CSB351 Term Test 2 Summary Notes

CSB351

Lecture 21 – Enteroviruses: Poliovirus, Rhinovirus
 So polio used to be a thing
o Ubiquitous vaccinaton has mostly eradicated it from the world
 But not completely, stll fares up in the Middle East/South Asia
o Been around forever
 FDR and Tutankhamun could get it
 Polio as a template: enteroviruses
o Specifc type of picornavirus
o Polio rapidly mutates in the gut, but is stable outside
 Hence, we can use polio vaccines from the 1950s and they’d stll work
 And we don’t need boosters
o Polio is paralytc because it moves to the brain
 Others move to skin, muscle or liver (foot and mouth, myocardits, hepatts A)
o Transmission of polio
 Oral-fecal-oral, and nasopharyngeal
 Infecton can create viremia, but most growth is in gut
 GALT
o Gut associated lymph tssue
o Polio grows in GALT for fve weeks
 Also grows in intestne, CCS, lymph tssues
 Mostly affects unvaccinated children
 Herd immunity
o Enough immunizatons mean polio dies out before it can fnd a
host
 Sanitaton
o Clean out the feces, that would help
 Some people are asymptomatc carriers
o Clinical features of infecton/pathology
 Types of infecton
 Asymptomatc (90%)
o Virus only in mouth, throat, gut
 Abortve poliomyelits
o Flu-like
 Fever, sore throat, headache, constpaton, vomitng
 Invasion of CCS (1-2%)
o Meningits, back pain, muscle spasm
o Stll no paralysis
 Paralytc poliomyelits (0.1-2%)
o 1-4 weeks afer infecton
o 10% mortality rate, 80% paralysis rate

, o Flaccid paralysis
 Weak, asymmetrical, no loss of sensaton
o 1/200 cases lead to irreversible paralysis
 Virus enters bloodstream, invades CCS, usually near
legs
 Virus destroys nerve cells, muscles atrophy and lose
total functon
 Acute faccis paralysis (ALP)
o Cranial (bulbar) paralysis
 Trunk, thorax muscles get infected and atrophy
 Worst case, polio gets to brain stem, atrophying
swallowing, speaking and breathing
 The iron lung is supposed to breathe for them
 Infecton route
 Virus enters orally, multplies in tonsils, lymph nodes, gut
 CCS infecton requires either viremia or infecton directly from intestne
 Preventon
 Salk vaccine
o Killed virus
o Inject formaldehyde-treated virus into patent
 Sabin vaccine
o Live, atenuated
o Drip atenuated virus onto tongue
 Eradicaton
o Cot totally eradicated like smallpox or rinderpest, but we’re
getting there
o Only endemic to Afghanistan, India, Pakistan, Cigeria
 Postpolio syndrome
 Cew-onset muscle atrophy and weakness, plus pain, 30-40 years afer
inital infecton with poliovirus
 VAPP
 Vaccine-associated paralytc poliomyelits
 Oral polio vaccine virus gets into unvaccinated individuals and causes
disease
o Oral vaccine partcles have probably reverted to virulence
 Rhinovirus
o The common cold
o Structure
 Icosahedral, non-enveloped
o Genome
 +ssRCA, like the other picornaviruses
 Over 100 serotypes
 Polyproteinous

,  Cleaved into individual proteins
o Replicaton
 Entry
 ICAM-1 receptor on cell matches with rhinovirus capsid with
capsomeres
 10% of rhinoviruses use some other receptor
 Uncoatng, transcripton of polyprotein mRCA (in cytosol), replicaton of
genome through –ssRCA intermediate, translaton and processing of
polyprotein, packaging
o Transmission
 Aerosol, airborne or direct contact
 Tropism for nasal mucosa
o Symptoms
 Sniffling, sneezing, aching, coughing, stuffy-head, etc.
o Cure for the common cold?
 Zinc, maybe?
 Zinc compettvely inhibits ICAM-1 before the cold shows up
 So it’s bad if you have a cold already
 Does not work orally, either
o Must stck zinc up your nose

Lecture 22 – Picornavirus: Hepatitis A, Coxsackie,
Aphthoviruses
 Con-polio enteroviruses
o Coxsackie A/B, echovirus, enterovirus D68; let’s look at coxsackie
 Coxsackie A
 Hand, foot and mouth virus
 Coxsackie B
 Pericardits/myocardits, Bornholm disease
o Distributon
 Global
o Host range
 Humans, maybe chimpanzees and monkeys
o Epidemiology
 Same as other enteroviruses
 Found in water, soil, vegetables, shellfsh
o Transmission/tropism
 Fecal-oral route
 Aerosol transmission if pulmonary symptoms are present, if there is
conjunctvits, or if subjects have it in their throat
o Pathogenicity
 Virus replicates in throat and small intestne, and lymph nodes around those

,  Via blood or lymph, virus reaches target organs
o Symptoms
 Many different clinical symptoms, hard to tell
 Enteroviruses usually have featureless diseases
 Fever, rash, fu-like syndrome
o Tissue-level effects
 Skin/mucosa
 Herpangina (mouth blisters)
 Stomatts (oral mucosa infammaton)
 Hand, fooy mouth disease
o Vesicles on palms, soles, mouth
 Striated muscle
 Pleurodynia (Bornholm disease)
o Sudden chest pain due to diaphragm
o General malaise
 Heart
 Myocardits, pericardits, myopericardits
o Infammaton of heart and/or heart sheath
 Ofen fatal in infants
 Gut, liver
 Abdominal pain, hepatts (rare)
 COT diarrhea
 Pancreas
 Strong implicatons of type I diabetes, which is the one where the
pancreas islet cells get destroyed
o Autoimmune reacton
 Respiratory
 Pneumonia, cold, respiratory tract infectons
 Eye
 Conjunctvits (pinkeye)
o Immune response
 Antbodies are lifelong, although it does depend on the circulaton of a virus in a
community
o Preventon/control
 Co vaccine
 Don’t poop where you eat
 Hepatoviruses
o Formerly enteroviruses, now classifed as their own thing
o Hepatts A
o Characteristc features
 Liver cell tropism
 Small/absent VP4 protein