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42 Cards in this Set
- Front
- Back
where do HSV-1 and HSV-2 remain latent
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HSV-1 in the trigenimal ganglia
HSV-2 in the sacral ganglia |
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why can herpes survive in small populations
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it remains latent in infected individuals for life
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why has there been an increase in type 2 HSV
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individuals with HSV-1 are less susceptible to HSV-2 and there has been a decline in HSV-1
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how does infection onf HSV-1 prevent infection with HSV-2
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they share glycoprotein D (gpD), which is a surface antigen for adhesion
gpG is diff between the 1 and 2 |
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genome of herpes
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linear ds DNA
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What keeps HSV latent
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epigenic DNA methylation
LAT (latency associated transcripts) are RNA that doesn't produce protein but maintains latency (microRNA) |
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how does infection with HSV occur
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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
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how do herpes lesions compare to other genital lesions
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they aren't as deep and remain in superficial layers
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what percent of people remain asymptomatic
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75%
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signs of HSV
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vesicles (crawl like a snake)
flu-like symtomes lymphadenopathy lesions rarely leads to ENCEPHALITIS Bells palsy |
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what is used to treat HSV
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acyclovir
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how does acyclovir work
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it is activated by phosphorylation by a herpes encoded thymidine kinase and inhibits the viral DNA polymerase
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what type of cancer is associated with EBV
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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 |
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what test is used to detect EBV
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monospot test (measures heterophil antibodies)
(also used for glandular fever) |
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How are antibodies to VCA and EBNA helpful in diagnosis of EBV
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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 |
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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 |
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How is EBV infection diff in children
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there immune system is immature so symptoms won't be apparent
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what are the signs and symptoms of EBV (IM)
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tiredness
enlarged spleen and lymph nodes atypical lymphocytes in blood |
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what is the pathogenesis of EBV
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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 |
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What causes lymphoproliferative disease
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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 |
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What is LMP-1
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it is a CD40 (inhibitor of apoptosis) that is encoded by EBV
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how do you treat mono
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steroids if there is a chance of splenic rupture (otherwise just rest)
there are no antivirals against EBV |
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what is a sign of EBV activation in HIV patients
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oral hairy leukoplakia
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what types of cancer can EBV lead to
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burketts lymphoma
nasopharyngeal carcinoma lymphoproliferative syndrome Hodgkin's disease T cell and NK cell cutaneous lymphoma (this effect is from the apoptosis suppression) |
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aspects of hodgkin's disease
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originating in B cells (EBV prevents apoptosis)
associated with mixed polarity |
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How is CMV transferred
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via body fluids (mainly urine)
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what are the consequences of CMV infection
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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
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why is CMV called cytomegalovirus
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large cytoplasmic inclusions
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Why is CMV common in tranplant patients
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If the donor or recipient is infected with CMV, the immunosuppressents willl allow it to spread throughout the body and cause disease
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How is IM caused by CMV differentiated from IM caused by EBV
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atypical IM patients don't have a sore throat and they give a negative monospot test
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what are the symptoms of CMV infection in immunosuppressed individuals
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IM
retinitis pneumonia neurological disorders |
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what are the symptoms of CMV infection in fetuses
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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 |
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what is used to treat CMV
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gancyclovir
gancyclovir pump can be inserted into the eye for retinitis |
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how is CMV diagnosis made
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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 |
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What is HHV-6 associated with
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Rosela infantum (maculopapular rash with central distribution but only when it infects babies)
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where does VZV remain latent
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in the sensory ganglia of the head and trunk
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what treatments are there for VZV
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zoster immune globulin and a live attenuated vaccine
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what are the presentation of lesions caused by VZV
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they are concentrated on the trunk and are at all stages of development
(smallpox has lesions on the extremities at all stages) |
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are fetuses at risk for VZV infection
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yes, if the mother gets a primary infection during pregnancy
VZV immunoglobulin should be given to protect the fetus |
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What type of cancer is HHV-8 associated with
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Kaposi's sarcoma
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who is at highest risk for Kaposi's sarcoma
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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) |
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what are characteristics of kaposi's sarcoma
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purple appearance (due to stimulation of blood vessel formation by VEGF)
Mixed cell polarity |