exam 3 Flashcards
define emergence of a virus
viral infection whose incidence is humans has increased within the past two decades
list 5 emerging viral diseases
hiv, west nile, sars, monkey pox, ebola
Which of the following is (are) reasons why epidemics of infectious organisms continue to occur?
a. continuous evolution of new strains of an organism
b. continuous evolution of new organisms
c. Both a and b are correct.
d. Neither a nor b is correct.
c
how do arboviruses spread
bites from arthropods (insects)
what type of genome do arboviruses all have
rna
west nile virus and yellow fever are examples of what arbovirus
flavivirus
name 3 viruses that are classified as arboviruses
flavivirus, hantavirus, rift valley fever virus
what accounts for 40-50% of all chronic liver disease
hepatitis c virus
how is hcv transmitted
blood, needles, std
why is there concern that hcv will be reemerging
unknown transmission route, larger reservoir of chronic carriers, significant health risk
give examples of viral factors as an cdc enabling factor
evolution (antigenic drift, coinfection)
give examples of human factors as an cdc enabling factor
behavior, genetics, age
2 ways coinfection as a viral factor can drive emergence
recombination-two viruses infect the same cell and recombine into one (covid)
reassortment-two viruses infect the same host and combine part of each (flu)
list some examples of human factors as an enabling factor for spread of disease
human demographics, urbanization, human movement, global economy, occupation
why is close proximity of humans to animals a concern (like free range farming)
can lead to viruses crossing the species barrier, potentially leading to reassortment
how can agricultural practices likes deforestation and dam construction lead to emergence
exposes farmers to zoonotic diseases, displaced animals
what structural viruses are usually viral contaminant on food due to use of raw human sewage as fertilizer
non enveloped icosahedral viruses because they are more stable in the environment
examples of viruses that are viral contaminants on food
hep a, noro, enterovirus, rotavirus
list some examples of ecological factors as enabling factors
changes in agricultural practices, population movement into new arthropod habitats, travel, livestock transportation
Which of the following contributes to the emergence of new disease
A. rapid transportation systems and the mobility of the population
B. ecological disruption such as loss of predators and/or loss of habitat
C. increased drug usage and sexual promiscuity
D. All of the above can contribute to the emergence of new diseases.
D
why won’t some viruses be eliminated
-viruses that cause persistent infections, virus that weaken immune system, viruses that have a non human reservoir (like arboviruses)
theory for origin of hiv
siv infected chimp was killed for bushmeet, blood entered wounds of hunter, crossed species barrier
how many people has aids killed
> 25 million
where is aids most prevalent
sub-saharan africa
4 most common ways hiv is transmitted
sex, needles, blood transfusions, congenital aids
what happens to cd4 t lympocytes overtime in an hiv patient
drops immediately with primary infection, then decreases steadily as you progress towards aids
how does hiv destroy the immune system
kills off helper t cells
what is a long term non progressor
-infected with hiv but have stable cd4 cells with no symptoms
how can some people be exposed but not infected with hiv
mutant co receptor ccr5
what happens if you have a mutant homozygous ccr5
no hiv infection
what happens if you have a mutant heterozygous ccr5
progress to aids more slowly
what is the theory for where the mutant chemokine co receptor ccr5 originated from
mutant ccr5 led to increased survival during small pox outbreaks, and resulted from natural selection
Individuals of genotype CCR5-∆32/ CCR5-∆32 are
A. more susceptible to HIV infection
B. more common in people of European descent
C. more common in people of African descent
D. None of the above
B-small pox epidemic in europe in 14th century
why does variola have a secret
encodes a protein whose c terminal contains a smallpox virus encoded chemokine receptor
what does the secret domain on variola virus do
acts as a chemokine inhibitor, allowing the virus to evade the immune system
what happens if an individual has a defective chemokine receptor for the secret protein
resist HIV or variola from evading the immune response
how might a mutation in the chemokine receptor affect the secret domain of variola and viral infection
a mutation means that variola cannot bind to the chemokine, therefore not inhibiting it. this means that the immune response will block the infection
what enzyme is packed into retroviruses
reverse transcriptase
describe replication of retroviral genome
parental rna is reverse transcribed into cDNA, then it is integrated into dna where it uses the host machinery
how do retroviruses transcribe from dna back to rna
they bring their own promoters and enhancers
how does the integrated form of retroviruses have more information than genomic rna
long terminal repeats-rt starts at u3, transpose over to r, goes all the way down, then goes all the back to u5 (copy and transpose)
what is a provirus
integrated dna
if all ltr have termination sequences, how do they not stop at the beginning
first termination site is supressed due to secondary structure regions in GAG
The HIV virus uses the host cell’s reverse transcriptase to manufacture DNA
True
False
False
why can’t you use drugs to block translation for hiv
it would kill the host because it uses the host cell machienery
name 4 targets for hiv antivirals
protease inhibitors (blocks it from cleaving to functional proteins, no maturation)
rt inhibitors, entry inhibitors, integrase inhibitors
2 types of RT Inhibitors
NRTI (inhibits hiv rt) NNRTI (binding non competeitively to rt)
what do fusion inhibitors target in hiv
