Bio 220: Lecture 22 - Lysogenic Consequences

Front 1

True/False: Lysogenic cells cannot be reinfected by the same prophage

Back 1

true
other phages however can still cause an infection

Front 2

True/False: Host cells may undergo lysogenic conversion where they now show THE SAME properties.

Back 2

false

Front 3

True/False: Host cells may undergo lysogenic conversion where they now show NEW properties

Back 3

true
• For example, the prophage may carry a gene coding for a toxin. As a result of this conversion, the bacterial call may now produce a dangerous protein toxin which is encoded by the viral genes.
• The following bacterial organisms are believed to have gained their toxic pro ducting capabilities as a result of lysogenic conversion:
∙ Corynebacterium diphtheriae
∙ Streptococcus pyogenes
∙ Clostridium botulinum
∙ Bacillus anthracis
∙ Yersina pestis

Front 4

True/False: Prophage in lysogenic cells can facilitate specialized (restricted) transduction.

Back 4

true
• The prophage can only attach in specific areas upon the host chromosome. When the prophage pulls away it can bring along the adjacent genes from the host cell.
• This feature has been used in advantageously by scientists to move about specific genes.

Front 5

What are the steps to the Replicative Cycle of Bacteriophage?

Back 5

1. Adsorption
2. Penetration
3. Biosynthesis
4. Maturation and assembly
5. Release

Front 6

Adsorption
(Replicative Cycle of Bacteriophage)

Back 6

adsorption is the attachment to solid surface. Through change collisions the appropriate phage bumps into the correct host cell bacterial cell. Specific receptors on the tail fibers will match up with receptor sites located on the cell wall, fimbriae, flagella or other external areas of the bacterial host cell. Viral adsorption involves steric complementarity of the virus and the host receptor sites. Weak electrostatic bonds are formed from chemical interactions.

Front 7

Penetration
(Replicative Cycle of Bacteriophage)

Back 7

after attachment, the T-even phage injects its DNA (viral genome) into the bacterial host cell. The remainder of this complex virus stays outside. The tail and associated enzymes of the T-even phage function in facilitating this penetration process. Phage lysozyme will help breakdown the bacterial cell wall.

Front 8

Biosynthesis
(Replicative Cycle of Bacteriophage)

Back 8

a. Host DNA is degraded and host protein synthesis is stopped. Viral proteins interfere with host cell transcription and translation
b. Host cell ribosomes, enzymes and amino aids are used for translation of viral proteins.
c. Phage nuclei acid, capsid proteins and phage enzymes are synthesized

The eclipse period is time in which complete infective visions are not present. It starts when the phage nucleic acid is injected into the host cell and ends after late maturation.

Polyribosomes may be observed in cells where viral particles are replicating. Normally there is only 1 ribosome on mRNA at a time. Viruses however, need to act quickly and efficiently and in infected cells many ribosomes may use the same mRNA at one time.

Front 9

Maturation and assembly
(Replicative Cycle of Bacteriophage)

Back 9

bacteriophage DNA (nucleic acid) and capsids are made separately and then assemble (copolymerized) in this phase. Tail fibers, the contractile sheath and the base plate are also made separately and then assembled. All of the viral components assemble spontaneously minimizing the number of viral genes assigned to this process.

Front 10

Release
(Replicative Cycle of Bacteriophage)

Back 10

viral genes encode for the enzyme lysozyme. This enzyme causes the bacterial cell wall to break down resulting in lysis of the host cell. Viral particles are now released
• Burst time is the total time from adsorption to release. This takes approximately 20 to 40 minutes.
• Burst size refers to the total number of viral particles that are formed in one host cell during the replicative cycle. Numbers vary from 100 to 1000 particles

Front 11

What are the step to a Replicative Cycle of an Animal Virus?

Back 11

1. Adsorption (Attachment)
2. Entry
3. Uncoating
4. Biosynthesis
5. Maturation and Release

Front 12

Adsorption
(Replicative Cycle of an Animal Virus)

Back 12

viral particle receptors target specific receptors upon host cells. The match is highly specific and like the phage model we see steric complementarity. With icosahedral viruses the viral receptor sites are located on the corners of the icosahedrons. Viral receptor sites can also be located upon spikes when these structures are present. Proteins and glycoproteins upon the host cell plasma membranes serve as the receptor sites on the host cells. Host cell plasma membranes can vary from one individual to another. This may explain why one person is susceptible to a virus while another is not.

Front 13

Entry
(Replicative Cycle of an Animal Virus)

Back 13

the entire viral particle may enter pinocytosis. The viral particle is surrounded by host cell plasma membrane and brought into the cell as the plasma membrane folds inward. Once inside the cell the virus is no in a vesicle. Enveloped viruses can be brought into the cell by a process known as fusion.

Front 14

Uncoating
(Replicative Cycle of an Animal Virus)

Back 14

unlike the phage model, the capsid along with the viral nucleic acid is brought inside the host cell and therefore must be removed in the uncoating process prior to biosynthesis. The eclipse phase does not start until after uncoating. Enzymes that remove the capsid are typically made from host cell enzymes. An exception to this rule occurs during the uncoating of the pox viruses. Pox viruses are large and they use their own genes to make enzymes for uncoating.

Front 15

Biosynthesis in DNA viruses
(Replicative Cycle of an Animal Virus)

Back 15

generally viral nucleic acid id replicated in the host cell nucleus using viral enzymes. The capsid and other proteins are made in the cytoplasm using host cell enzymes. Virions are assembled in the nucleus of the host cell. Pox viruses are the exception as they are DNA viruses that are completely synthesized in the cytoplasm

Front 16

Biosynthesis in RNA viruses
(Replicative Cycle of an Animal Virus)

Back 16

viral RNA (genes) is synthesized in the host cell cytoplasm. The capsid and other proteins are also made up in cytoplasm. Virions are assembled in the cytoplasm.

