MCM 2-18 DNA Viruses II Flashcards Preview

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Flashcards in MCM 2-18 DNA Viruses II Deck (37)
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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


Describe 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.

lesions contagious

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


EBV primary

transmission by saliva

EBV infects epithelial cells and B-cells in tonsils where it remains latent

Childhood - asymptomatic
Teens - mono


EBV recurrance

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
-stiff neck

recurrent HSV infections occasionally cause encephalitis
-neurological symtpoms

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


2 groups most at risk for CMV

aids patients and transplant recipients

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