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62 Cards in this Set

  • Front
  • Back
what are the 2 types of HSV infection
Type I: oral. get EARLY in life, fever blister

Type II: genital. more viscous, onset of sexual activity
HAV I and II are part of what viral family

whats the DNA
alpha-herpes virus

single linear dsDNA
what 2 thigns are important in HSV patogenicity
1. ability to penetrate CNS and replicate
(gets in and replicates locally but then gets into sensory ganglia and replicates there as well)

2. Ability to establish LATENCY
where does HSV replicate
in the host NUCLEUS

*at site of entry adn CNS

**causes DESTRUCTION
what happens to the host cell as HSV replicates
it replicates in the nucleas and this DESTROYS host- ballooning, intranuclear inclusions, giant cells form

**so this destructino can happen but it can also be latent and NOT cause damage
does HSV always get into host and just start replicating like crazy and destroy host cells
nope, hangs out quiet and latent
what type of HSV is...

1. oral
2. genital
3. more likely to recurr
oral I

genital II

reoccur: II

**these are guidlines, sexual practices can move these around, also there is some cross imminuty but NOT enough for resistance
what stain is used for HSV
Tzank
HSV...


1. Primary Infection
2. Recurrent Infection
3. Initial Infection
1. Primary infection: occurs after FIRST exposure, if type I primary infection occurs early in life NO HSV AB,

2. Recurrent infection: recrudescence of an established HSV infection

3. INITIAL: pts that have AB to one type but then are first exposed to a second type
what is the worst for preggo mom

primary
recurrent
initial
primary infection is a HUGE risk for the baby
ok so your pt has HSV I IgG but then recently is exposed to HSV II though sexual contact. what is the type of HSV II infection
INITIAL

**this is when you ahve one and then get the other

**primary is the first time you are exposed
**recrurrent is recrudescence of an establised infecion
what is does the primary HSV II infection look like
painful macules/papules --> vesicles (great spreading!!!) --> pustule/ulcer

**fever, maliase, lymphadenopathy

**more severe in females
**lasts about 3 weeks

**recall primary is the FIRST time you are exposed
what type of tissue does HSV LovE
transitional epithelium
what does an initial HSV 2 infection look like
this happens when you have been exposed previously to HSV 1 but are then exposed to HSV for the FIRST TIME

**less severe and heals faster (<3weeks) than a PRIMARY infection
why is an initial HSV 2 infection less severe than a primary HSV 2 infectino
in an initial infection you ahve been exposed to HSV 1 and so will have limited immunity

**can suppress initial infection w/acyclovir but can still be xmitted
in what cell type does HSV establish latency

will it remain in latency
ganglion cells

nope, recrudesence can occur even WITH good immune system- the more severe the intial outbreak the more liekly you will have lots of recurrence
do HSV lesions scar
not really, even if you have multiple outbreaks in the same ares
what is a discordant couple
if one has HSV and the other does not.
can you autoinoculate HSV
you bet

if you ahve a sore dont be touching thigns!
how often do HSV reinfections occutr
1/3 get 1-2
1/3 get 4-7
1/3 get >8
**if initial infection was SEVERE its more liekly to have recurrence
when is HSV infection spread
ANYTIME!!

if you have clinical sx its easier but can still xmit w/o sx
does humoral immunity (AB) prevent HSV reinfection
nope

**we often see recurrence when we are stressed and immunity is decreased

**transplacental AB from mom are NOT totally protective for baby
what other animals get HSV
NONE, humans are hte only reservoire

there is an increase in rate of xmission
how is HSV spread?

when is most spreading
from vesicular fluid, saliva and other secretions of infected ppl

**MOST ARE SPREAD WHEN ASX!!!!!!

**in order to infection the virus must enter mucosa through an abraision
HSV I is acquired when
what about II
I- young, early in life, from parnets

II- later, onset of sexual activity

MOST PPL q/HSV II dont know they have it. scary
if you have an acitve HSV I infection does this make it less likely to get HIV bc you have maximal AB
NO!!!! its EASIER to get HIV bc you have an open sore from the HSV I
who gets HAV more M or F

married or divorced
city or rural

what is stongest rpedictor of getting HSV infection
Female

more common in divorced/single
more common in cities

MULTIPLE sex partners
is neonatal HSV infection something to worry about
OH YA!

