The Viruses: Host-Pathogen Interactions Flashcards
Viral Sources (3)
- Humans
- Environment
- Animals/Insects
Human Reservoirs for Respiratory Viruses
- Coronavirus
- Influenza
- Parainfluenza
- RSV
- Rhinovirus
Human Reservoirs for Mucosal Viruses Oral
- HSV
- CMV
- EBV
Human Reservoirs for Mucosal Viruses Genital
- HBV, HCV
- HIV
- HSV
- HPV
Environmental Viruses
Fecal-oral
-norovirus, rotavirus, Hep A
Fomites
-adenovirus
Vector Borne Viruses
Mosquitoes -West Nile -Dengue Animals -Rabies -LCMV
Viral Factors Influencing Clinical Outcomes (5)
- viral inoculum
- virulence of virus
- efficiency of attachment to host cell
- ability to spread
- effect on cell (eg. cytopathic, transformative)
Stages of Viral Infections (3)
Acute
Latent
Chronic
Latent Ix
- no clinical presentation during latency
- can reactivate later
- dormancy
- eg. herpesviridae
Chronic Ix
- slow progression of clinical disease
- eg. HIV
Variability in viral populations due to (5)
- Large population
- Selective pressure
- Heterogeneity
- High mutability
- Genome structure
RNA vs. DNA viruses mutability
-higher in RNA virus, RNA pol lacks proofreading abilities
Quasispecies
- population of viruses infecting a host are not all exactly the same
- group of genetically similar viruses
- allows selective pressures (ie. antivirals) to select for resistance in the viral population
Influenza
- ssRNA virus
- segmented genome
- surface proteins - hemagluttinin and neuraminidase
Antigenic Drift
-mutations in genome cause slightly altered surface glycoproteins
Antigenic Shift
-rearrangement of genome causes different pairings of H’s and N’s to come together
Clinical Significance of Drift
- need for yearly vaccine
- antibodies from last year’s vaccines may not completely recognize this year’s strain
Clinical Significance of Shift
- abrupt reassortment results in virus to which immune system has little to no protection
- rearrangement with H’s and N’s from animal hosts
Spanish Influenza
- 1918
- H1N1, novel reassortment
Bird Flu
- H5N1, H7N9
- poor pt to pt spread
Neuraminidase Inhibitors
- influenza antivirals
- oseltamavir, zanamavir
- MOA: inhibit NA, prevents virus from cleaving sialic acid as it leaves cell, new viruses can’t be released
- covers A and B
M2 Inhibitors
- influenza antiviral
- amantadine
- MOA: inhibits M2 ion channel, preventing acidification of vision which is necessary for uncoating
Clinical Benefit of Influenza Antivirals
-if given within 24-48 hrs of symptom onset, reduce symptoms and recovery time
Acyclovir and Valacyclovir
- phosphorylated by viral and cellular kinases to become triphosphate form where they can be integrated into growing nucleic acids, prevent chain elongation and disrupt viral replication
- used in HSV and VZV
Gancyclovir
- only phosphorylated by cellular kinases to triphosphate form, prevents chain elongation and disrupts viral replication
- used in CMV
