MCM 2-18 DNA Viruses II

Question 1

key differences between herpesviruses and adenovirus life cycles

Answer 1

-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

Question 2

Describe latency

Answer 2

the genome present in the cell, but infectious virions are absent.

-major barrier to vaccines

Question 3

when can herpes be spread?

Answer 3

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

Question 4

the herpesviruses are enveloped or non-enveloped?

Answer 4

enveloped

Question 5

Describe HSV1 Primary infection

Answer 5

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

Question 6

describe HSV1 recurrent infection

Answer 6

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

Question 7

describe HSV2 primary infection

Answer 7

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

Question 8

HSV 2 recurrent infection

Answer 8

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

Question 9

what can distinguish HSV1 and 2?

Answer 9

serology and PCR

Question 10

HSV treament and prevention?

Answer 10

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.

Question 11

Primary VZV infection

Answer 11

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.

Question 12

Recurrence of VZV infection

Answer 12

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

Question 13

Diagnosis of VZV

Answer 13

initial - clinical signs

PCR to confirm

Question 14

treatment of varicella

Answer 14

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

Question 15

EBV primary

Answer 15

transmission by saliva

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

Childhood - asymptomatic
Teens - mono

Question 16

EBV recurrance

Answer 16

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

Question 17

diagnosis of EBV

Answer 17

initial - clinical

Serology/blood smear looking for high WBC and atypical lymphocytosis to confirm

Question 18

treatment of EBV malignancies?

Answer 18

supportive care (symptom management), alleviaton of immunosuppression, and oncotherapy.

No antivrials or prevention methods

Question 19

CMV

Answer 19

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

Question 20

CMV prevention and treatment

Answer 20

preemptive screening before transplant, prophylactic Antivirals

highly toxic ganiciclovir can treat, no prevention methods.

Question 21

diagnosis of CMV

Answer 21

serology, culture assays,and PCR

Question 22

HHV6 and HHV7 primary

Answer 22

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

Question 23

diagnosis of HHV6 and HHV7?

Answer 23

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

Question 24

viral genome expression phases

Answer 24

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.

Question 25

describe HSV in the brain

Answer 25

HSV 1 and 2 primary infections often cause meningitis

• stiff neck
• headache

recurrent HSV infections occasionally cause encephalitis

• fever
• neurological symtpoms

HSV targets the temporal lobe

Question 26

where does CMV stay latent?

Answer 26

in the cd34+ HSC cells - bone marrow hematopoietic stem cells

Question 27

Gingivostomatitis

Answer 27

HSV1 in children, causes lesions around the mouth

Question 28

what nerve do HSV 1 and 2 remain latent in?

Answer 28

trigeminal nerve ganglion

Question 29

oral hairy leukoplakia

Answer 29

caused by EBV

Question 30

2 groups most at risk for CMV

Answer 30

aids patients and transplant recipients

Question 31

HHV8

Answer 31

Kaposi sarcoma herpes virus. associated with immuncompromised, aids, higher prevalence in africa and mediterranean

Question 32

KSHV diseeases

Answer 32

infects B cells and endothelial cells

karposi sarcoma - endothelial cell proliferation
multicentric castleman’s disease

Dramatic B-cell tumors, treat underlying immunodeficiecny

Question 33

diagnosis of KSHV and treatment

Answer 33

lesion appearance, alleviate immunosuppresion, no antivirals

Question 34

37 year old male. loss of appetite, fatigue, faint rash on torso, jaundice, abdominal tenderness.

elevated WBC and liver enzymes. likely diagnosis?

Answer 34

CMV

• mono like (fatigue, swelling of spleen and liver)
• no sore throat (not EBV)
• Rash (not EBV)

Question 35

primary infection with CMV is characterized by

Answer 35

risk of congenital CMV in neonates

Question 36

what feature is common to all alpha herpes viruses (HSV1, 2, and VZW)

Answer 36

susceptible to acyclovir and derivatives

Question 37

how is roseola acquired in infants?

Answer 37

hhv-6b and 7 spread through saliva