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42 Cards in this Set

  • Front
  • Back
where do HSV-1 and HSV-2 remain latent
HSV-1 in the trigenimal ganglia
HSV-2 in the sacral ganglia
why can herpes survive in small populations
it remains latent in infected individuals for life
why has there been an increase in type 2 HSV
individuals with HSV-1 are less susceptible to HSV-2 and there has been a decline in HSV-1
how does infection onf HSV-1 prevent infection with HSV-2
they share glycoprotein D (gpD), which is a surface antigen for adhesion

gpG is diff between the 1 and 2
genome of herpes
linear ds DNA
What keeps HSV latent
epigenic DNA methylation

LAT (latency associated transcripts) are RNA that doesn't produce protein but maintains latency (microRNA)
how does infection with HSV occur
it goes thru a break in the skin and replicates in the epithelium (epidermal cells). it will travel from there thru neurons and remain latent in ganglia
how do herpes lesions compare to other genital lesions
they aren't as deep and remain in superficial layers
what percent of people remain asymptomatic
75%
signs of HSV
vesicles (crawl like a snake)
flu-like symtomes
lymphadenopathy
lesions
rarely leads to ENCEPHALITIS
Bells palsy
what is used to treat HSV
acyclovir
how does acyclovir work
it is activated by phosphorylation by a herpes encoded thymidine kinase and inhibits the viral DNA polymerase
what type of cancer is associated with EBV
burketts lymphoma (increased B cell proliferation predisposes cells to an 8:14 chromosomal translocation resulting in c-myc constitutive expression)

B cells are susceptible due to class switching and affinity maturation
what test is used to detect EBV
monospot test (measures heterophil antibodies)

(also used for glandular fever)
How are antibodies to VCA and EBNA helpful in diagnosis of EBV
antibodies to VCA rise quickly upon infection and persist for life and antibodies to EBNA rise about 1 month after infection and persist for life.

High VCA and no EBNA antibodies means recently infected
when are the following EBV antigens produced in cells
Viral capsid antigen (VCA)
EBV nuclear antigen (EBNA)
early antigen (EA)
VCA is only produced during active infection
EBNA and EA are expressed even during latency
EA is a good marker for chronic infection
How is EBV infection diff in children
there immune system is immature so symptoms won't be apparent
what are the signs and symptoms of EBV (IM)
tiredness
enlarged spleen and lymph nodes
atypical lymphocytes in blood
what is the pathogenesis of EBV
it infects the epithelial cells of the oral-pharyngeal region
It makes a jump to the blood where it binds to complement receptors on B lymphocytes
Infected B cells present EBNA to activate T cells
What causes lymphoproliferative disease
Reactivation of EBV from memory B cells

normally in an immunosuppressed individual or an individual that has a gene that predisposes them to this condition
What is LMP-1
it is a CD40 (inhibitor of apoptosis) that is encoded by EBV
how do you treat mono
steroids if there is a chance of splenic rupture (otherwise just rest)

there are no antivirals against EBV
what is a sign of EBV activation in HIV patients
oral hairy leukoplakia
what types of cancer can EBV lead to
burketts lymphoma
nasopharyngeal carcinoma
lymphoproliferative syndrome
Hodgkin's disease
T cell and NK cell cutaneous lymphoma
(this effect is from the apoptosis suppression)
aspects of hodgkin's disease
originating in B cells (EBV prevents apoptosis)
associated with mixed polarity
How is CMV transferred
via body fluids (mainly urine)
what are the consequences of CMV infection
it is usually asymptomatic except in immunocompromised people and fetuses whose mother become infected during pregnancy (common with second child because first child will bring the virus home from daycare). It remains latent for life
why is CMV called cytomegalovirus
large cytoplasmic inclusions
Why is CMV common in tranplant patients
If the donor or recipient is infected with CMV, the immunosuppressents willl allow it to spread throughout the body and cause disease
How is IM caused by CMV differentiated from IM caused by EBV
atypical IM patients don't have a sore throat and they give a negative monospot test
what are the symptoms of CMV infection in immunosuppressed individuals
IM
retinitis
pneumonia
neurological disorders
what are the symptoms of CMV infection in fetuses
wasting and death because oxygen can't be delivered to the fetus

if a baby aquires the disease shortly after birth, it is relatively benign
what is used to treat CMV
gancyclovir

gancyclovir pump can be inserted into the eye for retinitis
how is CMV diagnosis made
CMV shell viral culture (white blood cells are cultured overnight and centrafuged to release anigens, which are detected with monoclonal antibodies)

also you could just look for the inclusions
What is HHV-6 associated with
Rosela infantum (maculopapular rash with central distribution but only when it infects babies)
where does VZV remain latent
in the sensory ganglia of the head and trunk
what treatments are there for VZV
zoster immune globulin and a live attenuated vaccine
what are the presentation of lesions caused by VZV
they are concentrated on the trunk and are at all stages of development

(smallpox has lesions on the extremities at all stages)
are fetuses at risk for VZV infection
yes, if the mother gets a primary infection during pregnancy

VZV immunoglobulin should be given to protect the fetus
What type of cancer is HHV-8 associated with
Kaposi's sarcoma
who is at highest risk for Kaposi's sarcoma
patients that got AIDS from MSM (male sex with male)

it is endemic to western europe and equitorial africa (because it can be spread by the oral route)
what are characteristics of kaposi's sarcoma
purple appearance (due to stimulation of blood vessel formation by VEGF)
Mixed cell polarity