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aug 17

Shylla T Inglés 74 fichas

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  1. 1Virionthe mature infectious virus particle
  2. 2Capsidthe protein shell that encloses and protects the viral nucleic acid.
  3. 3Nucleocapsidthe internal part of the virus particle, which consists of the nucleic acid and closely associated capsid proteins.
  4. 4Envelopethe viral membrane, consisting of a lipid bilayer, proteins, and glycoproteins
  5. 5Sizetiny-most not visible under light microscope
  6. 6Nucleic Acid-genetic material.
    -amount varies from enough to code for only three to four proteins to enough to code for several hundred proteins.
    -some viruses have segmented genomes, others have a single piece of nucleic acid.
    -A single type of virus will have only one kind of nucleic acid, either DNA or RNA, in the virion as its genetic material.
  7. 7CapsidFormed of protein subunits called structural units or capsomers.
    Protects the enclosed nucleic acid
  8. 8Complex-found in poxviruses; their morphology is different from that of other viruses.
  9. 9IcosahedralSolid w/ 20 triangular faces, 12 vertices, 2, 3, 5 fold symmetry.
  10. 10Helicalhelical morphology.
  11. 11EnvelopeSurrounds the nucleocapsid.
    Formed from modified host cellular membrane.
    Contains host derived phospholipid bilayer.
    Contains virus-derived proteins and glycoproteins-for attachment and viral fusion.
  12. 12Matrix proteins (M proteins)are often found associated with the inner layer of the envelope. Aid in viral structure.
  13. 13Fusion proteins (F proteins)are found on the envelope surface, they cause viral membranes to fuse with cellular membranes.
  14. 14Membranes on enveloped viruses are essential for their functioning.These types of viruses cannot function without that lipid component.
    Membranes are much easier to strip away with detergents etc than proteins and so enveloped viruses are much more susceptible to inactivation than unenveloped viruses.
  15. 15Steps of Viral Infection of a Host CellAttachment to the host cell
    Entry of virus into the host cell
    Synthesis of viral proteins and genome
    Assembly and release
  16. 16Attachment to the host cellThe presence of viral receptors on the cell surface is the most important determinant of host specificity.
    Viruses tend to be very host specific and can be very tissue specific due to presence or absence of a receptor.
  17. 17example of attachmentCD4 is the receptor for HIV-1 and is present on Macrophages and T-cells, It normally binds to MHC class II and mediates the T-cell response
  18. 18Nonenveloped viruses-1) Bind to host cell surface and rearrangement of capsid proteins.
    2) Viruses engulfed by receptor mediated endocytosis. There is partial breakup of the capsid in the vacuole, followed by migration into the cytoplasm for further uncoating.
  19. 19Enveloped-1) Fusion of viral membrane and cell membrane mediated by a viral F protein (fusion protein).
    2) Phagocytosis (or endocytosis) with fusion of viral membrane with membrane of phagosome (or endosome) mediated by a viral F protein.
  20. 20Different strategies for entry into host cell and uncoatingat plasma membrane, in endosomes, or at the nuclear membrane
  21. 21We went over before that membranes on enveloped viruses are essential for their functioning. It is becausethe F protein or fusion protein is present in those membranes. Without the F protein, the virus cannot enter the host cell and has not evolved the mechanisms that unenveloped viruses possess to enter host cells.
  22. 22***removing the envelop (detergent)that will inactivate the virus
  23. 23The F ProteinThe F protein has a hydrophobic domain that can insert into the host cell membrane.
    The viral and host cell membrane are brought into juxtaposition and are ready to fuse.
    ***all envelop virus have F protein
  24. 24eclipse periodperiod-nucleic acid uncoated from its protective capsid, no infectious particles made
  25. 25latent periodno extracellular virus can be detected but intracellular virus present
  26. 26+ssRNApositive sense single stranded RNA is the same polarity as mRNA, it is mRNA.
    Therefore if you can get the +ssRNA into the host cell, this alone can initiate viral replication and growth without any other help or aid of accompanying viral enzymes.
  27. 27-ssRNAnegative sense single stranded RNA complementary to mRNA, the opposite strand.
    RNA dependent RNA polymerase enzyme must come with a –ssRNA genome into host cell to initiate infection.
  28. 28RNA dependent RNA polymerase-an enzyme that uses RNA as a template for producing RNA (RNA viruses use this to make mRNA and RNA genomes, enzyme not present in host)
  29. 29RNA dependent RNA polymerase shows ahigh mutation frequency, partly because of a lack of a proofreading function that assures fidelity in other processes such as DNA replication
  30. 30RNA dependent DNA polymerase (reverse transcriptase) is even more error prone.RNA viruses mostly replicate in cytoplasm.
  31. 31Most DNA viruses depend on thecellular RNA polymerase II, the enzyme that produces cellular mRNA.
    Most DNA viruses replicate in the nucleus.
    DNA viruses use cellular or viral DNA polymerases to replicate their genomes.
  32. 32Assembly of structural units of virion protein shells: can be fromindividual polypeptides, polyprotein precurser, and/or be chaperone mediated
  33. 33Viral proteins such as enzymes and glycoproteins may be sythesized aspolyproteins.
    Some viruses use proteases to cleave polyproteins into discrete functional viral proteins.
  34. 34Assembly and release of virus 2 mechanismsDisintegration of infected cell (burst)-especially in the case of naked nucleocapsids.
    Slow release- with acquisition of the envelope as the nucleocapsid buds through virus modified cellular membranes.
  35. 35The budding process itself does not harm some host cells significantly. Cells persistently infected with some viruses remain normal in appearance and continue to multiply for many generations while viruses bud from the cell surface. Howeversome cytopathic effects may be seen in infected cells.
