Lysogenic Replication

1
Lysogenic Replication
3
Prophagein chromosome
2
Entry
Lyticcycle
Lysogeny
Synthesis
6
Release
8
4
Replicationofchromosome(and progeny)cell
division
7
Assembly
Further cell divisionreplications
Induction
5
2
Lysogenic Conversion

• Prophage may confer new properties upon cell
• Corynebacterium
  diphtheriae
• Synthesis of diphtheria toxin
• Clostridium
  botulinum
• Synthesis of botulism toxin
• Streptococcus
  pyogenes (?-hemolytic)
• Streptoccal exotoxin responsible for scarlet
  fever
• Salmonella
• Modification of lipopolysaccharide of cell wall
• Vibrio cholerae
• Synthesis of cholera toxin

3
Eukaryotic Viruses (Animal viruses)

• Use to
  replicate
• Carry genes for
• Production of viral protein coat
• Assuring replication
• Moving virus in and out of the host cell
• Viral replication cycle
• ? ?
  ? ?

4
Entry of animal viruses Direct penetration
Receptors oncytoplasmic membrane
1
2
3
Capsid
Viral genome
Cut edge of hostcytoplasmic membrane
(a) Direct penetration
5
Entry of animal viruses Membrane fusion
1
Viral glycoproteins
2
Viral glycoproteinsremain in cytoplasmic membrane
Envelope
3
4
Viral genome
Receptors oncytoplasmic membrane
5
Uncoating capsid
(b) Membrane fusion
6
Entry of animal viruses Phagocytosis
2
1
Cytoplasmicmembraneengulfs virus
3
4
5
6
Uncoatingcapsid
(c) Phagocytosis
7
Synthesis of Animal Viruses
Table 13.3
8
Release of animal viruses - Budding
Viral glycoproteins
2
1
3
Budding ofenvelped virus
4
Cross sectionof hostcytoplasmicmembrane
Viral capsid
5
Envelopedvirion
9
Virion abundance for persistent infections
virus is shed
slowly and relatively steadily
10
Bacteriophage vs. Animal Virus Replication
Table 13.4
11
Latent Viruses

• Animal viruses may remain dormant in cells ?
• Provirus may or may not become
• Incorporation into host DNA is permanent
• ex chickenpox, herpes, HIV

12
Tumors and Oncogenes

• (mass of neoplastic
  cells) swelling caused by abnormal growth of
  cells
• 
  growth remains in defined region
• 
  growth metastasizes (cancer)
• cell
  division is tightly controlled
• occur when controls
  for cell division do not function properly
• genes
  code for proteins that control cell division
• Mutation in proto-oncogenes ? oncogenes ?
  abnormal protein function ? abnormal cell growth

13
How does a proto-oncogene become an oncogene

• Multiple hits -
  ? oncogenes
• Environmental factors
• Integration of virus into genes controlling cell
  division ?
  ? oncogenes ?
• virus does not kill cells, but changes cellular
  properties

14
Oncogene theory of cancer induction
Figure 13.15
15
Viruses Associated with Human Cancers
16
Cellular Effects of Animal Viruses
17
Prions

• Protein only
• Transmission
• Ingestion of infected tissue
• Transplant of infected tissue
• Contact of mucous membranes or skin abrasions
  with infected tissue
• 
  ? vacuoles and spongy appearance
  in brain tissue
• Infections are always fatal
• Not inactivated by UV light or nucleases
• Not destroyed by normal cooking or sterilization
• Inactivated by chemicals that denature proteins

18
Proposed mechanism of prion replication
Tertiary structures of PrP

• Change protein folding properties
• Prions catalyze conversion of

Normal PrP
Prion PrP
Figure 13.21
19
Infections caused by prions
20
Scrapie in sheep brain tissue
Figure 13.22