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- naked protein--variants of PrPc (involved in a number
- Interact with endogenous cellular proteins
- form neural plaques and tangles
- causes diseases called spongiform encephalopathies
- Two types: TSE (transmissible) and GSE (genetic/rare)
What is interesting about the variants of prions?
the variants have a primary sequence identical to the primary sequence of normal proteins; what differs is the secondary and tertiary structure
prions can dimerize/ acid resistant/ resistant to proteinases/ can't break them down
What does PrPc naturally do?
it naturally maintains myelin on myrlinated axons, prevents lysis from osmosis, etc.
- first observed?
- how obtained?
- prion involved?
- Observed in New Guinea during the 1920s
- Ritualistic cannibalism: consumed the tissues, including brain of deceased family and battle enemies; brain tissue from individuals with kuru was highly infectious; prion was transmitted via eating or sores/ cuts
Parkinsonian movement (6 ms-1 yr) and dementia (1-2 years)
three types: classic, variant, familial
- Parkinsonian symptoms
- new: 1999-2000
- onset over age 60
- sporadic (sCJD)
- onset below 30
- acquired (vCJD or iCJD);
- 2 years
familial; occurs in families where genetic mutations allow them to form
BSE/ Mad Cow Disease
- first identified?
- result of?
- first infections of BSE occurred in the 1970s; two being identified in 1986
- result of feeding cattle meat-and-bone meal that contained Scrapie/ BSE-infected material
- Strong epidemiologic evidence for a causal association with vCJD
- first reported from UK in 1996
- are what?
- infect what?
- reservoirs of them?
- related to?
- can be used in what?
naked nucleic acids that can be as small as 22 nucleotides
infects damaged plants, causing color changes, wilting leaves, root rot, plant death, stunted growth; affects chloroplast; uses it as a base to begin replication
- related to introns
two families (PSTVD/ ASBVd)
What are the mechanisms of action for the antiviral drugs?
- attachment blcokers
- penetration and uncoating blockers
- genome relication inhibitors
- gene expression
- inhibitors of assembly, aturation, and release
- viral attachment mimetic
- - Anti-receptor antibodies
- - Anti-idiotype antibody to viral particle
- - Natural receptor ligands & agonists
- - Peptides that mimic the receptor binding domains
What aren't viral drugs often prescribed?
they are unspecific and have several issues
- do what?
- include what?
- mimic the receptor and bind the virus
- anti-virus antibodies
- receptor anti-idiotyp antibodies
- extraneous receptor
- synthetic receptor mimetic (sialic acid for influenza)
Penetration and Uncoating
- •The drugs generally interfere with proteins
- –Two common drugs interfere with endosomal enzymes that inhibit HA conformational changes
- •Amantadine Rimantadine
The capsids can't break down and uncoat/ viral components can't get out
Genome Replication Inhibitors
- •These drugs are polymerase and protease inhibitors
- •Many of these drugs are nucleoside analogs
- –Phosphorylated for activity
- •Toxicity varies between analogs
- •Engineered proteins
- –Interfere with enzymes
- –Bind RNA
- •Non-nucleotide RT inhibitors
- –Bind enzymes directly
Assembly, Maturation and Release
- •Interfere with late stage processes
- •Tamiflu and Relenza
- two types
whole agent and subunit
- - live
- - inactivated by formalin (rabies, salk polio)
- - attenuated: replicate a very mild case; agent replication increases the dose; mutation issues; reuces the virulence of the pathogen
- what are the four
erecombinant: protein or portion expressed in a vector (Hep B)
toxoid: inactivated toxin (tetanus/ diptheria)
conjugated: immunogenic molecule fused to a protein (strep pneumonia)
acellular: fraction organisms (pertussis)