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CSB351 Term Test 2 Summary Notes

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Complete and in-depth Term Test 2 Summary Notes for CSB351 for EXAM prep. Kevin has combined notes from his peers and his own work to provide the most complete and comprehensive study guide for all types of students. He has achieved an overall cumulative GPA of 3.95 during his undergrad at the Univ...

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  • June 10, 2018
  • 43
  • 2017/2018
  • Summary

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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

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