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Virology > Exam I > Flashcards

Exam I Flashcards

1
Q

Discuss whether viruses are alive, and if they are not, how they evolve.

A

Viruses are not alive. To be alive, organisms must acquire and use energy and be able to reproduce on their own. Viruses don’t do this, so they are biological, because they are made of biological molecules, but not living. Viruses use the host cell’s machinery to replicate. Viruses evolve by undergoing natural selection, random mutation, and if two viruses were to infect the same cell at the same time, their genetic material can swap.

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2
Q

virus definition

A

a microorganism that infects cells and uses host cell machinery to replicate

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3
Q

genome definition

A

complete set of genes or genetic material present in a cell or organism

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4
Q

envelope definition

A

membrane protein that dissolves in detergent

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5
Q

capsid definition

A

protein shell that encloses nucleic acids

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6
Q

icosahedron definition

A

having 20 sides. It is the perfect shape for a phage head because it is very stable regarding the infectious phase where high energy states occur

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7
Q

eclipse period definition

A

the time between when the cell is infected and when the mature virus first appears

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8
Q

burst size definition

A

the expected number of virions produced by one infected cell over its lifetime

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9
Q

Discuss whether all viruses are related.

A

There is no viral tree of life and no DNA or RNA sequence has been found to be shared between all viruses. Viruses are not all related.

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10
Q

Discuss how viruses may be deadly, yet in some cases are life giving.

A

Viruses can kill you, but they can also be helpful. Viruses are used for viral gene therapy to insert corrected genes into humans. Oncolytic viruses are used to kill tumor cells. Viruses are how molecular biology started.

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11
Q

Define the central dogma of biology and indicate where viruses violate the central dogma.

A

RNA replicate via special enzyme
RNA can be reverse transcribed by reverse transcriptase
RNA dependent RNA polymerase uses an RNA template

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12
Q

Define the term metastable and how it relates to virions.

A

Capable of self-assembly
Stable carriers of genome outside of cell
Must disassemble to release their genome into host cell

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13
Q

Discuss steps that all viruses must accomplish in order to replicate.

A

Attachment
Entry
Transcription
Translation
Viral genome replication
Assembly
release

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14
Q

How were viruses discovered?

A

Dimitri Ivanovsky discovered tobacco mosaic virus in the late 1800’s. It could go through a filter that prevented bacteria or fungi from passing through.

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15
Q

What are the differences between viruses and other microbes?

A

Viruses are significantly smaller than the smallest bacteria. They are obligate intracellular pathogens, so they can only reproduce within a host cell.

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16
Q

How small are the largest and smallest viruses compared to the smallest thing you can see with your eyes?

A

Parvovirus is the smallest and it is 20 nm in diameter.
Mimivirus is the largest and it is 500 nm in diameter.
The smallest thing the human eye can see is 0.1 mm which is 10^5x bigger than the viruses.

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17
Q

What is an example of a helical virus?

A

tobacco mosaic

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18
Q

what is an example of a naked virus?

A

poliovirus

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19
Q

what is an example of an enveloped virus?

A

COVID

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20
Q

What is the difference between –RNA and +RNA?

A

+ Strand RNAs may be translated directly and they are identical to mRNAs. The - strand RNAs must be copied to form complementary + strand RNA before translation.

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21
Q

Virus genomes are often capable of non-canonical translation. How might this benefit the virus?

A

Non-canonical translation is when the virus uses a non-AUG start codon to regulate translation of a subset of mRNAs. This alternative open reading frame is advantageous because there are many alternative ways to express multiple proteins from a single mRNA.

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22
Q

Compare and contrast the different modes of influenza A evolution, antigenic shift, and antigenic shift.

A

Influenza A viruses have 8 different RNA genomic segments. They evolve quickly because there is no proofreading. Influenza viruses are highly prone to recombination (antigenic shift) whenever 2 virions infect the same cell. Antigenic drift is the accumulation of minor genetic mutations. Antigenic shift is when viral genomes recombine in the same cell after they infect the same cell, which makes reinfection highly likely.

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23
Q

Compare and contrast , transforming, lytic, chronic/persistent, and latent/proviral viral life styles.

A

Lytic- bacteriophage: attachment, penetration, transcription, biosynthesis, maturation, lysis.
Transforming- producing altered cell growth, usually only part of the viral genome is present. HPV
chronic/persistent- long-term infections with low levels of virus production. Hep B and C in the liver
Latent- viral genome is maintained in an inactive state within the cell. No replication occurs. Herpes

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24
Q

Describe differences in the classification systems of viruses and other organisms.

