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41 Cards in this Set

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Classification of Animal Viruses
-Superfamilies (DNA, RNA)
-Families (capsid type, presences of envelope, size, # of nucleic acid strands)
-Genera (host, target tissue, disease type)
Reproduction of Animal Viruses
Same steps as bacteriophage
1)Adsoption (attachment)
2)Penetration & uncoating
3)Replication of virus nucleic acids
4)Synthesis of viral coat proteins
5)Assenbly of Virons
6)Release
1)Adsorption of Virons
-glycoproteins mediate attachment
-Receptors play role in specificities of host and tissues
2)Penetration and Uncoating
-3 mechs:
A)Endocytosis of naked virus
B)Endocytosis of enveloped virus
C)Fusion of envelope with host membrane
-Uncoating occurs in different areas depending on virus
+Cytoplasm (HIV)
+Nucleus (Herpes Simplex Virus)
+Lysosome (Poxvirus)
A)Endocytosis of naked virus
-Nucleocapsid binds to receptors and is endocytosed
-Insert genome through vessicle membrane
B)Endocytosis of Enveloped Virus
-Receptor-mediated
-Form coated vesicle
-Genome released after fusion with organelle
C)Fusion of envelope with host membrane
-Nucleocapsid released into cytoplasm & uncoats
3)Replication and Transcription in DNA viruses
-Early genes- take over host, controls DNA RNA synthesis of host
-Viral DNA replication (nucleus)
-Early mRNA synthesis
-Some take control of cell functions
Replication of ssDNA Viruses
(parvovirus)
-Naked, icosahedral capsid
-small overlapping genome (3 overlapping genes)
-uses host for all biosynthetic processes (only during S period)
Replication of dsDNA viruses
(herpes simplex virus-1)
-icosahedral, enveloped
-linear genome (50-100 genes)
-host RNA polymerase for synthesis of viral mRNA
-Early genes
-DNA circularizes after 4 hours, viruses encoded DNA polymerase for replication
Replication of dsDNA viruses
(poxvirus)
-Largest (>200 genes)
-uncoating in lysosome
-DNA dependent RNA polymerase which synthesizes early mRNA
-Viral-associated= packaged in nucleocapsid
-starts after 1.5 hrs, spans 24 hrs
Replication and Transcription in RNA viruses
4 types:
1)Positive-sense ssRNA virus
2)Negative-sense ssRNA virus
3)dsRNA virus
4)Retrovirus
Positive-sense ssRNA viruses
look in notes pg122
Negative-sense ssRNA viruses
look in notes pg 122
dsRNA viruses
look in notes pg 122
Retroviruses
look in notes pg 123
Why does RNA viruses mutate more than DNA viruses?
-DNA has proofreading ability
-RNA no proofreading ability
4)Synthesis of virus capsids
-Capsid proteins (encoded by late genes)
-Naked virus
+procapsids formed then nucleic acid inserted
-Enveloped viruses
+same as naked, envelope acquired when released (budding)
-Matrix on some
5)Assembly of Virons
site of assembly and morphogenesis varies
6)Viron released
Naked virus
-lysis of host cell
Envelope viruses
-budding
-virus encoded protein incorperated into host membrane
-most release form plasma membrane but some from different membranes
HIV reproductive cycle
1)GP120 bind to CD4 of T cell, GP41 to accessory receptor
2)Fusion with PM
3)Reverse transcriptase (viral-assoc) makes dsDNA, enters nucleus, integrates using integrase (viral-assoc)
-Pos.-sense RNA made for genomes
4)mRNA transcribed & translated into polypeptide
-Protease (viral-assoc) cleaves into individual proteins
5)Assembles in cytoplasm
6)Buds from PM
HSV-1 reproductive cycle
1)Spike attaches to heparan sulfate on cell mem
2)Receptor-mediated endocytosis
-Vessicle fuses with outer nuc mem, envelope fuses with inner nuc mem to insert genome directly into nucleus
3)Early genes transcribed
-DNA circularizes, Viral DNA copied
4)Late mRNA transcribed
-Viral proteins made
5)Assembly in cytoplasm
6)Buds from PM
Influenza Reproductive cycle
1)Spike attaches to sialic acid containing glycoproteins
2)Receptor-mediated endocytosis
-vessicle fuses with endosome
-RNA released in the cytoplasm
3)Transcriptase (viral-assoc) transcribes mRNA
-Viral replicase make ds replicative form and -ssRNA
4)Late mRNA transcribed
-Viral proteins made in cytoplasm and rough ER
5)Assembly in cytoplasm
6)Buds from plasma membrane
Cytocidal Infections
7 types:

1) Inhibition of host mechs (DNA, RNA, Protein)
2)Lysosome damage
3)Alteration of plasma membrane
4)Toxicity from high concentrations of certain viral proteins
5)Formations of inclusion bodies (too many cells)
6)Chromosomal disruptions due to prophage insertion
7)Transformation of host cell into malignant cell
7 types
Tumor
Growth and lump of tissue
Neoplasia
Abnormal cell growth and replication due to regulation loss
Anaplasia
Reversion to a more primitive/ differentiated state
Metaplasia
spread of cancer cells throughout the body
Causes of cancer
5 types:

1)Spontaneous mutations
2)Chemicals (carcinogens)
3)Diet (30-60% of cancers)
4)Viruses
5)Radiation
5 types
Oncogenes
-cancer-causing genes
-most are proto-ocogenes (soon to be)
Possible Mechs by which Viruses Cause Cancer
4 mechs
1)Carry oncogene into cell and insert into genome
2)Altered cell regulations due to changes in kinase activity or production of regulatory proteins
3)Insertion of promoter or enhancer next to cellular oncogene
4)Insert into host chromosome and disrupt normal functioning proto-oncogene
4 mechs
Types of infections
3 types:
1)Acute
2)Persistent
3)Slow
1)Acute
Rapid onset and relatively short duration (ex flu)
2)Persistent
can last many years
2 types:
A)Chronic
B)Latent
3)Slow
Symptoms may take years to develop (ex HIV, Measles)
A)Chronic Infection
Virus is almost always detectable (diff from latent)

antibodies detected

slow repro w/o causing disease symptoms

symptoms mild or absent for long periods
B)Latent Infections
Remains dormant for some time

not detectable
(HSV, MONO, CHIC POX,)
Viroids
Infectious agents made only of circular ssRNA

cause disease in plants
Prions
-Infectious agent composed of only proteins
-Cause Neogenerative diseases (animals and humans)

-Transmissible Spongioform Encephalopathies (TSEs)
-microscopic holes in brain tissue
-Symptoms= dementia, mycolonia, cerebellar ataxia
PrP
prions protein, found in normal form of host animal
-protease sensitive
-alpha-helix
-soluble

altered PrP^Se(PrP-Res)
-protease resistant
-beta-sheet
-insoluble
PrP interaction and conversion
occurs at cell surface or in endocytic pathway

blocking interaction and conversion may lead to therapy

theories of conversion still not sure yet