DNA Viruses Flashcards
where does DNA viral transcription and replication occur?
In the nucleus (except poxvirus)
what enzymes transcribe and replicate genome?
Host RNA polymerase (except poxvirus) and either viral or host DNA polymerase for replication
what dictates whether a virus uses viral or host DNA polymerase?
how large the virus is
what is the order of replication, transcription and translation in the DNA viral life cycle?
transcription, translation then replication
how is RNA polymerase recruited to transcribe viral DNA?
viral DNA has promotors that are regulated by both cellular and viral transcription factors (as long as the cell is permissive)
in what cellular condition is viral DNA polymerase needed?
when cells are differentiated and nondividing
what are two examples of viruses that use their own DNA polymerase?
herpesvirus and adenovirus
why do DNA viruses have less random mutation than RNA viruses?
DNA polymerases have higher fidelity and proof reading. They are genetically more stable
where is most genetic diversity created in DNA viral genomes?
in recombination within and beteen genomes
what types of diseases does adenovirus cause?
respiratory (cold, pharyngoconjunctival fever, pneumonia), acute hemorrhagic cystitis, keratoconjunctivitis and gastroenteritis
what is the transmission of adenovirus?
aerosol, fecal-oral, objects and poorly chlorinated swimming pools
what are two particular susceptible populations to adenovirus?
children and military recruits
what part of the virus facilitates adenovirus entry into the cell into the cytoplasm and how?
fibers (spikes) bind to cell receptors to cause endocytosis and acidification causes the spikes to lyse the vesicle
where and how does the capsid of adenovirus uncoat?
it uncoats at nuclear pore by injecting it through (capsid docks at pore)
what are the adenovirus gene expression phases?
immediate early (transcribing transcription factors), early (replication) and late (capsid proteins)
does adenovirus use host or viral DNA pol?
viral
where does adenovirus capsid assembly occur and how does it egress from the cell?
In the nucleus and it lyses out of the cell
how is adenovirus diagnosed?
cell culture, antigen detection, PCR and serology
when and how is adenovirus treated?
with immunocompromised patients in only most dire cases with cidofovir (nephrotoxic)
is there a vaccine for adenovirus?
yes but it is only available to military personnel
what is the most commonly diagnosed STD in the US?
HPV
what epithelial diseases and malignancies are caused by HPV?
common warts, plantar warts and genital warts. head, neck, cervical and penile cancer
what is the tropism of HPV?
differentiated epithelial cells
what is the mechanism of wart formation associated with HPV?
HPV infects the precursor skin cells (stratum corneum) with little amplification. Once cells differentiate and become keratinized, the virus begins to replicate and cause hyperplasia
why is it difficult to study HPV in culture?
transcription factors in late keratinocytes promote gene transcription
what are the two possible courses of disease for a HPV wart?
it can be resolved by the host’s immune system or it may transform into a tumor from viral transcription factors E6 and E7 (oncogenes)
does HPV use host or viral polymerase?
Host
why is it important to diagnose ant type genital HPV?
there are 13 high risk types of cancer causing HPV (type with DNA tests)
how are HPV warts and malignancies treated?
cryotherapy, chemical ablation and colposcopy (excision in the cervix). ANy malignancies should be treated with oncotherapy
what are the types of vaccines for HPV and what types are they active against?
gardasil: 6,11,16 and 18
cervarix: 16 and 18
what is the vaccine to HPV comprised of?
VLPs: virus-like particles (empty capsids)
how many speicies of herpesviruses are there and what is the average number that people are infected with?
8 and most people are infected with >3
how long does a herpesvirus take to clear up?
it doesn’t
what is the host range and tropism of herpesvirus?
only infectious in humans and each virus prefers different cell types
where does herpesvirus transcription take place?
in the host cell nucleus
what phases of expression do herpesviruses have?
immediate early (transcription factors), early (replication of genome) and late (capsid proteins)
how does herpesvirus replicate its DNA?
viral polymerase and accessory factors
how does herpesvirus egress?
exocytosis
what is the definition of herpesvirus latency?
genome is present in cell but infectious virions are absent
what is a major barrier to vaccines with herpesviruses?
latency of the virus is established before it could be identified by the immune system and stays there for life
herpesvirus is only contagious during active disease periods. True or false?
false. they are transmissable during periods of latency as well (asymptomatic shedding)
how often do latent herpesviruses recur?
they may reoccur never or often
how is HSV-1 transmitted?
