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121 Cards in this Set
- Front
- Back
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t/f
viruses are sub-microscopic obligate extracelluar parasites |
f
intracellular |
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does the virus have a:
ribosome? protein synthesis? cell division? own toxic chemical? |
NO
NO NO NO |
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viruses are made from
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premade components
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t/f
viruses don't have dna or rna |
f
have either dna or rna single or double stranded |
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viruses are covered w/ ----, which are made of ---- components
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capsid/protein
individual |
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this is an additional layer of the virus which is taken from the host
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envelope
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can virues reproduce
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no
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t/f
viruses have their own metabolism proceses |
f
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virus is a ---- parasite
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energy
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the transmission form of a virus
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virion
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t/f
can view virus w/ reg microscope |
False!
need electron microscopy |
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this protect the fragile nucleic acid genome
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capsid: outer shell
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what does the the capsid protect from
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phy damage: shearing
chem damage: enzymatic |
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part that's responsible for recognition of the host
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outer surface
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how does the virus recognize the host
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binding to a specific virus-attachment protein to a cellular receptor molecule
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what initiates infection by delivering genome into host cell
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capsid
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structure of morphology depends on the ----
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capsule
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the outmost layer of enveloped viruses
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envelope
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viral envelope is composed of host ---- and viral ----
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lipid
proteins |
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what's often used for attachment to the host cell
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envelope
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viral proteins on the envelopes
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spike
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size of bac
size of virus |
0.45
0.22 so unfilterable to many |
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unique shape of virus
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icosonhidron
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what does it mean by host range
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viruses infect specific cells, tissues, bacterial, plants
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can an animal virus infect a plant
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no
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what does tissue tropism mean
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several viruses can have receptors for the same host
affinity for the same host |
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this one creates a monolayer and w/ a virus it will aggregat
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plaque assay
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study of viruses
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plaque assay
tissue culture tech plaque forming units |
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the number of plaques on the plaque assay directly relates to the number of ---- ---- ---- applied to the plate
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infectious virus particles
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lytic vs lysogenic
more common, part of course of virus no virus is produced, host accepts dna into chromosome, and is provirus/prophage |
lytic
lysogenic |
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classification of viruses based on
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virion
kingdom of host |
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classification based on
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host cell type
nucleic acid type +/- polarity virus coate morphology |
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types of viruses
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lytic
persistent transforming latent |
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this type causes a chronic infection, some viruses produced, host survives
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persistent
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this type alters dna of host; possibly causes CA
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transforming
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what type of virus:
host survives, feels normal, no virus produced |
latent
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two examples of persistent
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transforming
latent |
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best defense againt virus
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fever
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natural body chem against viruses
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interferon
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animal defenses against viruses
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fever
interferon antibodies drugs |
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which has more choices on how to infect
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animal
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fators that contribute to virulence
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abilty to enter cell
ability to grow w/in cell ability to combat host defense mechanism |
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can you observe virulence in vitro
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no
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viruses have the ability to produce temp or permanent damage in the host via
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cell lysis
production of toxic substances cell transformation |
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who makes the toxic substances the virus or the host
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host
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viruses induce which structural alteration of the host cell
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nuclear - including chromosomal
cytomplamic |
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viruses force some cells to fuse together. this is called
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syncthia
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how do viruses gain entry into host tissue
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trauma
insect bite mucous membranes of resp tract or alimentary tracts |
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thru mucous membranes what are the steps of virus
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1. survival
2. penetration 3. replication or pass thru |
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the host's antiviral defense include
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nonspecfic
specific |
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what the antiviral specific include
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antibody
phagocytes |
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non specific host defense mechanism include
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humoral factors
cellular factors |
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humoral factors in antiviral war include
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low pH of inflammatory exudates
enzymes mucous virocidins |
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cellular factors include
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nucleases
proteases interferon these can kill dna or rna |
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name 6 ways in which the virus can grow in the cell
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1. fast action
2. adapt to biochemical conditions insde the host 3. able to resist or not stimulate host defense mechanisms 4. go from cell to cell 5. antigenic shift 6. shape of protein |
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how do viruses avoid the immune system
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by going from cell to cell
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steps for viruses to be successful
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1. Attachment
2. Penetration 3. Synthesis of precursors of low molecular weight compound 4. Assembly |
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how is the host damaged due to viruses
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1. host lysis
2. production of toxic substances 3. cell transformation 4. suppression of the immune mechanisms |
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cell lysis occurs due to
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cytotoxic immunopathology
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how are the toxic substances produced
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complement fixation
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how is cell transformation done
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kill regulatory mechanisms
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how can cytopathology alter cells?
