Herpes Flashcards
Classify the herpesviruses
family: herpesviridae. enveloped. dsDNA icosahedral capsid
How many herpesviruses are there?
8
HSV-1 does what?
cold sores
HSV-2 does what?
genital herpes
VZV
Chickenpox, zoster
EBV
mono, oral hairy leukoplakia, B cell lymphoma, nasopharyngeal carcinoma
CMV
post transplant infections, retinitis
HHV-6
exanthem subitum or roseola infantum
HHV-7
no associated disease
HHV-8
Kaposi’s Sarcoma
What virus and what is herpetic gingivostomatotis
vesicular lesions on the oral mucous memranes that rupture and leave yellowish-gray ulcers or plaques. usually HSV-1
Herpes labialis
cold sores, fever blisters. vesicles at localized sites in the orofacial area that rupturea nd leave shallow ulcers or dry and form a scab.
genital herpes
HSV2. genital vesiceles that rupture forming ulcers in the genital region
neonatal herpes
infection of the newborn during delivery usually HSV2
herpes keratitis
acute necrotizing viral encephalitis usually HSV1
Describe pathogenesis of HSV
HSV is transmitted by direct contact of mucosal surfaces. Virus infects the epithelial cell and spreads causing primary lesion. Virus encounters sensory neuron ending where it binds and enters. It travels up via retrograde transport to the cell body and just hangs out there in a period of latency expressing LAT. Because there is no protein expression, it is not killed by a CTL response. At a later time, it will travel back down the neuron causing reactivation
What is the prevalence of HSV1
70% in the US. 90% in the developing world
What is the prevalence of HSV2
17% in the US. 50-80% in developing countries
Describe pathogenesis of VZV
VZV is inhaled as respiratory aerosols. Virus replicates in epithelial cells, then leads to the regional lymph nodes and infects T cells. Viremia then occurs in the blood. Leading to infection of liver and spleen. Infected mononuclear cells spreads then to the skin and mucousal membranes leading to pocks. Virus spreads to the dorsal root ganglia establishing latency there. Reactivation will then occur again along the dermatome usually on the body trunk.
Describe pathogenesis of EBV
transmitted by saliva. virus infects pharyngeal epithelial cells where it replicates and is shed in throat and saliva. EBV then infects the B cells (esp. those in the tonsils). EBV gene products stimulate proliferation of random B-cells which is why you can detect via monospot.
What drugs do we use to inhibit HSV
Acyclovir
Is there a vaccine for HSV?
No, but there is one in the pipelines
Is there a vaccine for VZV?
Yes
What actually causes the mono sx
T cell response to EBV
Does EBV persist?
Yes. It persists in the B cells in latent form
What are the sx of mono?
- enlarged lymph nodes
- sore throat
- fatigue
What are the lab results for mono?
heterophile antibodies react to antigens from animal RBC’s and thus agglutinate
What is a bad outcome of EBV infection?
enlarged spleen and potential rupture
What can happen long-term with EBV?
cancer
How is CMV spread?
ubiquitous virus that usually leads to asymptomatic sx, CMV is established from mother to child congenitally (transplacetally). Can also be with breast milk
HHV-6 does what?
Childhood disease that causes exanthum roseola, fever and rash. Can come back with bone marrow transplant recipients
What does HHV-8 do?
Kaposis Sarcoma which creates complex angioproliferative and inflammatory lesions.
how does acyclovir work?
It is a nucleoside analog which is incorporated in the DNA, but then lacks a special side chain moiety that prevents chain elongation and blocks viral DNA synthesis