A

They are grouped into clusters like phage. A new cluster is formed when the virus jumps into a new organism. Viruses don’t have kingdoms, phylums, or classes.

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25
Q

Describe the phrase “obligate intracellular parasite” and give examples.

A

It means that it needs a host cell to live and replicate in, otherwise it will not live. They are a parasite because when they exit the cell, they destroy it.

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26
Q

Define phylogeny and describe viral phylogenies.

A

Phylogeny- group of organisms that descend from a common ancestor
Viral phylogenies are basically clusters of related viruses, which researchers call quizispecies

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27
Q

Give examples of viral evolution.

A

Frameshift mutations, readthrough of stop codons, multiple start sites, overlapping genes, polyprotein cleavage, ribosomal frameshifting

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28
Q

Describe how viruses acquire envelopes.

A

Viruses acquire envelopes from stealing it from the host cell. During the budding process, the virus particles come enveloped in the cell’s plasma membrane.

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29
Q

Describe how different DNA and RNA viruses create mRNA.

A

dsDNA- + strand translatable
ssDNA- gets converted to dsDNA by DNA polymerase
dsRNA- one strand gets replicated by RDRP
+ssRNA- converted to -ssRNA then to mRNA by RDRP
-ssRNA- converted by RDRP
ssRNA-RT- converted to DNA/RNA then to dsDNA by RTase
dsDNA-RT- converted to mRNA

30
Q

Define “ambisense RNA genome”.

A

Has both - and + strands in RNA. The + strands can be directly translated to proteins.
Describe the Baltimore system of virus classification.
It is based on the replication strategy of the virus. It is broken down into dsDNA, ssDNA, dsRNA, ssRNA

31
Q

Define satellite virus

A

a virus that depends on a helper virus to replicate and disseminate. It has a very small genome that lacks some genes needed to replicate, so it relies on a larger helper virus.

32
Q

Define viroid

A

have no capsid. Transmitted from plant cell to plant cell via any contact. They don’t code for any proteins and are replicated from ssRNA.
Define prion.

33
Q

Define prion

A

A protein without genetic material that can infect humans and animals. They consist of a protein that has taken a misfolded shape. PrPsc is the misfolded one. PrPc is the normal one. They can basically not be destroyed and form long chains of these aggregates.

34
Q

Discuss where –strand RNA viruses get their RDRP enzymes.

A

They have to bring their own polymerase because no cells have them innately.

35
Q

Describe the Baltimore system of virus classification.

A

It is based on the replication strategy of the virus. It is broken down into dsDNA, ssDNA, dsRNA, ssRNA

36
Q

What are viral cellular receptors-What role do they play?

A

Viral cellular receptors are proteins found on the surface of host cells that act as the first point of contact between the virus and the host cell.

37
Q

Explain how direct plasma membrane fusion, endocytosis, endocytosis with endosome acidification, and direct capsid delivery play different roles in the entry of viral genomes to the cytoplasm.

A

Direct plasma membrane fusion

Endocytosis involves the internalization of the virus into a host cell via a vesicle, followed by the fusion of the vesicle with the endosome.

Endocytosis with endosome acidification involves a release of the viral genome into the cytoplasm through the endosome membrane.

Direct capsid delivery

38
Q

CD4

A

T cell to B cell

39
Q

CD8

A

T cell to any other cell

40
Q

What is a one step growth curve?

A

Used to estimate the life cycle of a virus for a specific host.

41
Q

Is entry into the nucleus required for all viruses?

A

It is required for -RNA viruses and dsDNA viruses

42
Q

Explain why the synthesis of viral proteins must take place in a highly organized manner.

A

Viral proteins are synthesized in a highly organized manner to ensure proper viral replication and assembly. This requires the coordination of various cellular and viral components to ensure that the right proteins are produced at the right time and in the right place. If this process is not properly organized, the virus may produce incorrect or non-functional proteins, leading to ineffective replication and assembly.

43
Q

What is the difference between rolling circle DNA replication and theta DNA replication?

A

Rolling circle replication is a process in which a circular DNA or RNA molecule is replicated in one direction. This particular process occurs in bacteria, plasmid and virus’s genome. Theta replication is a common type of replication that takes place in circular DNA of prokaryotic. Intermediate structure formed during the replication of a circular DNA molecule resembles the Greek letter theta (θ) and hence the name theta. Replication is either unidirectional or bidirectional. Theta replication does not involve breakage of nucleotide strands like that of rolling circle replication.

