The Viruses and VirusLike Agents

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Chapter 13

• The Viruses and Virus-Like Agents

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13.1 Foundations of Virology

• Many Scientists Contributed to the Early
  Understanding of Viruses
• Dimitri Ivanowsky and Martinus Beiherinck studied
  the tobacco mosaic virus
• Walter Reed studied foot-and-mouth disease and
  yellow fever

Figure 13.3b, page 371
Figure 13.4, page 373
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• Frederick Twort and Felix dHerelle studied
  bacteriophages
• In the 1930s, it was discovered that viruses are
  nonliving agents composed of nucleic acid and
  protein
• Alice M. Woodruff and Ernest W. Goodpasture
  developed a culture technique using chicken eggs

Figure 13.2, page 371
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13.2 What are Viruses?

• Viruses Are Tiny Infectious Agents
• Viruses are small, obligate intracellular
  parasites
• They lack the machinery for generating energy and
  large molecules
• They need a host eukaryote or prokaryote to
  replicate
• The viral genome contains either DNA or RNA, but
  not both

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• The capsid is the protein coat, made up of
  capsomeres
• The nucleocapsid is the capsid with its enclosed
  genome
• Some capsid proteins are spikes that help the
  virus attach to and penetrate the host cell

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• Naked viruses are composed only of a nucleocapsid
• Viruses surrounded by an envelope are enveloped
  viruses
• A virion is a completely assembled, infectious
  virus outside its host cell

Figure 13.5, page 374
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• Viruses Are Grouped by Their Shape
• Helical viruses have helical symmetry
• Isocahedral viruses have isocahedral symmetry
• Viruses that have both helical and isocahedral
  symmetry have complex symmetry

Figure 13.6, page 375
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• Viruses Have a Host Range and Tissue Specificity
• A host range refers to what organisms the virus
  can infect
• Host range depends on capsid structure
• Many viruses infect certain cell or tissue types
  within the host (tissue tropism)

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13.3 The Classification of Viruses

• Nomenclature and Classification Do Not Use
  Conventional Taxonomic Groups
• Viruses can be named according to a number of
  different conventions
• The International Committee on Taxonomy of
  Viruses (ICTV) is developing a classification
  system
• DNA viruses contain single- or double-stranded
  DNA genomes

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• RNA viruses contain single- or double-stranded
  RNA genomes
• strand RNA viruses have mRNA genomes
• strand RNA viruses have RNA strands that would
  be complementary to mRNA
• Retroviruses are replicated indirectly through a
  DNA intermediate

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13.4 Viral Replication and its Control

• The Replication of Bacteriophages Is a Five-Step
  Process
• T-even group bacteriophages are virulent viruses
  that carry out a lytic cycle of infection
• The phage nucleic acid contains only a few of the
  genes needed for viral synthesis and replication

Figure 13.7a, page 375
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• Phase 1 Attachment occurs when a phages tail
  fibers match with a receptor site on the
  bacteriums cell wall
• Phase 2 Penetration occurs when the phage tail
  releases lysozyme to dissolve a portion of the
  cell wall
• Phage DNA is injected into the bacterial
  cytoplasm
• Phase 3 Biosynthesis is the production of new
  phage genomes and capsid parts
• Phase 4 Maturation is the assembly of viral
  parts into complete virus particles
• Phase 5 Release is the exit of virions from the
  bacterium
• It is also called the lysis stage when the cell
  is ruptured

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• Temperate phages do not lyse the host
• They insert their DNA into the bacterial
  chromosome as a prophage (lysogenic cycle)

Figure 13.8, page 380
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• Animal Virus Replication Has Similarities to
  Phage Replication
• Animal viruses attach to host plasma membrane via
  spikes on the capsid or envelope

Figure 13.9, page 382
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• Since receptor sites vary from person to person,
  some people are more susceptible to a certain
  virus than others
• Animal viruses are usually taken into the
  cytoplasm as intact nucleocapsids
• Uncoating is the separation of the capsid from
  the genome
• This occurs as some animal viruses enter the cell

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• After the new viruses are assembled, envelope
  proteins are incorporated into a cellular
  membrane
• The virus buds, taking the membrane part with it
  as an envelope

Figure 13.10, page 383
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• Some Animal Viruses Can Exist as Proviruses
• Some DNA viruses and retroviruses insert their
  genome into the host chromosome as a provirus
• Retroviruses use reverse transcriptase to
  transcribe their RNA to DNA
• It can then be inserted into the host chromosome

Figure 13.11, page 384
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• The provirus encodes a repressor protein that
  prevents activation of the viral genes necessary
  for replication
• It is in a state of latency
• Latent proviruses are immune to the host bodys
  defenses
• They are propagated each time the cells
  chromosome is reproduced
• Eventually the provirus will be activated and
  replicate

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• Antiviral Drugs Can Be Used to Treat a Limited
  Number of Human Viral Diseases
• Antibiotics do not work against viruses
• Viruses lack the elements with which antibiotics
  interfere
• Some antivirals exist to affect
• viral penetration/uncoating
• genome replication
• maturation/release

