Repro: Test 2: 1&2. Blue : Viral Sexually Transmitted Diseases I & Ii

Front 1

What viral STD has the most new cases each year?

Which has the highest prevalence?

Back 1

new cases: Papillomaviruses

Prevalence: Herpes simplex type 2

Front 2

Once you are infected with papillomavirus, how long will you be infectious? Herpes?

Back 2

Papilloma: a few years

Herpes: rest of your life

Front 3

The majority of genital herpes is what kind?

Back 3

type 2

Front 4

Transmission of HSV-2? (4)

Back 4

Genital-genital;
genital-oral;
oral-oral;
mother to newborn

Front 5

how does HSV2 infection occur (mechanism)

Back 5

initial infection of epithelial cells

replication of the virus in epithelial cells (can be symptomatic or asymptomatic)

virus enters local nerve branch (on terminal) and move retrogradely to the nucleus where it replicates

Front 6

how does HSV-2 not get cleared from the system?

Back 6

tether themselves to chromosome...lets them hide in the DNA

LATENCY

Front 7

What is latency with respect to HSV2

Back 7

viral genome chromosomally tethered:
euchromatic in epithelial, heterochromatic in neuron
(limits expression).

Front 8

Why are recurrent flares of HSV2 marked by low symptomatology or even asymptomatic?

Back 8

2ndary Ab response is faster, and can clear the virus

Front 9

why are neurons that are infected with HSV not destroyed? 2

Back 9

Very small amount of replication going on which prevents its complete destruction

also the virus has protective factors to prevent destruction of the gene (miRNAi/siRNA's expressed block neuronal apoptosis upon primary/recurrent infection)

Front 10

Pt presents with Painful, usually multiple, blister-like
lesions on vulva, vagina, cervix, and
rectum. Additionally they ahve fever, chills, malaise, and headache...what do they have?

Back 10

HSV2

Front 11

How long during an infectious period of HSV is the virus shed?

Back 11

12 days

note that this can occur after the symptoms go away, so this is a likely means of how the disease is spread, people think "oh the disease is gone for now, I can go put my D in some V...womp womp)

Front 12

Why is genital herpes so prevalent?

**

Back 12

20% of people infected with HSV2 have no sx at all

60% of people have symptoms but don't know they are infected

20% of people infected with HSV2 have sx and know they have it

Front 13

how often do people have ASYMPTOMATIC viral shedding?

***

Back 13

up to 75% of days!!!

Front 14

If a pt has HSV2 what must they use during sex?

Back 14

PROTECTION

Front 15

How can a newborn get HSV2?

Back 15

ONLY if the virus is being shed in the vaginal canal

it cannot cross the placenta

Front 16

Complications of genital herpes?

Back 16

meningitis/encephalitis, (can be recurrent: Mollaret’s meningitis), congenital or neonatal infection

Front 17

is there an increased risk of the baby getting HSV2 fi the mom is infected during the pregnancy or has recurrent disease?

Back 17

During the pregnancy?

Front 18

What are the 3 clinical patterns of neonatal herpes?

Back 18

(1) SEM (skin, eyes, mouth)
(2) CNS (encephalitis)
(3) Disseminated

Front 19

The Tzanck smear is the classical way of diagnosing HSV-2, but what is the gold standard now?

Back 19

Viral culture

Front 20

Drugs used for tx HSV2

Back 20

Acyclovir

Continuous use reduces frequency, duration of symptomatic recurrence, shedding time. Do not eliminate transmission. Drug resistance develops over time

Front 21

What virus causes benign tumors (warts)?

Back 21

Papilloma virus

Front 22

What is responsible for 95% of malignant cervical (and 70% of anal) carcinoma?

**

Back 22

Papilloma virus

Front 23

What are the 2 most commonly sexually spread HPVs?

what are the 2 most potentially malignant sexually spread HPV?

***

Back 23

spread: 6 & 11

Malignant: 16 & 18

Front 24

What are the cells that indicate you have HPV (active replicating virus is within them)..you would see them on a papsmear

*

Back 24

Koilocytes

remember: you get an abrasion of the skin, this is how the virus gets in, but it cannot replicate here, it has to move with the layers of skin that build up until it can get to a place where it can replicate...this is the koilocyte

Front 25

What 4 locations can you get neoplasia from HPV?

Back 25

Cervical intraepithelial neoplasia (CIN)

Vulvular (VIN)
Vaginal (VAIN)
Anal (AIN)

Front 26

what is a major difference in the HPVs that are oncogenic and those that are not?

**

Back 26

oncogenic: integrates into the host chromosomal DNA; affinity to activate E6/7; E2 disrupted-->leads to decreased regulation of E6/7 (inactivating tumor suppression)

non: does not integrate; E2 maintained-->regulates E6/7

Front 27

major pathogenic genes in the malignant predisposed HPVs? 2

How do they do this?

**

Back 27

E6 and E7 genes (in HPV 16&18)

E6: inactivates p53 (prevents degradation), and activates telomerase (which immortalizes the cells)

E7: blocks Retinoblastoma gene (keeps cell cycle going indefinitely)

Front 28

At p53, what can make you more susceptible to type 16/18 HPV E6 induced degradation...?

Back 28

pro or arg at codon 72.77

Front 29

major detection of HPV?

Back 29

Papsmear

Front 30

Protection granted by Gardasil? Cervarix?

Back 30

Gardasil: 6/11, 16/18

Cervarix: 16/18

HPV