44
Q

Describe the role of 5’-caps and poly-A tails play in RNA translation in Eukaryotic cells?

A

5’ caps: Influenza A cap snatches. It allows synthesis of 5’ capped mRNAs, then cleaves the cellular mRNA at 5’ end. Influenza undergoes primes mRNA synthesis and transcription and the viral mRNA is made with the cap of the cell.
Poly A’s: The virus has to copy each U into an A or stutter to create the poly A tail. Some viruses can copy N methylguanine cap.

45
Q

What are polyproteins?

A

Polyproteins are long chains of amino acids that are joined together to form a single protein molecule. They are produced by the virus during replication and are typically composed of multiple individual viral proteins that are cleaved into their functional forms. In simple terms, polyproteins are like a kit of many different parts that are assembled together, but later separated into the individual parts needed for the virus to function. The cleavage of polyproteins into individual viral proteins is a critical step in the replication and assembly of many viruses, and it allows the virus to produce multiple different functional proteins from a single gene.

46
Q

Why do viruses with –sense RNA genomes require the presence of an RDRP in the virion?

A

Viruses with negative-sense RNA genomes require the presence of a RDRP in the virion because the negative-sense RNA is not directly usable as a template for protein synthesis. The RDRP is responsible for synthesizing a complementary positive-sense RNA copy of the viral genome, which can then be used as a template for protein synthesis by the host cell’s ribosomes. Without the RDRP in the virion, the negative-sense RNA genome would be unable to direct the synthesis of new viral proteins, and the virus would not be able to replicate. In simple terms, the presence of an RDRP in the virion is crucial because it allows the virus to make a copy of its genome that can be used to make new viral proteins, which is essential for the virus to continue replicating and infecting new cells.

47
Q

Identify the 6 specific attributes of an adaptive immune system.

A

Specificity: able to differentiate self from nonself
Diversity: can respond to a wide variety of pathogens
Memory: ability to remember invaders you have seen before
Clonality: can replicate immune tools and distribute them around the body for rapid defense
Lethality: ability to develop multitude of deadly tools to destroy invaders
Viruses in dead cells don’t replicate or evolve.
Antigen-driven expansion: able to increase number of immune cells specific to invading pathogen, strengthening overall response

48
Q

Describe the differences between humoral and cellular immunity, and indicate how these engage endogenous or exogenous antigens.

A

Humoral immunity: involved production of antibodies. Antibodies bind to pathogens, marking them for destruction and preventing them from spreading. Primary involved in exogenous pathogens.
Cellular immunity: involves activation of immune cells called T cells. T cells directly attack infected or cancerous cells, either by releasing toxic substances to kill them or making them for destruction. Primarily involved in endogenous pathogens, such as viruses within a cell.

49
Q

Pathogens can produce a nearly infinite number of different proteins. Describe how can the humoral and cellular immune systems attack these invaders without attacking self proteins?

A

B and T cells are programmed to recognize self antigens presented by antigen presenting cells. These cells present fragments of self and foreign antigens to immune cells. Self reactive cells are typically killed early in development.

50
Q

MHCI

A

displayed foreign antigens translated inside cells
Endogenous antigens
Found on ALL nucleated body cells

51
Q

MHCII

A

displays foreign antigens processed by phagocytosis
Exogenous antigens
Found on macrophages, dendritic cells, and B cells

52
Q

What cells display MHC I, and what type of antigens are presented to the cellular immune system?

A

It is on all nucleated cells in the body. MHCI presents endogenous antigens, which are proteins produced by the body’s own cells to the cellular immune system.

53
Q

What is the difference between B & T lymphocytes?

A

B cells are involved in humoral immunity and produce antibodies.
T cells are involved in cellular immunity and attack infected or cancerous cells.

54
Q

How do different T lymphocytes arise in the bone marrow? How do they mature in the thymus? How can they become activated to become Cytotoxic T cells and T-helper cells?

A

T lymphocytes arise in bone marrow and mature in the thymus. They differentiate into cytotoxic T cells or T helper cells through selection in the thymus. Activation occurs when T cells recognize antigens presented by antigen-presenting cells, leading to differentiation and expansion of cytotoxic T cells or T helper cells.

55
Q

What cells display MHC II, and what type of antigens are presented to the humoral immune system?

