Flashcards in MCM 2-18 DNA Viruses II Deck (37)
key differences between herpesviruses and adenovirus life cycles
-when herpesvirus attatches to cell membrane, fusion induced. Capsid brough tinto cytoplasm and transported to nuclear pore.
When DNA is uncoated in nucleus, rapidly circularizes
virions released without lysing cell: after virions are taken up by golgi (allows them to egress by exocytosis from cell) and can take up latency
the genome present in the cell, but infectious virions are absent.
-major barrier to vaccines
when can herpes be spread?
during the primary infection
during latency (asymptomatic shedding)
or during recurrence of the disease
all of these will cause the primary infection in the person who gets infected
the herpesviruses are enveloped or non-enveloped?
Describe HSV1 Primary infection
primary - spread by close contact with active lesions/asymtpomatic sheeding. Lesions can appear on nose/face/mouth/eyes. Usually not genital.
Latency in neurons - can cause meningitis
describe HSV1 recurrent infection
triggered by fever, sunlight, hormones, stress, trauma.
prodomal symptoms include tingling and itching
lesions appear on lips and inside of mouth, can also be on eyes/genital/fingers.
occasionally causes encephalitis
in brain, targets temporal lobe
describe HSV2 primary infection
spread by close contact of mucus membranes (genital/oral)
produces many lesions causing pain, itching, fever, malaise, headache.
Ussually below waist.
Latency in neurons
Double infection with HSV1 common
HSV 2 recurrent infection
itching/tingling at lesion sight day before outbreak as prodromal symtpoms
vesicular lesions appear on labia, penis, anus, mouth, eyes.
lesions contagious, but asymptomatic shedding occurs as well
what can distinguish HSV1 and 2?
serology and PCR
HSV treament and prevention?
treatment - antiviral therapy to shorten infections and reduce transmission of boht HSV types.
Antiviral prophalaxis for those with HSV-2 recurring
parent drug of valtrex is acyclovir.
Prevention - safe sex, avoid contact with cold sores. HSV outbreaks avoided with chemoprophalaxis.
Primary VZV infection
varicella (chicken pox) - highly contagious spread through aerosol
latency in dorsal root ganglia neurons
distinctive body-wide rashes (dew drop on rose petal)
complciations include hepatitis, encephalities, pneumotitis, and infection of the lesions by MRSA and STrep.
Recurrence of VZV infection
Herpes Zoster/Shingles - common in elderly/immunocompromised
burning,itching, tinging as prodromes
-bilateral rash - outbreak occurs along a single dermatome with itchy, painful contagious lesions
Complications - bells palsey, blindness, post therapeutic neuralgia, long lasting pain
Diagnosis of VZV
initial - clinical signs
PCR to confirm
treatment of varicella
uncomplicated VZV does not require treatment.
for Zoster - treatment only effective in first 3 days. acyclovir and derivatives marginally effective
foscarnet is second line therapy
VZV is only herpes with vaccine - live attenuated, highly effective
transmission by saliva
EBV infects epithelial cells and B-cells in tonsils where it remains latent
Childhood - asymptomatic
Teens - mono
rarely, as latency is established in only a few B-cells
linked to immunosuppression.
Recurrance can cause several malignancies including hodgkin lymphoma and burkitt lymphoma
diagnosis of EBV
initial - clinical
Serology/blood smear looking for high WBC and atypical lymphocytosis to confirm
treatment of EBV malignancies?
supportive care (symptom management), alleviaton of immunosuppression, and oncotherapy.
No antivrials or prevention methods
transmitted orally, sexually, perinatally, and through blood.
swelling of liver and spleen
Mono like symptoms, distinguishes itself by absence of sore throat and prescence of a rash
ussually asymptomatic, but causes high morbiditiy/mortality in AIDS patients or transplant recipients
CMV prevention and treatment
preemptive screening before transplant, prophylactic Antivirals
highly toxic ganiciclovir can treat, no prevention methods.
diagnosis of CMV
serology, culture assays,and PCR
HHV6 and HHV7 primary
roseola infantum - transmitted in saliva.
infects CD4 t-cells where it establishes latency.
Three days high fever, followed by rash on trunk.
Peak incidence between 7 years old and 13 months
diagnosis of HHV6 and HHV7?
based on ruling out allergic reaction to abx (looks similar to roseola)
no treatment or prevention options, supportive care to alleviate the fever
avoid giving antibiotics
viral genome expression phases
1. Genome enters the nucleus, circularizes. Transcription of some mRNA, mRNA leave and are translated into immediate early genes which transactivate gene expression
2. mRNA made and leaves nucleus, gets translated into early genes which are involved in DNA replication.
3. mRNA gets made later on, leaves nucleus and gets translated into the late genes = capsid proteins and glycoproteins. Glycoproteins mature in golgi. capsids buds bud out, lose bud, enter cytoplasm.
describe HSV in the brain
HSV 1 and 2 primary infections often cause meningitis
recurrent HSV infections occasionally cause encephalitis
HSV targets the temporal lobe
where does CMV stay latent?
in the cd34+ HSC cells - bone marrow hematopoietic stem cells
HSV1 in children, causes lesions around the mouth
what nerve do HSV 1 and 2 remain latent in?
trigeminal nerve ganglion
oral hairy leukoplakia
caused by EBV