close contact with active lesions or asymptomatic shedding
what is the primary disease of HSV1 in childhood?
gingivostomatitis
where are the primary lesions of HSV1 usually present and where is latency established?
above the waist (can be genital) and neurons
what triggers and precedes recurrence of HSV1?
triggered by fever, sunlight or stress (etc) and it is preceded by a tingling, itching prodrome
where are the lesions of HSV1 recurrence?
on lips or in mouth (may also be in eyes, on genitals or on fingers)
what is often a complication of primary infection with HSV1 and 2?
meningitis (stiff neck and headache)
could also cause encephalitis
what part of the brain is targeted by HSV1?
the temporal lobe
how is HSV2 disease spread?
by close contact between mucous membranes (usually acquired during adulthood)
what are the symptoms of primary HSV2 disease?
many lesions, pain, itching, fever and headache (not always but usually below the waist)
where is latency established?
in neurons
double infections with HSV1 and 2 are uncommon. True or False?
False. They are actually common
what are the symptoms of recurrent HSV 2 disease?
prodoromic itching and tingling followed by vesicular lesions on labia, penis, anus, mouth etc.
how is HSV diagnosed?
serology and PCR disinguish HSV 1 and 2 (differentiates risk for having children)
when are antivirals used for HSV?
to shorten an infection, reduce transmission and as prophylaxis when people have frequent outbreaks
what is the main antiviral used for HSV?
acyclovir
how is HSV prevented?
safe sex, avoidance of cold sores, and chemoprophylaxis to reduce shedding
are there any vaccines for HSV?
no
what is the primary infection of VZV?
chicken pox- “dew drops on rose petals” rash
how is Varicella transmitted?
aerosol (highly contagious)
what are some complications of VZV primary infection
hepatitis, encephalitis, pneumonitis or bacterial infection of lesions
what is recurrence of VZV and what latency is it caused by?
shingles (herpes zoster). caused by a latency in dorsal root ganglia
who is most likely to develop shingles?
elderly and immunocompromised carriers of VZV
where does outbreak of shingles occur?
along the skin surface of a single dermatome
what are some complications of shingles?
bell’s palsy, posterpetic neuralgia (indefinite pain) and retinitis (can cause infectious blindness)
what is shingles infection of the eye called?
Herpes Zoster Opthalmicus
what parts of the eye can be effected by zoster and what part can be destroyed?
all parts can be infected and it can destroy the retina
how is VZV diagnosed?
clinical signs, PCR, antigen and serology
how and when is VZV treated?
not required unless complicated. can be treated within 3 days of beginning of zoster symptoms to have relief. Treat with acyclovir and foscarnet (second line)
how is VZV prevented?
two live, attenuated vaccines:
varvax prevents varicella (1-50)
zostavax prevents zoster (>50 yo)
how is Epstein Barr Virus transmitted and what cells does it infect and become latent in?
it is transmitted in saliva and infects oral epithelial cells and B cells in tonsils. It remains latent in B cells
what are the usual symptoms of childhood Epstein Barr Viruses?
they are usually asymptomatic
when is EBV likely to recur?
during ties of imunosuppression (usually does not occur in healthy people)
what complications are associated with latent EBV virus?
many different types of malignancies and oral hairy leukoplakia
how is infectious EBV diagnosed?
clinical signs, serology and blood smear for elevated WBC and atypical lymphocytes
how are EBV associated malignancies treated?
alleviate symptoms, treat immunosupression and treat with oncotherapy
what antivirals and vaccines are available for EBV?
none
how does CMV spread and what are its symptoms?
many different routs. symptoms may like mono but are highly dependent upon the host (most people are asymptomatic)
how can CMV and EBV be differentiated clinically?
CMV has no sore throat but does have a rash
what is the result of primary infection with CMV in pregnancy?
increased risk of congenital malformations. primary cause of deafness
in which patients is CMV concerning?
pregnant women, AIDS patients and transplant recipients (frequent cause of transplant failure)
how is CMV diagnosed?
serology, culture and PCR
what antiviral drugs are used for CMV?
ganciclovir, foscarnet and cidofovir (last two nephrotoxic)
what disease is caused by HHV6b and HHV7 and how is it transmitted?
roseola infantum, transmitted orally
what are the symptoms of roseola and what age does it typically happen?
3 day high fever followed by faint rash. happens most at 7-13 months of age
how is roseola treated?
supportive care for fever but resist giving antibiotics
what must be ruled out when diagnising roseola infection?
drug allergy