  36. 36- Enveloped viruses are more sensitive to inactivation. Unenveloped viruses are more resistant..
  37. 37Enveloped viruses get into cells byfusing their membrane with the host cell via an F protein, they often bud from host cells to be released.
  38. 38Unenveloped virusesburst from host cells.
  39. 39+ssRNA infectious alone, -ssRNA requiresRNA dependent RNA polymerase enzyme to come with it into host cell.
  40. 40General rule (some exceptions)-RNA viruses replicate in the cytoplasm, DNA viruses replicate in the nucleus.
  41. 41Laboratory methods to confirm diagnosisIsolation and growth of virus
    Cytopathic effects in cells
    Electron microscopy to detect viral particles
    Detection of viral components (proteins, enzymes, nucleic acids using ELISA, PCR etc.)
    Evaluation of the patient’s immune response (serology using ELISA, PCR, hemagglutination etc.)
  42. 42Transfectioninfection of mammalian cells by bare viral nucleic acid.
  43. 43Transformation (in virology)a stable heritable change in the genetic makeup and phenotype of a cell resulting from the infection of that cell by a virus. (Usually implies converting to a neoplastic phenotype.)
  44. 44Permissive cellscells that support the complete virus life cycle, with production of infectious virus particles.
  45. 45Non-permissive cellscells which permit none of, or only part of the virus life cycle
  46. 46Defective virusa virus that is not capable of going through its entire replication cycle unless the cell is infected with a complete virus (helper) particle as well
  47. 47Cytopathic effect (CPEobservable damage to a cell resulting from virus infection
  48. 48Proliferation of host cell (transformation)-formation of masses of cells piled on one another (viruses often induce growth).
  49. 49Cell death and lysisRounding of cells and then lysis.
  50. 50Fusion of membranes of adjacent cells (syncytia)-formation of multinucleate giant cells (found especially with viruses that have an F protein).
  51. 51Inclusion bodiesAggregates of viral proteins, HSV: Cowdry type A, and Rabies: negri bodies.
  52. 52Determining infectious units of virus (live cultivation)Serial dilution end point method-looking for
    Plaque formation (viral lysis of cells in tissue culture)
    Focal cytopathic changes in tissue culture
    Focal proliferation of cells in tissue culture
    Pock formation in membranes of chicken embryonated egg
    Infection in experimental animals
  53. 53Cultivation of virusesTissue culture
    Embryonated egg
    Intact animal
  54. 54Enumeration of viral particles-*Electron microscopy
    *Hemagglutinin-some viruses bind red blood cells and make a lattice that prevents red blood cells from falling to bottom of tube
  55. 55Observation of virus or viral products through- immunological meanscomplement fixation- complement is consumed when it is activated by a virus antibody complex, and is unable to lyse red blood cells when these are
    added.
    *direct fluorescent antibody- antibody binds to virus
  56. 56Hemagglutination assayinfluenza virus is diluted and mixed with chicken red blood
  57. 57Western blotviral proteins run on a gel and
    visualized by antibody.
  58. 58* ELISAantibody binds to viral products.
  59. 59PCRpolymerase chain reaction amplifies specific DNA regions
  60. 60Neutralization of infectivity (these are usually antibodies produced to viral surface components) mechanismshinder absorption to cells
    stabilize virus capsid, prevents uncoating
    inhibits membrane fusion and entry into cells
  61. 61Measurement of antibodies produced in response to animal virusesNeutralization of infectivity
    Complement fixation
    Hemagglutination-inhibition
    Latex agglutination
    ELISA
    Indirect fluorescent antibody
    Western immunoblot
  62. 62Pattern of viral presence during infectionLocalized infections
    Disseminated infections-
  63. 63Localized infectionsviral multiplication and cell damage localized near the site of entry.
  64. 64Disseminated infections-1) Local multiplication at the site of entry.
    2) Spread through the lymphatics to the blood stream and circulation in the blood. (primary viremia)
    3) Multiplication at secondary sites
    4) Secondary viremia
    5) Infection of the target organ
    Often the infection is asymptomatic through the first four steps. We call this the incubation period.
  65. 65Inapparent Infections-asymptomatic viral infections (subclinical).
    These are very common, and may result from infection by an attenuated virus or from effective host defense mechanisms
  66. 66Acute Infections-Virus infects host, shortly after disease ensues.
  67. 67Latent infectionvirus particles are not demonstrable, but reappear during recurrences. Viral nucleic acid is demonstrable, even between recurrences. (Herpesvirus infections are the best characterized examples.)
  68. 68Chronic infectionVirus is always demonstrable and often shed. (Hepatitis B infection is the best-characterized example.) Infected cells produces and release virus, but cellular metabolism is little affected and the infected cells can grow and divide.
  69. 69Control of Viral DiseasesPrevention of transmission
    Public health surveillance
    Education
    Isolation of cases of diseases
    Passive immunization-serum
    Active immunization- either live attenuated, inactivated, or subunit vaccines are used.
  70. 70Treatment of Virus DiseasesSymptomatic
    Immune serum- most effective early, before exposure or during incubation period
    Drugs- A limited number of antivirals are available for the treatment of viral diseases.
  71. 71Cytopathic effects-lysis (unenveloped viruses), syncytia formation (F proteins enveloped viruses), inclusion bodies.
  72. 72Transformation of host cells-unrestricted replication of host cells facilitated by viral infection.
  73. 73Viral infections are localized or disseminated; acute, chronic, or latent..
  74. 74Immunity to viruses can beCD8 T-cells, antibodies, interferons, and natural killer cells

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Fichas sobre aug 17, creado por Shylla T el 17/08/2020.
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Shylla T
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