Herpes Flashcards
describe the structure of a herpes virus
DNA, double strand, enveloped, icos
describe the herpes life cycle
adsorption and fusion w/ host
nucleocapsid releases viral DNA into nucleus
DNA becomes circular
mRNA, viral protein synthesis inside nucleus
progeny nucleocapsids assemble in nucleus causing inclusion bodies
viral glycoproteins are inserted into membrane (can cause syncitia)
progeny bud out from membrane
**needs nucleus
describe how herpes is eliminated from the body
herpes is not eliminated from the body, even upon asymptomatic recovery. instead, herpes becomes latent. even in asymptomatic latency, pts may sporadically create infectious virions
describe the subclassifications of herpes virus and some examples
alphaherpesvirus- HSV1- wide host range, latency in neurons
betaherpesvirus- CMV- narrow host range, latency in monocytes
gammaherpesvirus- EBV- narrow host range, latency in B lymphocytes
latency
all herpes viruses can become latent:
non destructive
lifelong
persistence of viral genome in non infectious state
potential to be reactivated
is latency active or static?
active-
creating gene products that prevent apoptosis, but opens the virus to immune recognition
also have asymptomatic shedding
why could herpes be good for you?
chronic stimulation of immunity by non-lethal pathogens could be beneficial
HSV1- primary and recurrent infection mechanisms
“cold sores”
primary infection often subclinical and most commonly causes stomatitis
virions produced at the site of initial infection travel up sensory neurons to nearest ganglion (often trigeminal ganglia) and establish latent infection
recurrent infection occurs when viral multiplication resumes and virions are tranported down axons to cutaneous site of primary infection- results in cold sores
what % of the population has HSV1?
> 80%
what is the incubation period for HSV 1
1-2 weeks
what factors can aggravate latency, causing a recurrent infection?
UV light
fever
emotion
HSV1 vaccine
none
HSV2
“genital herpes”
primary infection of genital mucosa, virus follows sensory neurons back to ganglia and establishes latency (sacral ganglia)
HSV2 incubation period
1-2 weeks
what % of the population has HSV2?
20%
describe the complications of HSV2 and perinatal infection
virions released by vaginal secretions can cause systemic disease in newborns ~6 days after birth
disease is often fatal, with destruction of liver and adrenal
most dangerous scenario is when mother has just gotten primary infection and has no Ab
HSV2 shedding before deliver is indication for C-section
HSV1 and 2 also cause what in addition to skin lesions
encephalitis
ocular disease
herpes simplex encephalitis
most common cause of sporadic encephalitis- usually HSV1
causes high fever, confusion, lymphocytes in CSF, lesions on MRI
often death w/o early recognition
treatment for herpes simplex encephalitis
acyclovir
herpes simplex keratitis
herpes simplex infection of eye
unilateral red eye
can cause blindness if untreated
does herpes simplex cross placenta
no
how do you diagnose herpes simplex?
isolation and culture
ELISA
DNA PCR of CSF
serology (IgM in primary infection)
HSV2 vaccine
none
what are the treatments for herpes simplex
acyclovir- gold standard
herpes thymidine kinase will phosphorylate ACV, which can then be subsequently be phosphorylated by host and incorporated into DNA, which halts synthesis and causes death in infected cells
varicella zoster virus
chickenpox/shingles
primary infection causes chickenpox- infection through respiratory tract- causes viremia. then spreads to the skin and
causes small itchy vesicles (rash) and fever. then travels retrograde to sensory neurons
often fatal to immunosuppressed
varicella zoster virus transmission
aerosol
spread from mucosa in skin lesions to the respiratory tract. vesicles in respiratory tract may also rupture and spread disease
treatment for varicella zoster virus
can get IgG- VZIG
or
acyclovir
congenital varicella syndrome
fetal infection from a pregnant mother
causes limb atrophy and scarring of the skin
zoster
shingles- more common w/ age
reactivation in a sensory ganglia that results in pain distributed along a specific dermatome, followed by lesions
can be followed by post-herpetic neuralgia- residual pain
more
zoster treatment
acyclovir
vaccinations to varicella zoster virus
vaccines to both varicella (live attenuated, requires boosting) and zoster
CMV
causes enlarged cells w/ “owl eye” inclusion bodies
causes retinits, colitis, heterophile negative mono
leading cause of congenital abnormalities- from infection in 1st trimester- can go through placenta
CMV immune evasion
has 6 genes to evade T cell activation via disrupting antigen presentation
CMV transmission
blood/ bodily secretions (urine)
CMV infects what
epithelia- moves to ganglia- infects monocytes
easiest way to test for CMV in neonates
CMV in urine
CMV vaccine
none
CMV treatment
ganciclovir or foscarnet
CMV findings in newborns
retinal inflammation jaundice large spleen and liver low weight mineral deposits in brain rash seizures small head retardation deafness
EBV
causes heterophile positive mono and cancer
subclinical infections in kids, but more prevalent post puberty
1st symptom is sore throat
also: fever, sore throat, lethargy
EBV transmission
salvia or oral contact
seen in college aged people
infects mucosal epithelia before spreading to B lymphocytes. can become latent w/ these b lymphocytes
seen in people post puberty
EBV vaccine
none
EBV incubation period
2-4 weeks
% of population with EBV
90%
describe the immune response to EBV
CTLs develop to clear infected B cells, causing abnormal cellular phenotype in blood
develop Abs that cross react w/ sheep RBCs, creating a diagnostic test
diagnostic tests for EBV
look for CTLs or test for agglutination with sheep RBCs
Ig to viral capsid
EBV treatment
no treatment
HHV6
most prevalent herpes virus > 90%
genome can integrate w/ human genome and becomes heritable
causes: roseola infantum and exanthm subitum (rashes) w/ high fever
HHV7
causes infections but w/o symptoms
HHV8
Kaposis Herpesvirus
not seen in 1980s b/c of AIDS.
common in sexually transmitted HIV
forms spindle epidermal cells
also in GI and lungs
rarely seen in US b/c of antivirals
tumor virus
HHV8 treatments or vaccines
none
B virus
infection of rhesus macaques (benign in monkeys, not in humans)
very rare- seen in people who work in animal facilities
caueses encephalitis, serious neurological squelae, and death
B virus treatment
acyclovir
triflurodine
useful in treating keratitis simplex infections
causes nucleotide form of triflurodine to be incorporated into DNA and to halt DNA synthesis.
cells in cornea replicate slowly enough that only infected cells will die off
adenine arabinoside
analogue of deoxyadenosine that gets phosphorylated by host enzymes an incorporated into DNA, halting DNA synthesis
foscarnet
inhibits DNA polymerase of herpes virus selectively
alternative to ganciclovir in CMV
