Unit 2 (minus the first three lectures) Flashcards
what are the results of RNA viruses’ high mutation rates?
resistance to antivirals, barriers to vaccines, reassortment of genome segments, pandemics
“small RNA virus”
picornavirus
what is the purpose of RNA in an RNA virus
genetic material AND template for protein synthesis
what is the dual purpose of replication in the RNA virus
to copy the genome AND make mRNA
what are the characteristics of the rotovirus
dsRNA, eurkaryotic virus, icosahedral, enveloped
process that makes mRNA from RNA genome of RNA virus
transcription
process that makes RNA genome in RNA virus
replication
where do RNA viruses operate in the cell
cytoplasm
what is (+) RNA used for
mRNA sense strand, instructions for protein
what is (-) RNA used for
template for (+) strand
what do RNA viruses use to replicate the RNA genome
RNA dependent RNA Polymerase (RDRP)
(host/virus) ribosomes translate mRNA into proteins
host ribosomes
RDRP is highly (efficient/accurate) in replicating RNA virus genomes
efficient
exception to the rule that RDRP operates in the cytoplasm
influenza virus
where in the cytoplasm does RNA virus replication specifically occur
on cell membranes (endosomes, lysosomes, ER vesicles), this concentrates the components to increase efficiency
what contributes to RNA virus genetic diversity
low fidelity/no proofreading of RDRP, rapid evolution by recombination, reassortment of genome segments
classification of poliovirus
picornaviridae, enterovirus, (+)ssRNA genome, linear mRNA, infects human GI cells
poliovirus transmission of disease and where it persists
fecal-oral, water supply
how does poliovirus enter the host cell
binds receptor
capsids become hydrophobic > shape change
capsids form pore through membrane
RNA genome enters cell at plasma or endosome membrane
3Dpol
poliovirus RDRP
(the same/a different) enzyme copies (+) and (-) RNA strands in the RNA virus
same RDRP
when does the virus switch from translating mRNA to packaging it?
when there are enough capsid proteins that have accumulated
what happens to an RNA virus when RDRP is scarce
translation
what happens to an RNA virus when RDRP is abundant
(-) RNA synthesis
which RNA viruses (+/-) must package RDRP in the virion
(-)
which RNA viruses (+/-) may or may not package RDRP in the genome
(+)
why must RNA viruses code for RDRP in their own genomes
mammalian cells do not have enzymes to transcribe RNA from RNA templates
presentation of rotavirus disease
severe gastroenteritis–diarrhea, dehydration, malabsorption
key feature of rotavirus genome
segmented
accumulation of virus proteins in the cytoplasm that displaces the cytosol
viroplasm
how do rotavirus virions enter the rough ER
budding after assembly
two ways that rotaviruses exit the host cell
exocytosis/lysis
rotavirus prevention
live attenuated vaccines
presentation of uncomplicated influenza virus
respiratory tract involvement, fever, headache, myalgia, weakness
complicated influenza virus symtpoms
pneumonia, myositis (muscle pain), rhabdomyelitis (muscle break down)
where does influenza virus replicate
in the lungs
where in the cell does transcription and genome replication take place for influenza virus
the NUCLEUS
releases influenza virions from sialic acid on cell surface
N antigen (neuraminidase)
how are influenza virions shed
in respiratory droplets
characteristic of influenza vaccine
trivalent inactivated vaccine–two strands of A and one strand of B
virus binds to CD4 and chemokine receptors on T cells and macrophages
HIV
T cell count is (high/low) in HIV infection
low
key enzyme involved in converting (+)ssRNA HIV genome to dsDNA
reverse transcriptase (included in the virion)
what makes HIV so difficult to treat
dsDNA genome integrates into host chromosome for life
which enzyme transcribes mRNA from the integrated HIV genome
RNA Pol II
where does HIV virion maturation occur
outside the cell, while the viral protease cleaves the capsid proteins, forming the final trapezoid shape
how is the HIV virion released from host cell
budding
gold standard for HIV diagnosis
PCR
HIV treatment
ART antiretroviral therapy, many drugs must be combined
what causes the fever, body aches, and extreme fatigue in influenza virus infection
interferon induction
where do DNA viruses carry out transcription and replication (exception: poxvirus)
in the NUCLEUS
(host/virus) RNA Pol transcribes mRNA in DNA viruses (exception: poxvirus)
host
the viral or host DNA Pol replicates the genome for (DNA/RNA) viruses
DNA viruses
cells that have the right transcription factors for a DNA virus to undergo transcription are considered ____
permissive
two viruses that use viral DNA polymerase
herpesvirus, adenovirus
DNA polymerases for DNA viruses have (high/low) fidelity
high fidelity
origin of diversity in DNA viruses
recombination
DNA virus with symptoms such as infected conjunctivae, painful sore throat, pneumonia, bad cold with fever
adenovirus
particularly susceptible populations to adenovirus infections
military, children at camps or on sports teams
(host/viral) RNA Pol II makes adenovirus mRNA
host
where does the adenovirus genome replicate
nucleus
adenovirus genome is replicated by (host/viral) DNA Pol
viral
where does adenovirus capsid assembly take place
in the nucleus
how do adenovirus virions egress
lysis
there is an adenovirus vaccine but only a select group of people get it–who
