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Virions, Prions, and Viroids:
Infectious Agents of Animalsand PlantsTopics
StructureClassification
Methods of study
Viral infections
Viral tumors
Human tumors
Viral host range
Prions
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StructureAnalogous to bacteriophages
Capsid (protein coat) made up of capsomeres Naked vs. enveloped viruses Attachment proteins or spikes in enveloped viruses
Distinct from bacteriophages
Segmented viruses (contain more than one RNAmolecule)
Plant viruses do not enter via receptor attachment
Shapes:
Isometric
Helical
Pleomorphic
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Classification
Taxonomy in constant fluxMost common taxonomic criteria for animal viruses:
1. Genome structure (DNA or RNA, ss vs. ds,segmented or not)
2. Virus particle structure (isometric, helical,pleomorphic)
3. Presence or absence of viral envelope
Viruses infecting vertebrates are divided into 14 RNAfamilies and 7 DNA families (Ending: -viridae)
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Coronavirus
Classification:
Coronaviridae (Family)
Coronavirus (Genus)
Common cold virus (Species) (together
with rhinoviruses)
Structure: non-seg., lin., ssRNA, helical, env.
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Herpesvirus
Classification:
Herpesviridae (Family)
Herpesvirus (Genus)
Herpes simplex type 1 / type 2 (Species)
Structure:
non-seg., lin., dsDNA, helical, env.
http://darwin.bio.uci.edu/~faculty/wagner/movieindex.htm
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Cells Infected with a Herpes Virus
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Groupings Based on Routes ofTransmission
Not a taxonomic grouping more than one family may bincluded in one transmission grouping
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Methods of Study
Much more expensive and difficultto study animal viruses thanbacteriophages
Cultivation in host cells Living animal Embryonated chicken eggs
Cell or tissue culture (= invitro)
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Methods of Study cont: Quantitation
Plaque assay (useful for infective and lytic viruses)
Virion counting with EM
Quantal assay
(ID50 or LD50)
Hemagglutination(e.g.influenza virus)
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Acute Viral Infections
Productive infection of relative short duration
Naked viruses usually cause cell lysis, whileenveloped viruses do not
Symptoms due to localized or widespread tissue
damage
Host defense mechanisms gradually eliminate virus
Examples of acute infections
Time course
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Mumps, Measles, Influenza, andPoliomyelitis
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Time Course of Acute Viral Infection
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HEV
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Reproductive Cycle
1. Attachment
2. Entry
3. Uncoating
4. Replication of NA andprotein
5. Maturation of viral particles
6. Cell lysis
7. Spreading and shedding
8. Transmission to next host
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Transcription Strategy
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Mechanisms of Release
1. Cytopathic effect: Unlike virulentphages most animal viruses do not
encode for cell lytic enzymes.Instead degenerative changesassociated with the virus lead to
cell death.
2. Budding: from plasma membrane(most common) or from Golgi
apparatus. May or may not kill cell.Enveloped viruses
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Persistent Viral Infections
Virus continually present in body. Released by
budding.
May or may not cause disease
Carrier able to spread disease
Four categories (if more than one applies = complexinfections):
1. Late complications from acute infections
2. Latent infections
3. Chronic infections
4. Slow infections
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Late Complications from AcuteInfections
1. Subactue sclerosing panencephalitis (SSPE) -years following measles in 1 in 300,000. Viruspersistent in brain tissue with decreased
transcription of viral genome. Lack of envelopeprotein production prevents immune response toeliminate infected cells. High Ab, low CMI. Exactmechanism unknown.
2. Progressive (pan)encephalitis following rubella
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Latent Infections
Acute infection symptomless periodreactivation of disease
Symptoms of reactivation may differ fromoriginal disease
No measurable viral particles during
symptomless period
Examples: HSV-1 and HSV-2; varicella
C
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Chickenpox- Varicella
Blister-like rash on surfaceof skin and mucousmembranes. Blistersusually appear first ontrunk and face, thenspread to almost
everywhere else.
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Shingles orHerpes Zoster
About 20 % of those peoplewho have had chicken poxwill get zoster at some timeduring their lives. Most
people will get zoster onlyonce.
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Shingles comes frolatin cingulum, whichmeans girdle or belt.
It occurs in an area ofthe skin that is suppliedby the sensory fibers
a single nerve-dermatome. Rashappears as well-defineband on one side of
body, or on one side offace, arms or legs.
Ch i I f i
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Chronic Infections
Virus can be demonstrated at all times
Disease may or may not be present forextended time periods or show up late(carriers!)
Sl I f i
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Slow Infections
Gradual increase of infectious agent over long
time period often no apparent symptoms for longtime (=preclinical phase)
Usually slowly progressive lethal diseases
Examples AIDS
Lentivirus
prions
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HIV: Example of Complex Infection
Retrovirus ssRNA, envelope
RNA DNA (with the help of reversetranscriptase) permanent integration into host
genome (=provirus)
Polyprotein is cleaved into individual proteins withviral protease assembly of virions budding
Vi l T (N l )
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Viral Tumors (Neoplasms)
Benign
Malignant cancer, metastasizes
Proto-oncogenes and oncogenes are regulatorygenes
Properties of normal and transformed cells Only about 15% of human tumors are due to viruses
Examples of human tumors:
Kaposis sarcoma (herpes virus)
Squamous cell carcinomas (HPV)
Hepatocellular carcinoma (HBV and HCV)
K i S
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Kaposis Sarcoma
Purplish lesions of a
skin cancer not usuallyseen in young men
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Viral Host Range
Mostly species and even cell type specific
Exception:Zoonotic viruses are transmissiblefrom animals (arthropods, vertebrates) to man
(zoonosis) Arboviruses (West Nile virus), rabies etc.
Modification of host range due to
Phenotypic mixing Genetic reassortment
G ti R t t
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Genetic Reassortent
In segmented viruses
Simultaneous infection of onecell with 2 different types ofviruses leads to exchange of
genetic information
Creation of major new influenza
strains resulting in pandemics
Antigenic shift vs. antigenic drift
Oth I f ti A t P i
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Other Infectious Agents: Prions
Small proteinaceous infectious particles (resistinactivation by procedures that modify nucleic acids)
Prion diseases are often called spongiformencephalopathies because of the post mortemappearance of the brain with large vacuoles in the
cortex and cerebellum
Human prion diseases CJD: Creutzfeld-Jacob Disease
BSE: Mad cow disease (BSE) GSS: Gerstmann-Straussler-Scheinker syndrome
Kuru