Polio and Picornaviruses

Question 1

describe the nucleic acid structure of picornaviruses

Answer 1

small, single stranded RNA

Question 2

what are the 3 types of immunity?

Answer 2

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

Question 3

why did paralysis become more common in cases of polio, especially in more sanitized countries?

Answer 3

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

Question 4

what are the clinical features of polio?

Answer 4

1 subclinical infection
2 mild, non specific symptoms such as fever
3 aseptic meningitis- headache, stiff neck, fever, increased CSF leukocytes
4. paralysis

Question 5

describe the 2 types of paralytic polio

Answer 5

1. spinal- destruction of motor neurons

2. bulbar- attack on respiratory centers in medulla and cranial nerves (iron lung)

Question 6

how does polio spread within the body?

Answer 6

viremia

Question 7

how does polio spread?

Answer 7

encountered via fecal contamination, enters the body orally

Question 8

what is polios incubation period?

Answer 8

2-3 weeks

Question 9

where does viral polio multiplication occur?

Answer 9

primarily (day 0-1)- tonsils, peyers patches, lymph nodes of small intestine

secondary (day 6)- CNS

Question 10

when is the first Ab detectable against polio?

Answer 10

day 5

Question 11

rhinoviruses

Answer 11

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

Question 12

Salk v Sabin vaccines

Answer 12

Salk- inactivated

Sabin- live attenuated

Question 13

how does the shape of the virus capsid effect the ability for your immune system to combat it

Answer 13

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

Question 14

what are the consequences of having RNA vs DNA genomes?

Answer 14

DNA- low mutation rate (b/c of proofreading), species specific

RNA- high mutation rate (b/c no proof reading), low species specificity

Question 15

do enteroviruses have envelopes?

Answer 15

no- they invade through the gut and the digestive enzymes in the GI tract would strip the envelop away

Question 16

describe polio replication in the cell

Answer 16

1. • strand RNA is translated into polyprotein
2. polyprotein is cleaved inefficiently using cellular proteases
3. 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
4. proteases, in addition to cleaving polyprotein, cleaves CAP binding proteins necessary for host cell translation

Question 17

how does polio replicate without CAP dependent translation

Answer 17

they have IRES, with a secondary structure that attracts ribosomes w/o the need for CAP protein. allows them to overcome lack of CAP

Question 18

how is the IRES used in vaccines

Answer 18

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

Question 19

what “season” is polio most common in?

Answer 19

summer- playing outside in contaminated water

Question 20

what are the advantages of the live attenuated polio vaccines

Answer 20

1. more effective at stimulating long term protection- stimulates both IgG and IgA. IgA in the gut neutralizes polio in the gut.
2. prevents infected individuals from shedding in their feces
3. live vaccine spreads from person to person, spreading vaccination

Question 21

formaldehyde-virus killing curve

Answer 21

too much formaldehyde = destroys the antigenicity
not enough = residual live virus

need to get the amount correct

Question 22

compare and contrast the live and dead vaccines

Answer 22

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

Question 23

which vaccine does the US use?

Answer 23

dead

Question 24

describe the replication cycle of coxsackie

Answer 24

same as polio

Question 25

describe the transmission of coxsackie

Answer 25

fecal to oral

Question 26

is coxsackie virus enveloped or naked?

Answer 26

naked

Question 27

describe the 2 subtypes of Coxsackie

Answer 27

A- tropism for skin and mucous membranes
 hand foot mouth disease
aseptic meningitis
rare paralysis
herpangina (fever, sore throat, pharyngeal lesions)

B- viscerotropism
pleurodynia-  targets intercostal muscles causing chest pain
orchitis- inflammation of the scrotum
myocarditis
aseptic meningitis
paralytic disease

Question 28

Describe coxsackie diagnosis and treatment

Answer 28

treatment- supportive, no vaccines, no antiviral therapy

diagnosis- growth in cell cultures, Ab titers, or PCR for RNA, especially w/ meningitis

Question 29

ECHO viruses

Answer 29

fecal-oral transmission
stable in environment- no envelope
replication similar to polio
32 sterotypes- lots of varition

symptoms-
rash
leading cause of aseptic meningitis

treatment-
none, no antivirals or vaccines

Question 30

other enteroviruses

Answer 30

enterovirus 70- acute hemorrhagic conjunctivitis
71- Hand foot mouth disease, CNS infections
72- hepatitis A

Question 31

reovirus

Answer 31

double stranded RNA segments, but nucleic acid is not infectious, and it needs RNA dependent RNA polymerase

important virus is Rotaviruses

Question 32

Rotaviruses

Answer 32

spread fecal to oral route- unenveloped
common cause of death in kids under 2 via dehydration
2 day incubation period followed by vomiting and diarrhea
seasonal peak in winter
not common in US

vaccine under development- 2 live attenuated viruses
Rotarix- human virus

Question 33

Calcivirus

Answer 33

small, non enveloped + strand RNA
larger than picornaviruses
poorly understood replication

Norovirus- most common cause of viral gasteroenteritis
bad on cruise ships
2 day course
causes vomiting

Question 34

Astrovirus

Answer 34

small, RNA + strand viruses
peaks in winter
causes diarrhea and vomiting
spread by contaminated food and water

Question 35

Adenovirus

Answer 35

DNA virus, non enveloped
lots of sterotypes
3-10 incubation period

causes: respiratory disease
conjunctivitis
gastroenteritis

spread: hand to hand contact, doorknobs, fecal-oral