Virology Exam Questions 2011

Front 1

Define a virus

Back 1

A genetic element containing either RNA or DNA that is able to alternated between intra- and extracellular states, the latter being the infectious state.

Front 2

Why do virologists refer to the term "quasispecies?"

Back 2

because virus replication can have error rate of 10^-4 which results in a population of dynamic contributions of nonidentical but related replicons.

Front 3

What is the origin of the naming picornavirus?

Back 3

due to the physical characteristic of the virus. Pico = small + RNA since has a RNA genome.

Front 4

What is the origin of naming tobacco mosaic virus?

Back 4

Based on the how the disease looks, the mosaic pattern it creates on plants and that it was found to infect tobacco plants.

Front 5

what is the origin of naming Herpesvirus

Back 5

by the symptom or disease caused by the virus. Herpes produces scaly, (snake skin) leasions.

Front 6

What is the origin of the naming retrovirus

Back 6

based on physical characteristics of the virus, it uses retrotransposition to replicate.

Front 7

How do yearly Influenza A vaccination campaigns affect the evolution of this virus? What is this called? How does this affect the ongoing formulation of flu vaccines?

Back 7

influenza A vaccines produce a genetic bottleneck which prevents this highly mutagenic disease from creating too many quasispecies to be able to control. By creating a new vaccine each year they are able to contain the virus species to few mutational variants in order to reduce the risk of mass casualties.

Front 8

Why do helical viruses take on that particular shape?

Back 8

formed mostly by a single major protein that stacks the amino acides in a helical shape which is energetically favorable and allows for flexibility. the charge components on the viral capsid will form it into a helical structure.

Front 9

Why do icosahedral viruses take on their shape?

Back 9

has three rotational axis. the viral capsid protein interactions is what forms the triangulation unit that then forms the icosahedral shape. The more proteins on each triangulation unit the smoother the morphological unit looks.

Front 10

Viruses that cause acute infections typically shed from which side of the cell? Why would they choose that side? Why is that ultimately good for the host?

Back 10

apical side
-so they can get out quickly and spread to next host
-limits infection to the external epithelial surface to the body. limits spread to body

Front 11

Viruses with what type of genomes are most responsible for causing cancer? Why?

Back 11

viruses with DNA genomes. cause they need to stimulate cells to enter S phase in order to get viral genomes replicated. this also gets cell genome replicated, leading to cell proliferation and division which leads to cancer.

Front 12

There are more than 100 cytokines, but fortunately for students they can be divided into three classes. name the 3 classes. why do we need these classes?

Back 12

1-pro-inflammatory
2-anti-inflammatory
3-chemokines.
-a cytokine is A small protein released by cells that has a specific effect on the interactions between cells, on communications between cells or on the behavior of cells. The cytokines includes the interleukins, lymphokines and cell signal molecules, such as tumor necrosis factor and the interferons, which trigger inflammation and respond to infections.
-we need three classes to protect from all types of varying infectious particles trying to affect our immune system

Front 13

Successful viruses have evolved strategies to deal with cytokines, e.g. virokines and viroreceptors. What are these and what do they do?

Back 13

virokines look like cytokines. bind to cytokine receptors on cells but do not activate them.

viroreceptors- look like cytokine receptors, they bind to cytokines and take them out.

Front 14

What pathway are Dicer and the RISC complex part of? What turns on this pathway? What is the product of this pathway? Give an example of how a virus might evolve a strategy to deal with this product so as to avoid the consequences of this cellular defense.

Back 14

pathway: part of RNAI pathway
-dsRNA turns on pathway
-product of pathway is very small dsRNA (approx. 21 nucleotides)
-strategies: sequestoring/degrading RNA or mislocalizing the product to get rid of it somehow.

Front 15

MHC class I molecules are expressed on which types of cells in our bodies? What is their function? Give a general example of how a virus might deal with this.