military personnel
why is HPV hard to replicate in lab
only amplifies when transcription factors in the host cell are just right (different stages of epithelial cells)
(host/viral) RNA pol transcribes HPV mRNA
host
(host/viral) DNA Pol synthesizes HPV genomes
host
viral factors of HPV E6 and E7 are ___
oncogenes
how does the HPV vaccine work
no viral DNA, just viral capsid to induce correct antibodies
DNA viruses (except poxvirus) use the host RNA Pol II enzyme and what else to synthesize mRNA
viral and cellular transcription factors that bind to viral gene promoters
viral DNA polymerase and accessory proteins are required to replicate what type of viral DNA genomes
large DNA genomes
DNA virus associated with: gastroenteritis, keratoconjunctivitis, pharyngoconjunctival fever, pneumonia
adenovirus
cidofovir is used to treat which DNA virus
adenovirus
the initial phase of HPV infection occurs in which cell type
basal epithelium
treatments for this DNA virus include: chemical ablation, cryotherapy, colposcopy, VLP vaccine
HPV
how many human herpes viruses are there
8
most people are infected with __ herpesviruses
three or more
major barrier to herpesvirus vaccines
latency
classification of herpesvirus
icosahedral, tegument, dsDNA
herpesvirus genome replication is by (host/viral) polymerase and (host/viral) accessory factors
viral, viral
how is HSV-1 primary infection spread
close contact with active lesions or asymptomatic shedding, usually above waist
characteristics of HSV-1 recurrent disease
tingling and itching precede outbreaks, lesions on eyes/genitals/fingers/mouth,
what triggers HSV-1 recurrent disease
fever, sunlight, hormones, stress, physical trauma
are HSV-1 recurrent disease lesions contagious
yes
which herpesviruses cause meningitis
HSV1 and HSV2 primary infections
what does HSV recurrent infection cause in the brain
encephalitis
how is HSV2 primary infection acquired, and when
adulthood, oral-genital STD
HSV2 recurrent disease prodome
itching, tingling at lesion site a day before outbreak
can HSV2 recurrent infection spread in the absence of lesions
yes
what test is used to distinguish between HSV1 and HSV2
PCR
parent drug used to treat HSV2
acyclovir
where does chicken pox remain latent in the body after infection
ganglia
primary vzv aka
chicken pox
how is primary VZV transmitted
aerosol, highly contagious
complications possible with primary VZV infection
hepatitis, encephalitis, pneumonitis, bacterial infection of lesions
VZV recurrence
herpes Zoster (shingles)
complications of VZV recurrence
Bell’s palsy, neuralgia, retinitis
common sites of shingles
back, shoulder
30% of herpes zoster outbreaks affect face, destroying the ____ and leading to _____
retina, blindness
when is herpes zoster treatment effective
only during first three days of outbreak
vaccines for VZV (exist/do not exist)
exist–live, attenuated virus
where does Epstein Barr Virus remain latent
small fraction of B cells
what causes EBV recurrences?
immunosuppression
EBV recurrences can lead to:
malignancies
what are the diagnostic tests for mono
clinical signs, serology for heterophile antibodies, blood smear for elevated WBCs and atypical lymphocytosis
does prevention exist for EBV
no
CMV
cytomegalovirus
presentation of primary CMV infection
usually asymptomatic
how is CMV differentiated from EBV
absence of sore throat and presence of rash (not mono!)
permanent outcomes of congenital CMV disease
hearing loss, MR, vision loss, seizures, death
virus that is a frequent cause of transplant failure
CMV
CMV diagnostic methods
serology, culture, PCR
does treatment exist for CMV
yes, antiviral drugs
does prevention exist for CMV
no–vaccine ineffective
what cells does HSV6, 7 infect
CD4+ T cells
where does HSV6, 7 remain latent
CD4+ T cells
how is HSV6, 7 transmitted
saliva
at what age does HSV 6, 7 infection primarily occur
7-13 months of age
diagnostic test for Roseola HSV6, 7
clinical manifestations, rule out drug allergy
treatment for Roseola HSV6,7
none, treat symptoms, don’t give antibiotics
prevention for Roseola HSV6, 7
none
what is reactivation of HSV 1 characterized by
viral shedding from vesicular or asymptomatic lesions
reactivation of VZV is characterized by
painful, unilateral rash
risk associated with primary CMV infection
congenital CMV syndrome in neonates
EBV infection presentation in children
asymptomatic (teens get mono)
acyclovir works for:
HSV 1, HSV 2, VZV
how is viral gene expression induced
by binding of cellular transcription factors to promoter regions
viral genes are (prokaryotic/eukaryotic)
eukaryotic
viral genes in a linear arrangement on one RNA strand, with only a single promoter
simple genome, eg retrovirus
viral genes on both strands of DNA, often overlapping, and each with its own promoter
complex genomes, eg adenovirus, herpesvirus, poxvirus
how do transcription factors affect cell permissiveness to viruses
only certain cells in certain tissues express the transcription factors needed for the virus to grow (HPV-epithelial, Hep B-liver)
viral genomes (have/do not have) non-coding regions
do not have
viral genomes (have/do not have) overlapping reading frames
have
viral genomes (have/do have) alternative splicing of RNA
have
the goal of alternative splicing of RNA is to change the ___ sequence
aa
why are viral proteases targets for antivirals
to prevent polyproteins from being divided into appropriate proteins
