Micro Exam 3 Test Questions – Flashcards

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question
3 virus epidemics
answer

1. influenza- spanish flu 1918 - crossed the country in 3 days, over 100 million deaths

2. Four corners disease- Western state - native americans come down with pulmonary disease - hantavirus and sin nombre

3. Norovirus - from cruise ships - vomiting and diarrhea; morbidity

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Hantavirus
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- related to four corners disease

- found in rodents

- sin nombre is the strain that jumped the species barrier

- increased rate of mortality

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Virus classification (5)
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1. host range

2. size

3. virion type

4. viral symmetry

5. nature/expression of the genome

 

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Host range
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- what types of organisms are effected

 - bacteriophage - virus that infects bacteria only

- eukaryotic cells like protozoa, plants, fungi and algae are effected

- viruses that effect animals may or may not effect us

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Size of virus
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- electron or light microscopy

- very small (molecular size) to large (barely visible under light microscopy)

- poxvirus and mimivirus are the 2 largest viruses

- mimivirus is a potention evolutionary bridge

- hemoglobin is one of the smallest

- how large virus is reflect how much genetic information they have; more info, less dependent

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virion type
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- nucleic acid/viral core

- protein capsid

- naked virus: nucleocapsid, less susceptible

- enveloped virus: ether sensitive, envelope around protein coat, no effective without enveloped (cannot infect or replicate)

 

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Peplomers
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- AKA spikes

- on the envelope

- not all viruses have them

- important to coronavirus (SARS)

- crown-like appearence

- imporant for attachment

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Viral structural organization
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- nucleic acid core

- proten capsid

- capsid is made up of capsomers - discreet, small, protein subunits

- capsomers are made up of protomers

- virion is the entire infected particle made up of all the parts listed

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Viral symmetry
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- TMV- tobacco mosaic virus

- helical symmetry: capsomers attached to core and compressed in a circle because of envelope

- helical structure is also filamentous

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Neuraminidase & hemagglutin
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Ne or N / He or H

- orthomyxoviridae

- change on an annual basis

- why we are immunized every year- different strains

- ex) h1n1, h1n2, h3n1 etc.

- cause of antigenic drift

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Antigenic shift vs. anigenic drift
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shift: major changes that can occur in the antigens of a virus -- epidemics

drift: slight changes that occur in the antigens of a virus; specific antibodies made in response to the antigen before the change occurred are only partially protective -- exterior of virus shifts away

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Icosahedral vs. complex/binal symmetry
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- i: cubic, regular, polyhedral, isometric

--> 12 vertices/points, 20 faces, 30 edges

--> pentons at points, hexons at edges

--> capsomers not attached to core, core is free

--> more volume/surface area

--> no filaments

- complex/binal: reminiscent of bacterial cells with nucleoid ex) poxvirus

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Nature of the genome
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- RNA vs. DNA

- double vs. single stranded

- circular vs. filamentous

- segemented

- both can never make up core; one or the other

- monopartit vs. multipartite

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Dependent/polymerase combinations
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- DNA dependent/RNA polymerase: produces RNA from DNA

- RNA dependent/DNA polymerase: produces DNA from RNA

--> AKA retrovirus

--> reverse transcriptase

--> oncogenic- capable of causing cancer

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Viral core "sense"
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RNA- single stranded

- RNA +: mRNA transcription, translated by eukaryotic cell

- RNA-: needs to be manipulated/altered so a + sense  can be produced from it; replication intermediate

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How do we prevent drug resistance? (7)
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1. educate the public- viral vs. bacteria, costs

2. antibiotic sensitivity testing- avoid encouraging resistance

3. use narrow spectrum compounds- avoid super infection

4. use combinations (synergy)

5. rigidly contain resistant organism (isolation/quarantine)

6. take all required medication on schedule - on time to maintain constant levels, full days supply

7. restrict use of therapeutically valuable antimicrobics for nonmedical purposes- ex) cattle - leads to food poisoning

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Mechanism of bacterial resistance to antibiotics (7)
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1. enzymatic cleavage

2. chemical modifations- inactivation

3. reduced uptake- due to mutation

4. active efflux of antibiotic from cell- pumped out as same rate of entry

5. eliminate/reduce binding to target

6. metabolic bypass of inhibited reactions(salvage pathway)- bypass, shunt, work around

7. overproduction of target- ratio of enzyme/metabolite to antimicrobial (sulfa/PABA)

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Chemical modification / inactivation (3 ways)
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1. acetylation

2. phosphorylated

3. adenylated

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Development of antibiotics resistance (3)
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1. spontaneous mutation- vertical gene transfer

2. gene transfer- horizontal gene transfer; includes conjugation, transformation, transduction

3. plasmid promiscuity- transfer is extensive; r-plasmids

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Viral replication based on genome
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6 types:

1.+/- DNA

2. - DNA

3-5 RNA

6. reverse transcriptase

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Replication intermediates
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dsDNA

ssDNA

dsRNA

ssRNA

* intermediate needed to get to + mRNA

* important in synthesis/replication

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Viral replication steps (6)
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1. Adsorption/attachment

2. Penetration

3. Uncoating- liberation from capsid, protease/protein splitter

4. Synthesis/replication

5. Assembly/maturation

6. Release

* time varies; rhino and adenovirus can take as little as 24 hours, others take years

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Adsorption
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- naked virus: receptors on capsid

- enveloped virus: receoptrs on envelope

- adsorption can be increased by density or amount of viruses

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Tropism examples (6)
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- Neurotropic: rabies- effects neurons, localized in NS

- Pneumotropic: influenza- effects respiratory epithelium

- Viscerotropic: rotavirus, noravirus, poliovirus- effects intestinal epithelium

- Immunotropic: HIV- t-helper cells (on CD4 cells) become infected and dysfunctional

