Polio and Picornaviruses Flashcards
describe the nucleic acid structure of picornaviruses
small, single stranded RNA
what are the 3 types of immunity?
active- host makes Ab
passive- host given Ab
passive-active- host has passive immunity, becomes infected but with limited severity d/t existing immunity, but acquires active immunity
why did paralysis become more common in cases of polio, especially in more sanitized countries?
polio is spread fecal-orally. in countries with low sanitary conditions, exposure to polio was high. however, there was also passive immunity to polio acquired maternally. therefore, people would become infected, but it would present less severely and without paralysis, and they would then acquire active immunity.
in more sanitized environments, this passive immunity did not exist. therefore, infectious polio could spread to the nervous system more easily, resulting in more cases of paralysis
what are the clinical features of polio?
1 subclinical infection
2 mild, non specific symptoms such as fever
3 aseptic meningitis- headache, stiff neck, fever, increased CSF leukocytes
4. paralysis
describe the 2 types of paralytic polio
- spinal- destruction of motor neurons
2. bulbar- attack on respiratory centers in medulla and cranial nerves (iron lung)
how does polio spread within the body?
viremia
how does polio spread?
encountered via fecal contamination, enters the body orally
what is polios incubation period?
2-3 weeks
where does viral polio multiplication occur?
primarily (day 0-1)- tonsils, peyers patches, lymph nodes of small intestine
secondary (day 6)- CNS
when is the first Ab detectable against polio?
day 5
rhinoviruses
enters through the respiratory tract, common cause of cold
do not survive well at high temps or low pHs- cannot enter through the gut
treatment- heat yourself up to slow down virus
spread via aerosol
highly antigenic- no good vaccines or antivirals
Salk v Sabin vaccines
Salk- inactivated
Sabin- live attenuated
how does the shape of the virus capsid effect the ability for your immune system to combat it
the virus self assembles into a capsid, and the surface of the capsid has both plateaus and canyons. the CD155 binding site is inside a canyon, which makes it slightly more difficult to neutralize
what are the consequences of having RNA vs DNA genomes?
DNA- low mutation rate (b/c of proofreading), species specific
RNA- high mutation rate (b/c no proof reading), low species specificity
do enteroviruses have envelopes?
no- they invade through the gut and the digestive enzymes in the GI tract would strip the envelop away
describe polio replication in the cell
- strand RNA is translated into polyprotein
- polyprotein is cleaved inefficiently using cellular proteases
- polyprotein codes for RNA replicase, proteases, and structural coat proteins
4 RNA replicase- feeds back and starts making - strand from the + strand, which will serve as the templates for future + strands - proteases, in addition to cleaving polyprotein, cleaves CAP binding proteins necessary for host cell translation
how does polio replicate without CAP dependent translation
they have IRES, with a secondary structure that attracts ribosomes w/o the need for CAP protein. allows them to overcome lack of CAP
how is the IRES used in vaccines
in the live attenuated virus, several mutations are inserted into the IRES to inhibit its ability to attract ribosomes
mutations can revert live attenuated virus back to virulent strains
what “season” is polio most common in?
summer- playing outside in contaminated water
what are the advantages of the live attenuated polio vaccines
- more effective at stimulating long term protection- stimulates both IgG and IgA. IgA in the gut neutralizes polio in the gut.
- prevents infected individuals from shedding in their feces
- live vaccine spreads from person to person, spreading vaccination
formaldehyde-virus killing curve
too much formaldehyde = destroys the antigenicity
not enough = residual live virus
need to get the amount correct
compare and contrast the live and dead vaccines
both effective, longer term immunity from live, dead needs boosters, live isnt safe for pregnant or immunocompromised, live can spread immunization, but live can also revert, killed vaccine is more stable, live generates IgA in addition to IgG, dead sheds live virus b/c they lack of IgA
which vaccine does the US use?
dead
describe the replication cycle of coxsackie
same as polio