Front 17

Maturation and Release
(Replicative Cycle of an Animal Virus)

Back 17

the capsid is assembled spontaneously. Some viruses have envelopes. Envelopes consist of protein, lipid and carbohydrate components. The protein component is made from viral genes and is incorporated into the plasma membrane of the host cells. The other components are made from host cell genes and are already within the membrane. The envelope is picked up when the virus leaves the host cell in a process called budding (extrusion). The host cell is not destroyed in this process. Viruses that are non-enveloped (naked) leave through ruptures in the host cell plasma membrane. The host cell is usually destroyed in this process.

Front 18

± DNA → ∓
DNA

Back 18

± DNA → ∓
DNA
The DNA replicates by semi-conservative replication. Examples include the adenovirus and herpes virus.

Front 19

± RNA → ∓ RNA


Back 19

± RNA → ∓ RNA

The RNA replicates by semi-conservative replication. Example includes the arbovirus that causes Colorado Tick Fever

Front 20

+ RNA → ± RNA → + RNA


Back 20

+ RNA → ± RNA → + RNA

The -RNA is used as a template to make +RNA and is eventually broken down and discarded after use. Remember the +RNA (infecting strand/genome) can also act as mRNA for translation to proteins as well as a strand to manufacture the template (- RNA). An example includes the polio virus.

Front 21

- RNA→± RNA → - RNA


Back 21

- RNA→± RNA → - RNA

The + RNA is used as mRNA and then as a template for new –RNA and then discarded. An example includes the rabies virus.

Front 22

+ RNA → + DNA → ± DNA → + RNA

± DNA → Provirus (integrated onto the host chromosome)

Back 22

The enzyme reverse transcriptase catalyzes the conversion of + RNA → + DNA. A complimentary strand of DNA is now manufactured off of this + DNA to create ± DNA. The ± DNA can now integrate into the host cell genetic material in the form of a provirus. This is analogous to the prophage in bacterial host cells however, unlike the prophage; the provirus never comes out of the chromosome. The provirus can remain latent for extended periods of time or the provirus can be activated to produce + RNA through transcription and initiate viral replication. The retroviruses including HIV and HTLV-I and HTLV-II are examples of viruses that behave in this fashion.

Front 23

True/False: In the animal virus replicative process, host cell DNA, mRNA, protein synthesis and overall metabolism is NOT broken down.

Back 23

true

Front 24

True/False: In the animal virus replicative process, host cell DNA, mRNA, protein synthesis and overall metabolism is broken down.

Back 24

false

Front 25

True/False: Many viruses will use the host enzymes transcriptase or RNA polymerase.

Back 25

true

Front 26

True/False: Sometimes host cell protein synthesis is not only continued, but it is accelerated as increased cellular metabolic activity is observed.

Back 26

true

Front 27

True/False: Warts represent areas of increased epithelial growth due to papillomaviruses (non-enveloped DS DNA viruses)

Back 27

true

Front 28

What is some evidence that host cell is infected by a virus?

Back 28

1. CPE’s
2. Inclusion bodies in the host cell-these are aggregations of viral material that were not present
prior to infection. These typically display regular geometric patterns and are observable using EM. Sometimes, a virus will make more capsid material than it needs. Inclusions may be found in the nucleus (Herpes virus) or the cytoplasm. Negri bodies are inclusion bodies found in the cytoplasm of nerve cells. They are diagnostic of the rabies virus. Guarnieri bodies are found in the cytoplasm of epithelial cells infected by the smallpox virus.
3. Viruses can create polykaryocytes, the fusion of several adjacent cells.
4. Viruses can cause polyribosomes to occur.
5. Viruses are sometimes responsible for chromosomal damage or breakage.
6. Viruses can affect general cell function. For example, viruses can induce cells to produce
interferon.

Front 29

What are Latent Viral Infections?

Back 29

This is a situation where a virus can remain quiet or latent within a host cell and not go into replication phase and produce disease for an extended period, perhaps years. In bacterial cells this is analogous to lysogeny. In animal cells the classic example of this type of pattern is seen in Herpes simplex infections. A period of no symptoms followed by a period where there is an outbreak of lesions or sores. Another example would be the varicella-zoster virus as it re-emerges years later in the form of shingles. The retroviruses can integrate in the form of a provirus and also stay in a latent form until reactivation. A disease called subacute sclerosing panencephalitis (SSPE) can cause severe neurological symptoms. SSPE is rare and occurs 1 to 10 years following an active measles virus infection. The measles virus has also been implicated in multiple sclerosis. Various factors can trigger the activity of a latent virus including, UV light, fever, temperature changes, immune system changes, hormone imbalances, pH changes and stress.

Front 30

What are Persistent (Chronic) Viral Type Infections

Back 30

These are infections that occur gradually over an extended period of time. They are characterized as insidious, progressive, and degenerative in a neurological way. In addition to viruses the persistent or chronic infections are also associated with some other less conventional agents including viroids and prions. Viroids are naked loops of ssRNA found to be plant pathogens and suspected agents of some slow viral type diseases.

Front 31

± DNA =

Back 31

DS DNA (viral genome)

Front 32

+ DNA =

Back 32

SS DNA (viral genome); sense strand

Front 33

– DNA =

Back 33

SS DNA; antisense strand and template for +DNA

Front 34

± RNA =

Back 34

SS RNA (viral genome)

Front 35

+ RNA =

Back 35

SS RNA (viral genome); mRNA; template for – RNA

Front 36

– RNA =

Back 36

SS RNA (viral genome); template for + RNA