- Cytomegalovirus: effects many systems- epilthelium, monocytes, lymphocytes

- EB: epstein barr- mononucleosis (mono)

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Penetration
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- depends on kind of virus and if it is enveloped

- can identify viruses by probes due to proteins

- penetration and uncoating can occur simultaneously

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Penetration of naked virus vs. enveloped virus
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- naked: not just endocytosis; capid is unstable

- enveloped: endocytosis and fusogenic proteins on plasma membrane

--> endocytosis forms double membrane

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DNA vs. RNA synthesis/replication
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RNA- in cytoplasm

DNA- in nucleus

* exceptions: varcinia (cowpox), variella (smallpox)

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Single strand DNA
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+ssDNA, AKA +D1

-ssDNA, AKA -D1

* +/- ssRNA forms dsDNA intermediate to make mRNA with help of reverse transcriptase from +ssRNA

* dsDNA can jump in whenever it wants; bad results

 

 

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Single strand RNA
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+ssRNA- AKA +R1

--> can be used directly to form +mRNA at right polarity and sense

--> template to form -ssRNA

--> +/- ssRNA combination makes a lot of +mRNA

-ssRNA- AKA -R1

--> needs RNA dependent RNA polymerase

--> contributes to translation

--> second intermediate may be needed to reach genome

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Replication stages
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1. early transcription

2. early mRNA

3. early protein

* switches to late once viral cores have been synthesized (genome copies)

* compromises host cell as it is making virus instead of maintaining the cell (morphological changes)

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CPE
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- cytopathic effects

- viral induced damage to infected cell that alters microscopic appearence

- occurs during synthetic phase

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CPE examples (5)
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1. cell rounding- lose membrane

2. cell lysis

3. nuclear pyknosis- nucleus becomes coarse and clumps together; intense stain

4. Nuclear/cytoplasmic inclusion bodies

5. Multinucleated giant cell formation 

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Multinucleated giant cell formation
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- AKA: syncytial formation

- nuclei cluster in middle or periphery

- negri bodies- neuronal tissue characteristic of rabies

- basophilic bodies- characterization of hepatitis (liver tissue)

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Assembly/maturation
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- varies with different viruses

- core encased in capsid material

- can be self assembling (encapsidation)

- location varies as well; some will assemble where they undergo synthesis

ex) Dna=nucleus, Rna=cytoplasm

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Acute viral infection
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- AKA: productive or lytic

- virus remains localized and disappears when disease ends

- activitity shutdown; cells killed (rupture)

- release of virus is dependent on cell dying

 - virus is released after cell lyses

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Multiplicity of infection
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MOI

- number of virus particles that are released

- range for 10 to thousands

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Budding in viral infections
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- enveloped viruses

- cell membrane is modified by removing proteins and adding virus matrix proteins (exit proteins)

- phospholipid bilayer is left in tact

- virus matrix proteins fuse to cell membrane and undergo endocytosis

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Sialic acid
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- neuraminidase cleaves sialic acid on the membrane/envelope in order to release virus

- neuraminidase inhibitors limit influenze infection

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Persistent viral infection
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- virus that is released by budding usually survives

- viral infection does not always result in death, just alteration

- establishes infection and remains for a long time period

- no symptoms

- may or may not cause disease; person can be a potential source of infection

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Tumor cells
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- oncogenic- capable of causing cancer

- damage to cells can lead to tumor cell formation

- virus integrates into host cell chromosome

- can jump in anywhere: regulatory protein, plasmid or chromosome

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Latent infection
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- integrate into host of chromosome but no abnormal changes of host cell (provirus)

- can cause infection by plasmid replication

- symptomless period followed by reactivation

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Reactivation of viral disease (4)
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1. latent virus

2. Herpes simplex virus (HSV-1, HSV-2)- cold sore, fever blister, lesion that is reactivated due to stress, additional disease, or depressed immune system

3. VZ virus- varicella zoster - chicken pox is reactivated as shingles (herpes virus, not poxvirus)

4. EB- ebstein barr- mononucleosis and burkitt's lymphoma (hepes virus)

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Cancer in animals (3)
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- role of viruses and cancers:

1. bittner mammary tumor virus

2. gross murine leukemia virus

3. raus sarcoma virus

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Cancer in humans (5)
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- role of viruses and cancers:

1. t-cell leukemia caused by human t-cell leukemia virus type 1 (RNA)

2. Burkitts lymphoma caused by;epstein barr (DNA)

3. Nasopharyngeal carcinoma caused by epstein barr (DNA)

4. Hepatocellular carcinoma caused by hepatitis B (DNA)

5. skin and cervical cancer caused by papilloma (DNA)

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How do we study viruses?
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- need living systems since viruses are obligate intracellular parasites

1. laboratory animals

2. embryonated eggs

3. cell, tissue and organ cultures- Robert Enders

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Embryonated eggs
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- membrane- herpes, pox, raus sarcoma

- amniotic- influenza, mumps

- yolk sac- herpes

- allantoic- influenza, mumps, newcastle, adenovirus

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Colony forming units calculation
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# of colonies / 1

x 1 / aliquout

x 1 / microliter amt

;

ex) 74/1 x 1/10^-6 x 1/100 microliters

7.4x10^1 x 10^6 x 10^1 = 7.4x10^8 CFU/mL

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Axenic, pure, mixed cultures
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a: culture that contains a signle known genus and species of bacteria

p: signle genus and species of bacteria but identity of the organism may not be known

m: two different types of bacteria

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E. coli, Serratia marcesens, Micrococcus luteus colors
answer

e: cream, white colonies

s: red colonies (from prodigosin)

m: yellow colonies

;

* use tstreak technique to streak for isolation from mixture

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