A

MHCII is displayed on antigen presenting cells, such as dendritic cells, macrophages and B cells. MHCII presents exogenous antigens to the humoral system. This allows B cells to recognize and respond to these antigens, producing antibodies to mark them for destruction.

56
Q

What are memory cells? What do they do?

A

A type of immune cell formed after initial exposure to pathogen or antigen. They protect against reinfection by recognizing and responding rapidly to subsequent exposure to the same pathogen.

57
Q

How do different B lymphocytes arise in the bone marrow, how do they mature? How can they become activated to become antibody secreting plasma cells and memory cells?

A

B lymphocytes come from stem cells in bone marrow and mature there. They differentiate into either plasma cells or memory cells through activation by antigens presented by antigen presenting cells.

58
Q

What is the difference between a primary response to antigen, and a secondary response to antigen?

A

A primary response to an antigen is the initial response to a new antigen. It is a slower response and less effective. A secondary response to an antigen is the response of the immune system to a previously encountered antigen. It is faster and memory cells and plasma cells can respond.

59
Q

What is Somatic Hypermutation?

A

Somatic hypermutation is the process of random mutation in genes that code for antibody molecules in B cells during an immune response. This is done to create a diverse range of antibodies with different binding affinities, allowing the immune system to find the most effective antibody to neutralize the antigen.

60
Q

What is Affinity Maturation?

A

Affinity maturation is when B cells with high affinity antibodies survive and proliferate while those with low affinity antibodies die off. This results in a gradual increase in overall affinity of the antibody population over time leading to more effective elimination of the antigen.

61
Q

Natural active immunity

A

infection and recovery. Memory cells formed

62
Q

Artificial active immunity

A

deliberate antigen exposure. vaccination. memory cells formed

63
Q

natural passive immunity

A

maternal antibodies acquired in utero or from nursing. short term protection. only antibodies

64
Q

artificial passive immunity

A

purified antibodies from an alternative source antitoxins or antivenoms. monoclonal antibodies and only antibodies.

65
Q

Differentiate between oral poliovirus vaccine and the inactivated poliovirus vaccine.

A

Salk: first inactivated vaccine. cannot replicate. cannot present polio from replicating in the gut so it doesn’t block transmission
Sabin: oral. live attenuated. can back mutate so people are shedding wild type virus. can replicate in IPV people and spread polio.

66
Q

Discuss Vaccine Derived Polio Virus? How does it arise? How is it spread?

A

Vaccine-derived polio virus is a strain of polio virus that originates from oral polio vaccine. OPV contains a weakened form of the virus that is used to stimulate immunity, but the virus can revert to a more virulent form in some individuals, leading to VDPV outbreaks. VDPV is spread through human feces, just like wild-type polio virus, and can cause paralytic polio.

67
Q

Discuss the likelihood AND complications of poliovirus eradication in the world.

A

The likelihood of poliovirus eradication in the world is high but ongoing efforts are still necessary. The World Health Organization has been leading global efforts to eradicate polio since 1988 and has made significant progress. However, ongoing challenges include access to populations in conflict-affected areas, vaccine hesitancy, and importation of wild poliovirus from countries where the disease still persists. Complications of poliovirus eradication include the need for continued surveillance and vaccination efforts, and the risk of vaccine-derived outbreaks.

68
Q

Identify the major lymphocytes involved in adaptive immunity and correlate them with
humoral and cellular immunity.

A

Th1- inflammation cytotoxicity
Th2- humoral immunity

69
Q

MHCI activation steps

A

foreign protein in cell is recycled in proteasomes and peptide fragments make their way to ER lumen and bind MHCI and remain on cell surface
CD8+ (cytotoxic T lymphocyte) binds foreign peptide fragment with T cell receptor
Perforins and granzymes released by CD8+
apoptosis is induced, pinches off into vesicles and macrophages mop up debris

70
Q

MHCII activation steps

A

macrophage or dendritic cell undergoes phagocytosis of uk material
T helper cell with TCR will recognize MHCII presentation
T helper cell secretes cytokines to activate phagocyte
B cell receptor on naive B cell recognizes same protein and phagocytoses it and presents fragments on MHCII
T helper cell from before binds peptide fragment on MHCII randomly
B cell somatic hypermutation and selection
B cell differentiates into plasma and memory cells
It hangs out in the lymph node until it’s stimulated by another T cell

Virology (1 decks)

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