blocks fusion of viral gp41
name of hiv protease inhibitor
saquinavir
where does uncoating and rt happen for hiv
cytoplasm
why was harrt awesome
lowered hiv viremia, increased cd4 cells
why was harrt bad
expensive, people failed to take it correctly, could create resistant mutants if not taken correctly
what inhibitors is prep made of
nrtis
how did covid spread so effectively
you can transmit it before you show symptoms
what receptor does covid bind to
ace-2 in lungs
how does covid cause cytokine storm
infects cells in the lungs, cytokines released, t cells and macrophages join, positive feedback loop
what do monoclonal antibodies do as a treatment for covid
block entry into cell by binding to virus
types of covid vaccines
mrna, inactivated viral vector (janssen), injecting protein from covid, inactive virus
how does covid get in cell
fusion
how does cov make so many proteins
ribosomal frameshifting, cleavage of polyproteins (nonstructural), subgenomic rnas (structural)
in the latent life cycle of tumor viruses, what is it called when a virus early proteins are expressed that cause cause changes in the properties of host cell
virally transformed cell
tumor formation results from a failure of regulatory mechanisms which control what boundary in the cell cycle
g0/g1 boundary
resting phase
g0
stimulate cell growth, cause cancer when hyperactive
oncogene
inhibit cell growth, cause cancer when turned off
tumor supressor genes
dominant or recessive mutation-oncogene, and why
dominant, binding is a gain of function, under normal conditions the gene only binds when a signal is recieved to grow but a mutant binds all the time
dominant or recessive mutation-tsg, and why
recessive, normal gene always binds to control cell cycle, a mutant does not bind and function is lost
oncogene transmitted by virus
v-onc
cellular proto-oncogene
c-onc
examples of tumor supressor genes
rb, p53
how does rb control cell cycle
binds to e2f to control inappropriate entry into s phase
how does p53 control cell cycle
stops it if theres damage to the dna
what type of virus is rsv
retrovirus
what happens when a retrovirs has an oncogene instead of its regular gene
needs a helper virus for co infecting
difference between acute and chronic transforming retroviruses
acute has a v-onc, chronic cause cancer on accident
difference between cis and trans activation of cellular oncogenes
cis happens on the same location, trans can happen on different chromosomes
Acutely transforming retroviruses may deregulate cell division by
A. Bringing in a v-onc
B. Insertional mutagenesis
C. Overexpression of a c-onc
D. Destruction of tumor suppressor
A
Cellular transformation by retroviruses does not involve which of the following events?
A. Expression of a v-onc, which causes deregulated cell growth.
B. The overexpression of c-onc, which causes deregulated cell growth
C. Insertional mutagenesis results in disruption of a cellular tumor suppressor gene.
D. The virus is able to make a DNA copy from its RNA genome using reverse transcriptase, which causes deregulated cell growth.
D
what type of cell, permissive or non permissive, is more likely to interate into host genome for dna tumor viruses
non permissive
example of dna tumor virus associated with warts and cancer
hpv
warts vs cancer of hpv
cancer has abnormal differentiation, expresses e6 and e7, genetic damage
what does e6 of hpv do
degrades p53 so cell does not ever commit apoptosis and there is uncontrolled cell growth
what does e7 of hpv do
attacks p21 and pRB, releasing e2F to go into s phase
hpv genome
non enveloped, circular dna genome
hpv vaccine
empty viral capsid elicits immune response
what cancer is adenovirus associated with
retinoblastoma
e1a and e1b
e1a-adenovirus, inactivation of rb function e1b-adeno-blocks activation of p53
why does burkitts lymphoma cause cancer
translocation to chromosome 14, puts myc gene under the control of a very active promoter
Burkitt’s lymphoma is associated with EBV infection. How might this virus promote cell growth, leading to tumor formation.
Herpesviruses tend to cause dsDNA breaks
Translocation of a c-onc
Overexpression of a c-onc
All of the above
None of the above
D
what does an ideal viral vector look like
deliver therapeutic gene, allow good expression, maintain expression, selectively interact with specific tissues
what is a concern of using viral vectors and how can we avoid it
loss of therapeutic gene expression because virus tries to avoid immune response. add inducible promoter
adenovirus as a viral vector advantage
effects dividing and non dividing cells
adenovirus as a viral vector disadvantage
elicits immune response
advantage of aav
infects dividing and non dividing cells, no negative effects
disadvantage of aav
needs helper virus, small insert size
retroviral vector advantage
long term expression, infect non diciding cells
retroviral vector disadvantage
chronic overexpression, insertional mutagenesis
advantage as hsv as a vector
potential delivery to neurological tissue, acceps large inserts, latent infection
disadvantages of hsv as a viral vector
cant replicate in a dividing tumor cell yet
vaccinia virus advantage as a vector
replicates in cytoplasm so no need to deliver to nucleus, takes the largest genome size
ebola genome
enveloped, helical
how does ebola evade immune response
comes on really quickly, virus infects immune cells, cytokine storm damages other cells
what mechanism does ebola use to create more proteins
frameshifting
why is there no interferon response from ebola
vp35 binds dsRNA and hides it from RIG-I
Ebola is often fatal because the virus kills the host. How does Ebola do this
Blocks the host immune response
Causes a cytokine storm which damages other cells.
Cytokine storm kills endothelial cells which leads to vascular instability/ hypovolemic shock
Patient usually dies before they can make antibodies
All of the above
All of the above
