Week 6 (Part 2): Viruses Flashcards

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1
Q

What are 4 characteristics of viruses?

A
  1. Obligate Intracellular organisms
  2. DNA or RNA
  3. Unable to grow or undergo binary fission
  4. Composed of capsid and genetic material
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2
Q

T/F

Viruses are Obligate intracellular organisms that require a living cell or organism for it’s multiplication

A

True

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3
Q

T/F

Viruses are energy-less and float around until they come in contact with an appropriate cell

A

True

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4
Q

Define virus:

A

“Viruses are entities whose genomes are elements of nucleic acid that replicate inside living cells, using the cellular synthetic machinery and causing the synthesis of specialized elements that can transfer the viral genome to other cells.” - Luria & Darnell

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5
Q

What must a virus be able to do?

A

A virus must attach to a living cell, be taken inside, manufacture its proteins and copy its genome, and find a way to escape the cell so that the virus can infect other cells.
q

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6
Q

How does a virus replicate?

A

Replication of the genetic material occurs when the virus takes control of the host cell’s synthetic machinery – viruses contain all the genetic information, but not the enzymes, needed to build millions of replicas of the original virus

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7
Q

What is a virus composed of?

A

Viruses are basic life forms composed of a protein coat, called a capsid, that surrounds genetic material.

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8
Q

T/F

Viruses do have organelles, such as flagella and pili, or ribosomes like bacteria do

A

False

- Viruses do not have organelles, such as flagella and pili, or ribosomes like bacteria do

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9
Q

What are characteristics used to classify viruses? (4)

A
  1. Type of viral Genome (Single-stranded or double-stranded DNA or RNA)
    - Can use DNA or RNA!
  2. Type of symmetry of the virus capsid (helical vs icosahedral)
  3. Presence or absence of a lipid envelope (Naked or enveloped)
  4. Size
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10
Q

What is the first step in viral replication?

A
  1. Absorption and penetration

Absorption:

  • A virus attaches to a specific receptor site on the host cell membrane through attachment proteins in the capsid or via glycoproteins embedded in the viral envelope.
  • The specificity of this interaction determines the host—and the cells within the host—that can be infected by a particular virus.
  • This can be illustrated by thinking of several keys and several locks, where each key will fit only one specific lock.

Penetration:
- The nucleic acid of bacteriophages enters the host cell naked, leaving the capsid outside the cell.
Plant and animal viruses can enter through endocytosis, in which the cell membrane surrounds and engulfs the entire virus.
- Some enveloped viruses enter the cell when the viral envelope fuses directly with the cell membrane.

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11
Q

What is the second step of virus replication?

A
  1. Uncoating of the virus
    - Once inside the cell, the viral capsid is degraded, and the viral nucleic acid is released, which then becomes available for replication and transcription.
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12
Q

What is the third step of virus replication?

A
  1. Genome replication
    - The replication mechanism depends on the viral genome. - DNA viruses usually use host cell proteins and enzymes to make additional DNA that is transcribed to messenger RNA (mRNA), which is then used to direct protein synthesis.
    - RNA viruses usually use the RNA core as a template for synthesis of viral genomic RNA and mRNA.
    - The viral mRNA directs the host cell to synthesize viral enzymes and capsid proteins, and assemble new virions
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13
Q

What is the last step of virus replication?

A
  1. Release of virion from the host cell
    - The last stage of viral replication is the release of the new virions produced in the host organism, where they are able to infect adjacent cells and repeat the replication cycle.
    - Some viruses are released when the host cell dies, and other viruses can leave infected cells by budding through the membrane without directly killing the cell.
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14
Q

What are the 4 hot cell outcomes?

A
  1. Death
  2. Transformation
  3. Latent Infection
  4. Chronic slow infection
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15
Q

Describe the host cell outcome:

- Death

A

Death:

  • The viral replication cycle can produce dramatic biochemical and structural changes in the host cell, which may cause cell damage.
  • These changes, calledcytopathic(causing cell damage) effects, can change cell functions or even destroy the cell.
  • Some infected cells, such as those infected by the common cold virus known as rhinovirus, die throughlysis(bursting) or apoptosis (programmed cell death or “cell suicide”), releasing all progeny virions at once.

Death: With the viral infection, the host cell’s own function shuts down as the cell is commandeered for virion replication.
-This can result in cell death.

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16
Q

Describe the host cell outcome:

- Transformation

A

Transformation:
- Infection can activate or introduce oncogenes.
- This results in uncontrolled and uninhibited cell growth.
- Some animal-infecting viruses, including the hepatitis C virus discussed above, are known asoncogenic viruses: They have the ability to cause cancer.
- These viruses interfere with the normal regulation of the host cell cycle either by either introducing genes that stimulate unregulated cell growth (oncogenes) or by interfering with the expression of genes that inhibit cell growth.
- Oncogenic viruses can be either DNA or RNA viruses.
Cancers known to be associated with viral infections include cervical cancer caused by human papillomavirus (HPV) , liver cancer caused by hepatitis B virus, T-cell leukemia, and several types of lymphoma.

17
Q

Describe the host cell outcome:

- Latent infection

A

Latent Infection:

  • The virus can survive in a sleeping stat surviving but not producing clinically overt infections.
  • Various factors can result in viral reactivation.
  • Herpes simplex virus can remain in a state of latency in nervous tissue for months, even years.
  • As the virus “hides” in the tissue and makes few if any viral proteins, there is nothing for the immune response to act against, and immunity to the virus slowly declines.
  • Under certain conditions, including various types of physical and psychological stress, the latent herpes simplex virus may be reactivated and undergo a lytic replication cycle in the skin, causing the lesions associated with the disease.
  • Once virions are produced in the skin and viral proteins are synthesized, the immune response is again stimulated and resolves the skin lesions in a few days by destroying viruses in the skin.
  • As a result of this type of replicative cycle, appearances of cold sores and genital herpes outbreaks only occur intermittently, even though the viruses remain in the nervous tissue for life.

Latent infections are common with other herpesviruses as well, including the varicella-zoster virus that causes chickenpox.
- After having a chickenpox infection in childhood, the varicella-zoster virus can remain latent for many years and reactivate in adults to cause the painful condition known as “shingles”

18
Q

Describe the host cell outcome:

- Chronic slow infection

A

Chronic slow infection:

  • Some viruses will cause disease only after many years, often decades of indolent infection.
  • In hepatitis C infections, the virus grows and reproduces in liver cells, causing low levels of liver damage.
  • The damage is so low that infected individuals are often unaware that they are infected, and many infections are detected only by routine blood work on patients with risk factors such as intravenous drug use.
  • On the other hand, since many of the symptoms of viral diseases are caused by immune responses, a lack of symptoms is an indication of a weak immune response to the virus.
  • This allows for the virus to escape elimination by the immune system and persist in individuals for years, all the while producing low levels of progeny virions in what is known as a chronic viral disease.