what can occur due to this |
alter by cell lysis, syncytia
can possibly be cancerous |
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in host damage there's induction of --- ----- host specified products
there's also of --- alterations in the host cell |
non-normal
structural |
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in type 1 the --- antibodies are fixed to --- --- to react w/ complete virus or w/ viral components
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Ig E
mast cells |
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what's involved w/ type 2
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IgG
IgM |
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in type 3 the virus- ---- antibody ----- is fixed to a cell
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complement
complex Results in complement cascade; cellular apoptosis with subsequent inflammation response. |
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in 4 the virus component, commonly the ---- protein, is expressed on the surface of the infected cell
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capsid
Virus component (portion of capsid) expressed on cell surface. This would occur in antigen presenting cells (APE), namely cells with the MHC I complex. |
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in type 4 what's the target
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cmi target
phagocytic cells |
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flu like symptoms due to
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interferons
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complement fixation might be a result of
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immunocomplex
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how can viruses evade the immune resoponse
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1. inhibition fo MHC class 1 restricted antigen presentation
2. inhibition of MHC class 2 restricted-antigen presentation 3. inhibition of natural killer cell lysis 4. inhibition of cytokine aciton 5. evasion of humoral immunity |
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routes of entry
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resp tract
alimentary tract skin genital tract conjunctiva |
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most common route of entry for viruses
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mucous membrane
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of hte routes of entry which is not a mucous membrane
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skin
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what's 2ndary viremia
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enter goes to blood, to lymph, other organs
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main route for viremia
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resp tract
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name some 2ndary viremia
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CNS
other organs after entrance fetus |
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viremia is when the virus spread by the ---
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bloodstream
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two types of persistent
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latent
transforming |
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# 1 site of viral shedding
# 2 |
1. resp and oropharygeal secretions
2. feces |
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other routes of shedding
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urine
milk genital secretions blood |
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type of viral interactions
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permissive or productive
abortive or nonproductive persistent latent cytopathic effects |
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in this virus cell interaction some cellsa re infected due to receptors, virus is produced, and the host dies
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permissive or productive infection
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which is the norm course of action in the types of virus-cell interactions
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permissive or productive infection
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in abortive or nonproductive the virus enters cell, --- genes are turned on, no futher expression occurs. the ---- survives. --- is unsuccessful.
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few
host virus virus cannot replicate inside host |
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how do viruses increase the risk of cancer
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make cells more prone to mutation
cell to cell contact inhibition disrupted increase metabolism |
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viruse carry -----genes which can cause cancer
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onco
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how are the viruses in persistent infectio released:
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exocytosis
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(Many/Few) cells are produced after permissive cells die
Most cells are inhibited, but don't die |
Few
virus slowly reproduced host lives |
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ex of latent viral infection
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herpes
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which type of virus cell interaction:
part of the host forever replicate w/in host no harm done to the host |
latent
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latent infection: the virus might become part of the the ----
provirus |
DNA
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why is the virus latent
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host does not have nulceases to kill
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in which interaction is their plaque formation
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cytopathic
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what structures are changed in cytopathic
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mucleus
membrane fibroblast viral budding |
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this virus interaction has Syncytia formation, lysosomes leaking, inclusion bodies by staining
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cytopathic
CPE |
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inhibition of host protein synthesis lead to inhibion of host ---- synthesis
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macromolecular
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integration of viral genome into host - alters host
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transformation
can cause CA |
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lytic virus complete ---- interaction
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celll
productve infection results in multiplication and release of virus |
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steps of one step growth cycle
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1. attach or adsorb to cell
2. penetration by fusio or endoctyosis 3. eclipse: infectious virus not detectable 4. rise: infectious particles detecable |
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early rise:
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before nulceic acid synthesis
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late rise:
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after nucleic acid synthesis
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when the virus goes inside host was does it bring
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RNA/DNA
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viral replication steps
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1. attachment
2. penetration 3. replication 4. assembly/maturation 5. morphogenensis/release |
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types of attachment/adsorption
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ionic attraction
peplomers, spikes, capsomers, or glycoproteins intera w/ cellular receptor |
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what brings the virus in?
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receptor mediated endocytosis
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what's necessary after inside cell
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uncoating
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what determines entry into cell
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EM
no longer being able to neutralize virus |
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penetration and uncoatig allowed by ---- to microvilli or the ---- coated pits
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adsorption
clathrin |
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penetration by:
endocytosis, ------ or ---- |
invagination
viroplexis |
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--- coated vesicles in cytoplasm funs w/ ----- for transport to nucleus or uncoating in cytoplasm
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clathrin
endosome |
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----- fusion virus goes directly into cytoplasm
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membrane
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------- partially uncoated to subviral particle in cytoplasm
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reovirus
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--- coated vesicles are on surface to the cells. the virus recognizes, binds and goes inside
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clathrin
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low/high pH needed to open up and release virus
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low
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low pH causes --- of virus to endosome and uncoats
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fusion
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t/f
viruses uses their own enzymes and structural components such as actin fibers, membranes, and ribosomes |
f
they use the host |
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influenza virus has a ---- and ---
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spike
envelope |
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where does the membrane origninate?
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inside cell
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when the virus buds what does it have?
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full membrane
envelope |
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no viruses in the
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hair
ear |
