Micro Viruses Answers – Flashcards
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| what is a nucleocaspid |
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| genetic material and capsid of a virus |
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| what is a viron |
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| nucleocaspid plus the viral envelope |
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| what are the possible shapes of a nucleocaspid |
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| symmetrical: icosahederal or helical complex |
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| what is a viral envelope made of |
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| lipid bilayer of the host and viral glycopeoteins |
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| what are the down sides of a virus that needs an envelope |
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| more susceptible without host to drying and acidity |
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| what are the benifits of being a virus that does not need an envelope |
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| more resistant to acid, survive better without a host |
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| what are the options for composition and shape of the genetic material in a virus, how many combinations of this can a virus have |
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| DNA, RNA, single stranded, double stranded, circular, linear they can only be DNA OR RNA, circular OR linear |
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| how does a virus replicate its genetic material and make babies, why does it do it like this |
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| uses host machines to duplicate the genetic material because it has no reproduction machines, ribosomes, membranes, or enzymes of its own |
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| what is a capsid, where is it located, what is it made of, how is it compositionally organized, what is its function |
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| it is the proteiin coat around the virus made of capsomere proteins that are repeating units because the virus has little genetic material its job is to attach to host cell receptors |
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| name a bunch of ways viruses can be named and classified (8) |
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| capsid proteins nucleic acid composition and shape envelop or none size shape mode of replication and transmission (DNA, +/- RNA) target host type of infection where it was discovered |
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| list the virus shapes and an example for each (4) |
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| icosahederal: 20 faces on the capsomere. adenovirus (DNA virus that infects GI and upper respiratory) complex: pox virus rotavirus: wheel like (causes watery diarrhea in kids) corona: club like glycoproteins on the surface (respiratory viruses like SARS) |
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| what is the primary way to identify a virus in clinical situations |
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| serology |
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| what are the methods of viral transmission (11): give a few examples for each |
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| aerosol: rhinovirus, influenza dust: urine, feces ingested: HepA, norovirus transplacental: HIV, HepB sexual: HIV, HPV, HBV, HSV-2 skin contact organ transplant: CMV, HepC, HIV injection: HBV, HCV, iV drugs bites: rabies trauma arthropod bite: yello fever, west nile, dengue, encephalitis |
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| what makes viruses host or cell specific |
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| ability of virus to attach to the cells due to intermolecular forces, interactions between nucleocapsid (in naked virus) and virus membrane (in enveloped virus) with host membrane |
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| what occurs in the eclipse phase |
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| virus genetic material is in cytoplasm and the virus is no longer infectous, the envelope of capsid has ben shed upon entry |
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| where does viral replication take place, what viruses are exceptions |
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| in the nucleus except pox and rabies which is in the cytoplasm |
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| define trophism, where might it take place for example |
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| virus travels to preferred tissue some viruses replicate and remain at site (rotavirus in the GI) some viruses replicate and disseminate |
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| give examples of viruses that replicate and disseminate and their locations |
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| viremia: measles travels from URT to skin to CNS HIV: macrophage takes it to lymph then CD4 to CNS rabies: skin to peripherial neuron to CNS |
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| when a virus gets up to the cell how does it attach, what receptors |
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| viral glycoproteins attach to cell membrane salic acid receptors then penetrates with fusion proteins, shedding capsid |
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| explain how retroviral genetic material is replicated |
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| +ssRNA and viral reverse transcriptase make -ssDNA -ssDNA is duplicated with cellular DNA polymerase to dsDNA dsDNA is integrated into host genome host polymerase makes mRNA which causes translation |
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| explain how a dsDNA virus replicates its genetic material |
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| host polymerase turns dsDNA into mRNA which causes translation |
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| explain how a RNA virus relicates its genetic materal |
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| viral polymerase turns RNA into mRNA if mRNA is positive it can proceede to translation if mRNA is negative a viral RNA polymerase makes a positive mRNA from it then it goes to translation |
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| what is the order viral proteins are made in |
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| 1: enzymes and regulatory molecules for nucleic acid replication 2: proteins for capsid formation 3: genetic material |
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| oh no. the virus is simple and can only make one protein... how will it make all of the parts of the babies?? |
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| its ok. the one protein is made in the ribosome of the host then proken apart into the many proteins needed |
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| explain how budding works |
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| envelope proteins and glycoproteins are made and inserted into the host membrane nucleocapsid associates with membrane glycoproteins host enzymes cleave membrane virus acquires host membrane envelope |
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| what glycoproteins does a budding virus make |
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| hemagglutinin and neuraminidase |
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| why does a budding virus suck even more for the cell |
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| insertion of viral molecules into the membrane, pre budding, causes the cell to be antigenically different allowing immune response |
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| what types of viruses replicate via lysis |
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| naked ones that kill cells |
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| what are the different types of viral infection (4) |
