation to viral load and immune detection
ie: apathogenic
Describe how factors like the route of entry and tissue specificity affect the disease outcome
HHV-3 = Chickenpox = disseminated skin rashes
Shingles => avoid detection ‘clinical latency’ via hiding in peripheral nerves
= immuno-privilage and ⬇️ transcription of viral proteins
triggered by random insult allows viral load to travel down axon into sector specific outbreaks via mucosal / vascular travel and infection
Discriminate between acute infections, latent infections, and chronic/persistent infections
acute = sudden onset, short duration of symptoms eg: flu/influenza
latent infections = AIDS , herpes (HHV-1) which allow minimisation of re-infection, RSV
CHRONIC = hepatitis C
Discriminate between cytopathogenic and non-cytopathogenic infections or how viruses damage host tissues
cytopathogenic = relies on host destruction
eg:
- EBOLA epithelial damage / invasion = XS replication causing death of epithelial lining = vascular leakage / causing pathological changes in infected cells
- RSV syncytia = cell fusion w/in megakaryocytes
non-cytopathogenic = propagate production w/out relying on destroying host cells
eg: Hepatitis C: recruitment of leukocytes and CB8 cytotoxic cells to destroy infected cells causes onset of symptoms from pro-inflammatory response
Appreciate to what extent the symptoms of infection a result of the host’s immunological response
Dengue fever
- caused by antibody dependant enhancements due to 4 different serotypes
- allows recruitment of phagocytes which can be invaded for viral replication = depletion of immune cells & response + access to vascular transport
RSV: severe secondary infection responses come from instigating TH-2 allergen/parasite response which cause disease onset instead of pro inflammatory TH-1 responses to recruit and destroy infected cells.