**can be acquired in utero bc moms AB are NOT protective or as babe passes through birth canal (a primary infection is esp worrysome)

**fetal scalp monitors can be a site of viral inoculation, CI in mom w/Hx HSV 2
whats the most common form of HSV infection during preggo
recurrent infection, good bc its less severe and worrysome (primay infectino is BAD, initial is also not good)
what are 3 pays HSV can be given to neonate
1. in utero (rare)

2. during birth

3. post natal- from mom kissing the babe or whatever

**mom having HSV AB are good bc they can help protect but BAD bc they put baby at risk for exposure
we know some HSV infectinos are asx (most ppl doent know they have it) is this true for neonatal infection
nope, almost always sx, sometimes lethal
what are some manifestations of neonatal HSV infection
1. Encephalitis (micro/hydroencephalopathy)
2. skin disease
3. eye disease

**disseminated disease has WORST prognosis
how is HSV dx
tissue sample: ballooning pathology (from viral replication), Tzank smear, COWDRY A inclusions

PCR to detect HSV DNA- wont ID active/latent infection

Culture > PCR

test for AB is asx pts
does PCR ID active vs latent HSV infections, what is a better method
nope

culture > PCR

**if you sample the tissue you can have Tzank cells, coqqdry A inclusions etc
whats the tx for HSV
acyclovir will suppress but...

NO Tx will elimiate latency/recurrent infection

**also can still spread
long term tx of acyclovir for HSV is good for what
decrease recurrence, will STILL shed virus
how is HSV prevented in babes
c section, major infection risk is initial or primary infection. so its in moms who are HSV - but become + at some point in preggo

vaccine in works
what is the deal with HPV
initial infection is manageable but can progress to...

1. warts (6,11)
2. Cervical cancer (16,18)
what viral family is HPV in
papova virus

HPV is the largest and most complex virus in this family

circular dsDNA
we know HSV causes latent infection, what about HPV
yep
are HPV virus resistant
ya! they are TOUGH!!!

resist ether, acid, heat. this means that its hard to kill it with laser surgery or coagulation procedure
what cells are infected with HPV

how is HPV replicated
basal epithelium (so as the infected cell divides the daughter cell moves away from the BM and differentiates into epithelium)

**replication of HPV is not well understood. linked to host cell division. virions are made only in the differentiated cells
hoe does HPV get into the basal cells
through breaks in skin

**the HPV then stim the basal cells to divide and differnetiate into epithelium. the virion is only released through differentiated epithelium NOT hte basal cells.

**evades immune system
what causes the wart in HPV
its viral induced division which increases numper of cells and causes thickening whoch is the wart (6/11)
common warts

what are they called, what are they caused by
common (cutaneous warts) are called verruca vulgaris and are caused by HPV 1-4. flat!!
whats a plantar wart
flat hyperkeratotic region on the feet, can be painful!!!

the common warts on teh skin are caused by HPV 1-4 and are called common (cutaneous) warts (verruca vulgaris)
whats condylomata acuminta
genital warts

caused by HPV 6 or 11

**grey, fleshy color
cervical dysplasia is caused by what
HPV 16,18

Precancerous lesion of cervical epithelium
what are respiratory papillomatosis
juveline form of HPV <5 yp

caused by 6/11

**kid aspirated warts from the mom during birth (condylomata acuminata)
how does HPV 16 18 cause cervical cancer
E6: degrades p53
E7: binds to and inactivated Rb
p53
Rb

**net= trigger cell cycle progression

**this alone does NOT explain development into cancer, there are way more NON malignant infections
when we have HPV that does indeed cause cancer what can be said about the genetics
Viral DNA is integrated into host and E6/7 are expressed. E2 is inactivated

*in NON malignant cells E2 is still expressed and so E6 and E7 are not overexpressed
how is HPV spread
direct skin contact, genital contact, fomite transmission

ENDEMIC
what increases the transmission of plantar warts
seen more in winter
associated with heated swimming pools and communal baths

**common warts are in kids and are HPV 1-4

**ppl who handle meat, pultry, fish are lieky to get wart infections
HIV infection affectes HPV infection how
more likely to get HPV if you have HIV

**the immune suppression in HIV makes it more likely to get anogenital HPV infection
whats the most common VD in US
HPV
what HPV is in the vaccine
6 11- warts

16 18- cancer
how is HPV dx
clinical findings- pap, warts

Hiso is NO good for latent infection. but for active infection will see koilocyte- large vacules
is recurrence of HPV common
ya
how is HPV prevented
pap smear

HPV DNA test <30yo
molluscum contagiosum is part of what viral family
pox virus

DNA, replication in our cytoplasm

typically we fight this off so easily, bigger problem for our HIV pts
what is clinical manifectation of MCV infection
Molluscum contagiosum

skin infection- multiple, small white lesions. seen in genital/anal area.

not a big problem when healthy but big problem in HIV
whats the spread of MCV
direct contact, usually sexual contact

**lesion goes away on own. its NOT inflammatory

This disease was regarded as trivial and treated for largely cosmetic reasons until the advent of large numbers of AIDS patients