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BIO 202 Chapter Notes - Chapter 19: Viral Envelope, Lytic Cycle, Prophage

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Stony Brook University
Department
Biology
Course
BIO 202
Professor
susanerster

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Document Summary

They are useless on their own so they have to go from one cell to another to replicate itself. However, they all have capsids, which built of a large number of identical proteins around the virus. It is shaped however the virus is shaped: some viruses have viral envelopes, which are membranes that cloak the capsids. The viral envelopes are taken from the membrane of the host cell, which can help infect another cell: a type of virus is called the bacteriophage (bacteria eaters). It can sneak in a few different ways: by the transporter, receptors, cell pores, etc. Hiv can get in by fusing with the host cell. Influenza uses the receptor-mediated endocytosis (the process of capturing a substance from outside the cell). Many viruses have virally encoded glycoproteins in the cell membrane that triggers when the capsid proteins approaches.

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Related Questions

1. Select all of the true statements regarding phageconversion.

-The incorporation of viral genesinto the host cell's DNA is an example of phage conversion.
-The expression of the incorporatedgenes and the resulting alteration of the bacterial phenotype is anexample of phage conversion.
-Cholera toxin genes have a viralorigin.
-The cholera toxin is produced bythe virus.

-The cholera toxin itself is transferred to Vibriocholerae by a virus.

2. Viruses grown in media with radioactive sulfur haveradioactive capsids. Why?

Nucleotides contain sulfur
Cysteine amino acids containsulfur
Capsid peptidoglycans containsulfur

Phospholipids contain sulfur

3. Integrase inhibitors work by:

Agglutinating the reversetranscriptase inhibitors
Preventing the incorporation of theviral DNA into the genome
Blocking the final viralassembly

Degrading the viral envelope

4. Once a prophage is formed, the viral genes are reproducedevery time the bacterium multiplies. The genes that encode thelytic cycle are held in check by a repressor protein. Stressinduces the formation of proteases that degrade the repressor. Howwould this affect the prophage?

Apoptosis would be induced.
The virus enters the lyticcycle.
The bacterial genome isdenatured.

The bacterium rejects the viral genes.

5. Can a virus be killed?

No, viruses are non-living andcannot die.
No, viruses are capable ofself-assembly and cannot be permanently killed.
Yes, separating the genes from thecapsid kills it.

Yes, destroying its genome kills it.

6. Which class of drugs would be effective against HIV but notagainst most other pathogenic viruses?

Translation inhibitors that stopassembly of viral proteins.
Nucleotide analogs that haltreplication.
Non-nucleoside reversetranscriptase inhibitors that block reverse transcription.

Receptor antagonists that block viral entry.

7. An unscrupulous malcontent writes a computer program andembeds it in an e-mail that promises lucrative investmentopportunities. The e-mail is sent to thousands of anonymous users,when they open it the program copies itself into the computer'shard drive. The hard drive begins to fill up with copies of theprogram, once it is completely full the computer crashes. Match thecomponents of this story with the components of a viral lifecycle.

1. e-mail containing virus Virus
2. Innocent user Binding site onhostcell
3. User's hard drive andCPU Host cell'sribosomes
4. Program Uninfected host cell

8. Vaccines work by priming the immune system and inducing theformation of antibodies and memory cells. When the actual virusinfects the host the host's immune system recognizes it andresponds to it. Which feature of viruses helps them thwart thissystem?

The envelops prevents immune systemrecognition.
Autocatalytic proteins replicatewithout genetic material.
The high mutation rate of the viralgenome.
Integration of viral genescamouflages the virus.
Shedding the capsid inactivates theantibodies.

2.)

a.) Are viruses that infect Archaea different from other bacterial viruses?

Yes, they do not have protein coats because of the extreme conditions where they live.
No, they consist of nucleic acid and protein just like other bacterial viruses.
Yes, the structure of archaeal viruses is always completely different from other bacterial viruses.

Yes, they have only DNA genomes.

b.) Of the following examples, which is not a common part of many viral life cycles?

The pox virus genome is replicated by DNA polymerase.
Adenoviruses attach to the cell and the nucleocapsid is taken up by the cell.
Pox viruses replicate in the cytoplasm of the cell.

Once an adenovirus virion is inside a cell, host RNA polymerases transcribe early genes

c.) Some viruses are associated with cancer. There are a variety of ways in which viruses may affect a cell in a way that may lead to cancer. Based on your knowledge of the life cycles of viruses and of molecular genetics, what is one way that this might happen?

Viral genetic material inserts into a host genome close to the termination sequence, far downstream of the promoter, and causes a silent mutation.
Viral genetic material inserts into a host genome in a repetitive noncoding region.
Viral genetic material inserts into a host genome, placing a promoter in a new location and turning on a gene that had previously been turned off.
Viral genetic material inserts into a host genome and causes a mutation in a promoter, turning off a gene that had previously been turned on.

d.) Which statement describes the difference between the normal neuron protein PrPC and the pathogenic version PrPSc?

PrPC is just a protein and the PrPSc is a protein with nucleic acid inside.
The PrPC protein contains more beta sheets while the PrPSc protein contains more alpha helices.
The three-dimensional conformation is identical, but the amino acid sequence is different.
The amino acid sequence is identical, but the three-dimensional conformation is different.

Below is a paragraph describing HIV infection as they relate to the progress of infection. Please help choose the correct answer in each parentheses.

HIV initially infects (CD4+, or CD8+, or B) cells. These are helper T cells that activate (CD4+ or ,CD8+ or, B) cytotoxic T cells and (CD4+, or CD8+, or B) cells which produce antibodies. If HIV kills (CD4+, or CD8+) T cells then they cannot to do their job of activating these cells thus causing HIV infected people to be immunocompromised. Sometimes HIV infected people enter a latency period where the virus is inactive. This latency period can last for several years. During latency HIV (DNA, or RNA) becomes integrated into the (CD4+ or CD8+, or B) host cells genome and stops producing viral HIV RNA and new HIV virions. However, for some unknown reason, HIV comes out of dormancy and the viral (RNA, or DNA ) that was integrated in the (CD4+ , or CD8+,) T cell genome begins to transcribe more viral (DNA , or RNA) to make more viral (DNA, or RNA) using the host cells machinery. The viral (DNA, or RNA) then gets translated by host cell ribosomes to make viral proteins that eventually become packaged into new HIV virions. Consequently, after the latency period HIV becomes activated in the host cell. These cells present HIV antigen on their cell surface and alert (CD8+ or CD4+ or B) cells to kill them. As they are killed the infected (CD4+, or CD8+, or B) cells release the HIV virions into the blood stream to infect other (CD4+ or CD8+) cells such as macrophages and dendritic cells. This explains why after latency we see (CD4+, or CD8+) T cells continue to decrease while at the same time viral (DNA, or RNA) levels increase.

Based on your answers to the fill in paragraph, which statement is true?

A. Once active in CD8+ T cells, HIV can now replicate with impunity and infect other cells which explains the increase in HIV RNA after latency.

B. The increase in active HIV after latency accounts for why HIV can remain dormant for years after the initial infection.

C. CD4+ levels stabilize after the latency period and explain why there is little increase in HIV RNA levels.

D. Opportunist infections can occur after HIV latency because there are very few helper T cells to left to activate cytotoxic T cells and B cells to mount an immune response.