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| lytic, persistant, latent/incubation, transofrmative |
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| what is a lytic infection, what type of virus may do this |
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| causes cell lysis upon release of replicated virons polio |
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| what is a persistant infection, why can this type be sacary |
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| cell remains alive and releases particles at a slow rate someone can be a symptomless carrier and be passing around the disease |
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| what is a latent infection? how does it work? what viruses do this? |
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| genetic material hides in cytoplasm or genome replication is slow so immune system dosent react stress enhances the replication, then the immune system responds |
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| define a transformative virus infection |
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| virus transforms host cell into milignant cell by changing morphology or cell chemistry |
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| why do the changes in a transformative infection cause milignancy |
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| interfere with regulation of division or promote growth cells divide or arregrate |
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| what are examples of viruses that can cause a transformative infection (10) |
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| human T cell lymphotrophic virus type 1 epstin-barr virus HPV 16, 18, 31, 45 HepB HepC adenovirus HVB ECV HCV HHV-8 |
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| explain the two MOA transformative viruses use to cause milignancy |
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| direct mechanism: expression of viral oncogenes that transform cells indirect mechanism: chronically infect cells causing inflammation and mutations, production of proteins causes oncogenic mutations |
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| oncogenes: where do they come from and what evidence is there for their origin, why did god invent them initially |
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| come from virus or host. introns suggest they originated in the host origional oncogenes in the host (protoncogenes) code for growth factors for development and such but are supposed to be turned off or controlled |
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| how do oncogenes cause milignancy (3) |
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| when inserted into the genome the genes around them become uncontrolled can inhibit growth regulator p53 can inhibit apoptosis |
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| how are oncogenes transmitted (2 main methods) |
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| vertical: mother to offspring via gametes, placenta, or milk horizontal: saliva, urine, etc |
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| how do viruses effect the body |
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| protein synthesis synctia: fusion of cells cytoskeleton disruption DNA synthesis inhibition inclusion body firmation activate apoptosis inhibit apoptosis prodromal effects immune response damage cytotoxicity neurological symptoms chronic infection congenital infection |
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| what viruses cause chronic and congenital infections |
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| congenital: parovirus B19, rubella, CMV chronic: HBV, HCV, HIV |
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| what viruses cause neurological symptoms |
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| encaphalitis: rabies, west nile, EEE lower motor neuron: polio |
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| what viruses cause cytotoxicity |
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| herpes simplex |
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| what viruses cause immune response damage, specifically what damage |
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| measles chicken pox chronic hepatitis: chirrosis loss of CD4: HIV abnormal B cells: epstein barr splenomeagly: epstein barr development of immunity: measles dengue hemorrhagic fever |
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| what are prodromal effects, give an example |
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| inflammatory response via cytokines headachem body ache, chills influenze: cough, fever, congestion, gastroenteritis |
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| how can you block attachment of a viral capsid |
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| neutralize the antibodies on its surface |
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| what does pleconaril do |
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| block uncoating of enterovirus, treats influenza |
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| what does neuraminidase do |
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| stops influenza |
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| what does interferon alpha beta do |
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| stops protein synthesis in viruses |
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| what antivirals stop viral polymerase (protease inhibitors) |
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| saquinavir, indinavir |
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| what antiviral nucleotide analogs are there,how do they work, what viruses do they target |
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| target nucleic acid synthesis from viral nucleic acid template acyclovir: HSV, VSV grancyclovir: CMV ravavirinL RSV, parainfluenza |
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| what drugs are reverse transcriptase inhibitors |
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| zidovudine lamivudine |
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| what does atazanivir do |
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| nucleoside reverse transcriptase inhibitor |
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| what does the invluenza antiviral drugs target |
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| the budding process |
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| how do HIV antivirals work |
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| fusion inhibitor: peptide interferes with gp41 RSV: activates F protein |
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| wha are some innate host defenses (5) |
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| skin, mucosa, pH, tears, salts/bile |
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| what are the types of vaccine, give examples for each |
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| killed: influenza, salk polio, Hav attenuated: measles, mumps, rubella subunit: HBV |
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| how do macrophages find viruses |
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| macrophages target dsRNA and viral DNA |
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| what cytokines find viruses |
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| IL-1 and TNF |
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| what interferons find viruses, what do they do to them |
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| alpha and beta, stop protein synthesis gamma activates t and NK cells |
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| when IgG finds a virus, what happens next |
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| allows NK Fc receptors to attach signaling apoptosis |
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| how does CD8 cause apoptosis |
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| perforins and granzymes activate capsases |