Back 15

-expressed on all nucleated cells
-function: to present proteins samples from being reduced inside of cells to surface of cells and cells of the immune system (normally cytotoxic T cells)
example of virus - mislocalize the gene products, internalize them, send to proteosome

Front 16

What is antigenic shift? What property of the influenza A genome lends itself to this phenomenon?

Back 16

-segmented genome (8 diff. segments) get shuffled in antigenic shift

Front 17

Define Rhinovirus

Back 17

-inflammation of the nose, common cold.

Front 18

Define Papular Rash

Back 18

-raised bump without liquid

Front 19

Define Retinopathy

Back 19

-degeneration of the retina

Front 20

Define secondary viremia

Back 20

-release of virus into bloodstream subsequent to infection of organ that was not first organ to be infected

Front 21

define viral shedding.

Back 21

-release of virus from infected cells/tissues

Front 22

Why do attenuated live vaccines provide better protection than killed virus vaccines vaccines?

Back 22

-mimic natural infection and induce T cell or cell mediated immune response

Front 23

What is downside to attenuated live vaccines?

Back 23

-we can get revertants that mutate back to pathogenic form that can cause disease

Front 24

Viral infection stresses cells. p53 if a major tumor suppressor Protein that responds to cellular stresses. What does it do? How could this limit virus replication? Give strategy that viruses have evolved to deal with this.

Back 24

-prevents cells from entering G1 until stress is gone. if stress does not stop then it initiates apoptosis
-limits DNA viruses from replicating because it prevents cell from going into S phase
-strategy-having proteins that specifically block, degrade, or mislocalize p53 to get rid of it and allow cell to go into S phase

Front 25

Why was smallpox a good candidate for eradication using vaccines while influenza is not?

Back 25

-smallpox has only one serotype, no antigenic drift and no natural reservoir.
-Influenza has a large animal reservoir, multiple serotypes (always evolving), has antigenic drift and shift.

Front 26

Why is West Nile virus infection limited to May-October in the US but is yearlong in its native Egypt

Back 26

-transmitted by mosquitos and US only has mosquitos in spring/summer/fall months and not during the month. Egypt has mosquitos year long due to subtropical climate

Front 27

Why have drug companies adopted a strategy to develop "skin wart vaccine" against HPV instead of one that is labeled a "cervical cancer vaccine"? How can a skin wart vaccine also be made to prevent cervical cancer?

Back 27

-to do with politics and public relations. from standpoint of parents they do not want to think of their children having unprotected sex but would like to prevent from skin warts on hand and feet.
-add specific antigens HPV-16 and HPV-18 into vaccine to also reduce risk of cervical cancers

Front 28

Define "Portal of Entry"? List three of them.

Back 28

-any part of body through which viruses can enter and access targeted tissues.
-eyes, respiratory tract, breaks in skin, eurogenital tract, alimentary tract

Front 29

Natural passive immunity protects fetuses and newborns against infectious diseases. Where does this come from, and name two sources for it.

Back 29

-comes from - mother's immune system,
-circulating immunoglobin G from blood to placenta to fetus
-IGA's secreted breast milk

Front 30

what is the thesis of the evolutionary DNA vs. RNA viruses?

Back 30

-based on RNA world hypothesis the idea was that RNA came before DNA.
3 theories of virus evolutions
-1 theory - came from protobiotic world, leftovers of RNA world
-2nd theory - evolved from selfish DNA elements that figured out they did could move from cell to cell
-3rd theory - deevolved from preliving organisms.

Front 31

if one thing Dr. Dinman wants you to learn from this class it is?

Back 31

there is no one right answer especially where evolution is concerned.
-many ways to evolve.

Front 32

What is Dinman's full name

Back 32

Jonathan Dinman

Front 33

What does Dinman's lab study?

Back 33

virology, ribosome structure/function relationship, regulation of gene expression

Front 34

What is his current grant from NIH?

Back 34

BCHM of programmed ribosomal frameshifting