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• Most antivirals target the replication enzymes of
  the virus by
• inserting base analogs in the replicating DNA
  strand
• blocking replication of the viral genome
• Reverse transcriptase inhibitors prevent the
  synthesis of DNA in retroviruses
• Protease inhibitors impede the HIV protease that
  trims viral proteins in capsid construction
• Neuraminidase inhibitors block an enzyme in the
  spike of influenzaviruses
• This prevents the release of new virions into the
  body

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• Interferon Puts Cells in an Antiviral State
• Interferon (IFN) is a group of naturally-produced
  proteins that alert cells to a viral infection
• Some IFNs have anti-cancer properties
• Cells in an antiviral state can inhibit viral
  replication by preventing protein synthesis

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• IFNs bind to receptors on cells, triggering them
  to produce antiviral proteins

Figure 13.12, page 388
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13.5 The Cultivation and Detection of Viruses

• Detection of Viruses Often Is Critical to Disease
  Identification
• Rivers postulates expand upon Kochs postulates
  to help identify viruses
• Filtrates of infectious material shown not to
  contain bacterial or other cultivatable organisms
  must produce the disease or its counterpart
• Filtrates must produce specific antibodies in
  appropriate animals

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• Cytology uses light microscopy to examine cells
  for cytopathic effects (CPEs) of viral infection
• Unusually, viruses can be observed directly by
  electron microscopy

Figure 13.13, page 390
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• Cultivation and Detection of Viruses Most Often
  Uses Cells in Culture
• In a primary cell culture, cells form a monolayer
  in a culture dish
• The type of cell culture depends on the virus to
  be cultivated in the monolayer
• Viruses can be detected by the formation of
  plaques, a clear zone within the monolayer

Figure 13.14c, page 391
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13.6 Cancer and Viruses

• Cancer Is an Uncontrolled Growth and Spread of
  Cells
• A tumor is a clone of abnormal cells
• Normally, the body surrounds a tumor with a
  capsule of connective tissue
• a benign tumor
• Tumor cells can break free from the capsule and
  spread to other tissues of the body (metastasis)
• a malignant tumor

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• Viruses Are Responsible for Up to 20 Percent of
  Human Tumors
• 60-90 of human cancers are associated with
  carcinogens

Figure 13.15, page 393
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• Oncogenic viruses include
• Epstein-Barr virus is linked to Burkitt Lymphoma,
  a tumor of the jaw
• Human papilloma virus (HPV) is associated with
  cervical cancer
• There is now a vaccine against the 2 most common
  strains of HPV

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• Oncogenic Viruses Transform Infected Cells
• The oncogene theory suggests that protooncogenes
  normally reside in the chromosomal DNA of a cell
• They can be transformed to oncogenes by
• radiation
• chemical carcinogens
• DNA damage
• viruses

Figure 13.16, page 395
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• Sometimes a virus inserts its DNA (as a provirus)
  into a cells chromosome next to a protooncogene
• When virus replication is triggered, the provirus
  replicates its only DNA as well as a few adjacent
  host genes
• V-oncogenes are protooncogenes captured in the
  viral genome
• When the oncogenic viruses infect another cell,
  the v-oncogene is under the virus control not
  the cells control
• The v-oncogene can then code of growth factors
  stimulating uncontrolled cell proliferation

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Figure 13.17, page 396
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13.7 Emerging Viruses and Viral Evolution

• Emerging Viruses Usually Arise Through Natural
  Phenomena
• Emerging viruses may spread to new populations,
  or may expand host range
• Genetic recombination can lead to new viruses
• Mutation can occasionally be advantageous and
  create a new or new strain of virus

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• There Are Three Hypotheses for the Origin of
  Viruses
• The regressive evolution hypothesis
• Viruses are degenerate life-forms
• The cellular origins hypothesis
• Viruses are derived from subcellular components
  and macromolecules that escaped from cell walls
  and replicated inside hosts
• The independent entities hypothesis
• Viruses coevolved with cellular organisms from a
  self-replicating molecule present on primitive
  Earth

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13.8 Virus-Like Agents

• Viroids Are Infectious RNA particles
• Viroids are tiny fragments of RNA that cause
  diseases in crop plants
• The replication cycle and disease causation
  process of viroids are not understood
• One hypothesis suggests they originated as introns

Figure 13.18, page 400
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• Prions Are Infectious Proteins
• Transmissible spongiform ecephalopathies (TSEs)
  can occur in humans and other animals
• For example, mad cow disease
• TSEs are neurologic degenerative diseases that
  can be transmitted within or between species
• Originally, scientists believed TSEs were caused
  by a virus
• Stanley Prusiner discovered the proteinaceous
  infectious particle (prion)

Figure 13.19a, page 401
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• The protein-only hypothesis predicts that prions
  are composed only of protein and contain no
  nucleic acids
• Normal cellular prions have a different shape
  than abnormal prions, the latter of which cause
  TSEs
• TSEs may spread when infectious prions bind to
  normal prions
• This causes normal prions to change shape and
  become abnormal
• Abnormal prions do not trigger an immune response

Figure 13.19b, page 401
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• Death of the host occurs from nerve cell death
  leading to sponge-like holes in brain tissue
• Symptoms include
• dementia
• weakened muscles
• loss of balance
• This results from insoluble aggregates of
  abnormal prions in the brain
• The human form of TSE is called variant CJD
  (Creutzfeldt-Jakob disease)