Polio, Polyoma, Prions 'n Shit Flashcards
Polyoma is in this family of viruses:
Papovaviridiae
In non-permissive cells, Polyoma virus can lead to:
Viral transformation—> tumor
Polyoma further subdivided into two viruses:
Both are very common in this demographic:
BK and JC
Both very common in kids. BK 3-4 yo. JC 10-14yo.
JC and BK are generally not a big deal in healthy individuals. Viruses are REALLY BAD FOR:
Immunocompromised pts.
Transplant pts: 80% mortality
AIDS pts: change of HAART can improve survival to 50%
Your rural 3rd world pt has flaccid paralysis. PCR determines they are suffering the neurological deficits associated w/ this viral infection:
Polio
Polio spreads:
Fecal-oral route
Tx of pts w/ Polio within this time frame can spare them of permanent paralysis.
6 months since onset
In the US, we recommend pts be vaccinated with the live (OPV) or inactivated (IPV) form of the Polio vaccine? Why?
IPV- fear of OPV reversion to virulent form
In 3rd world countries, they get the OPV form. Why is that?
IPV does not protect you from contracting the wild-type Polio that still exists in 3rd world countries due to incomplete vaccination campaigns. IPV does protect against paralysis.
In the past, children were first vaccinated with IPV and then given OPV as a booster (remember OPV stands for Oral Polio Vaccine). Why?
Oral booster ensures they have mucosal IgA.
What are the diseases of prions causing transmissible spongiform encephalioathies (TSE)?
Kuru CJD GSS FFI vCJD Animal Scrapie
Not only are prions proteins that are resistant to degradation by proteosomes, but they are also resistant to these commonly used forms of disinfection:
Radiation, EtOH
Describe the prion theory, i.e. why they are pathological. How are they different from normal proteins?
Where do they come from?
All based on ^ conservation of prion protein on Ch. 20 expressed in neurons and lymphocytes.
PrPc- normal
PrP-Sc- Scrapie, Dz prion due to sporadic, familial, infxn etiologies
These are normal sequences of AAs, that have FOLDED incorrectly, making them resistant to degradation—> accumulation—> death of cells (MC neurons)
How do prions replicate?
PrP* is the unfavored conformation of the good protein PrPc.
A PrPsc prion crashes into a PrP* protein and forces it to conform into PrPsc. The PrPsc acts as a “template” that reforms the PrP* into PrPsc. The more PrPsc is present, the bigger the problem, hence why re-infections cause worse dz.
Which is the most common prion dz?
Describe the clinical manifestations.
Creutzfeldt-Jakob Disease (CJD) Manifestations: (ACDC mnemonic) Akinetic mutism- late in dz Cerebellar dysfxn- ataxia Dementia- as w/ all TSEs Clonus- myoclonus
