17. Herpesvirus 1 Flashcards
when did publications about herpesvirus start to increase?
1960s
what type of genome does herpesvirus have? size?
dsDNA –> 125,000-229,000 bp
shape of herpesvirus capsid?
icosahedral
is herpesvirus enveloped or naked?
enveloped
where does herpesvirus envelope come from?
come from nuclear membrane from budding
how many capsomeres are there?
162
what surrounds the capsid?
tegument
is herpesvirus a complex virus?
yes –> over 100 transcripts and over 70 ORFs
all human herpesviruses have identical ___________
all human herpesviruses have identical EM morphology
are herpesviruses ubiquitous or rare?
ubiquitous –> infect a majority of all humans
can herpesviruses be latent?
yes, ALL remain latent lifelong and may reactivate
8 human herpesviruses:
- HSV1 (HHV1)
- HSV2 (HHV2)
- Varicella-zoster virus (HHV3)
- EBV (HHV4)
- Cytomegalovirus (CMV, HHV5)
- HHV6
- HHV7
- Kaposi sarcoma-associated virus (KSHV, HHV8)
a) What cell does HSV1/HHV1 target?
b) Pathophysiology of HHV1
c) Site of HHV1 latency
d) Means of spread
a) Mucoepithelial cells
b) Oral and/or genital herpes, usually orofacial
c) Latent in neurons
d) Spread by close contact –> oral or sexual
a) What cell does HSV2/HHV2 target?
b) Pathophysiology of HHV2
c) Site of HHV2 latency
d) Means of spread
a) Mucoepithelial cells
b) Oral and/or genital herpes
c) Latent in neurons
d) Spread by close contact –> oral or sexual
a) What cell does Varicella zoster virus/HHV3 target?
b) Pathophysiology of HHV3
c) Site of HHV3 latency
d) Means of spread
a) Mucoepithelial cells
b) Chicken pox, shingles
c) Latent in neurons
d) Spread by respiratory and close contact
a) What cell does EBV/HHV4 target?
b) Pathophysiology of HHV4 (4)
c) Site of HHV4 latency
d) Means of spread (4)
a) B cells/epithelial cells
b) - Infectious mononucleosis
- Burkitt’s lymphoma
- Hodgkin’s lymphoma
- post-transplant lymphoproliferative disease
c) Latent in B cells
d) Spread by:
- close contact
- transfusions
- tissue transplant
- congenital transmission
a) What cell does Cytomegalovirus/HHV5 target?
b) Pathophysiology of HHV5
c) Site of HHV5 latency
d) Means of spread
a) Monocytes and epithelial cells
b) Infectious mononucleosis-like syndrome, retinitis
c) Latent in monocytes
d) Spread by saliva, urine, blood, breast milk
what type of people are infected with cytomegalovirus/HHV5?
immunocompromised people
(ex. AIDS patients)
what 2 type of disease does cytomegalovirus cause in immunocompromised ppl?
hematologic disease and solid organ cancer
4 locations of CMV infections in immunocompromised ppl
- Brain –> encephalitis
- Eye –> retinitis
- Lung –> pneumonia
- Stomach/intestines –> gastroenteritis
treatment for CMV infection? and most common type
treat with biologic modifying infections, most commonly Mab
downside of Mab?
all have complications –> relative immunosuppression, infections, etc.
a) What cell does Roseolovirus/HHV6 target?
b) Pathophysiology of HHV6
c) Site of HHV6 latency
d) Means of spread
a) T cells
b) Sixth disease, Roseola infantum, exanthem subitum
c) Latent in T cells
d) Respiratory, saliva, close contact
a) What cell does Roseolovirus/HHV7 target?
b) Pathophysiology of Roseolovirus/HHV7
c) Site of Roseolovirus/HHV7 latency
d) Means of spread
a) T cells
b) pathophysiology not well-defined
c) latent in T cells
d) unknown means of spread
what type of ppl does roseolovirus typically infect?
immunocompromised ppl
what disease do infants infected with primary roseolovirus infection get? how is it spread?
infants get EXANTHUM SUBITUM –> spread by people’s saliva when they kiss the baby, etc.
a) What cell does Kaposi’s sarcoma-associated herpesvirus/HHV8 target?
b) Pathophysiology of HHV8
c) Site of HHV8 latency
d) Means of spread
a) Lymphocytes
b) Kaposi’s sarcoma, primary cavity lymphoma
c) B cell
d) close contact, saliva
what strength of therapies do patients with KSHV/HHV8 need? why?
need very toxic therapies bc virus can infect internal organs
describe HSV1/HSV2 membrane glycoproteins
HSV1 and HSV2 have serologically distinct membrane glycoproteins
do HSV1/HSV2 cause similar symptoms?
yes, when infecting identical sites
do HSV1/HSV2 have the same epidemiological pattern?
different but converging epidemiological pattern
describe Herpes B virus
found in Macaques and only found in ppl who interact with Macaques –> leads to fatal encephalitis
HSV1 or HSV2 more common in urogenital infection?
HSV2
HSV1 or HSV2 more common in labial infection?
HSV1
HSV1 or HSV2 more common in ocular keratitis?
HSV1
HSV1 or HSV2 more common in Whitlow/Hand infection?
equal
HSV1 or HSV2 more common in encephalitis?
HSV1
HSV1 or HSV2 more common in meningitis?
HSV2
why is HSV2 more common in meningitis?
HSV1 is latent in nerve ganglia and travels to brain along axons, but HSV2 does not have access to brain bc it only travels thru blood
HSV1 or HSV2 more common in neonatal infection? why?
HSV2 –> mothers with genital infection pass it on
HSV1 commonly causes:
HSV1 commonly causes Herpes labialis
HSV2 commonly causes:
HSV2 commonly causes Herpes genitalis
what percent of the population is infected with HSV1/2 by age 5?
30-100%
what is a factor that affects which ppl are infected with HSV1/2?
class –> 30-50% of middle class children get infected while 80-100% of poorer populations get infected
describe primary HSV1/2 infection
usually asymptomatic but may present as SEVERE gingivostomatitis
why are some primary HSV1/2 infections symptomatic but most are asymptomatic?
everyone has different immune systems that work differently
how long is HSV1/2 incubation period?
2-12 days (i.e. time from infection to symptoms)
what can happen at the same time as primary HSV1/2 infection?
eye, hand, or other sites can be infected de novo or auto-innoculation
describe primary HSV1/2 infection in ppl who are not immunocompromised
usually no serious symptoms and treatment is optional
where does HSV1/2 sit latent?
sensory ganglia
where does recurrent HSV1/2 infection occur?
in same site as primary infection
what causes recurrent HSV1/2 infection?
- concurrent infection, fever
- stress, menses, exposure to UV light
describe asymptomatic recurrent HSV1/2 infection
small quantities of HSV1/2 can periodically be shed asymptomatically
do asymptomatic men or women spread virus more?
asymptomatic women spread the virus more bc lesions less visible
describe herpes infantum
how do we prevent this?
infected at birth from mother with latent genital herpes
- baby develops herpes encephalitis with herpes all over the skin
- pregnant person is continually checked for herpes if previously had herpes and treated with antiviral
describe whitlow
scratch herpes lesions –> get infection on finger
are STDs caught on public toilets? why?
NO
herpes is enveloped so it is very fragile
- envelope disintegrates in non-aqueous state
- virus need body temp to survive
2 types of VZV
- Varicella –> chicken pox
- Zoster –> shingles
describe varicella/chicken pox
PRIMARY infection throughout body
describe zoster/shingles
LOCAL recurrence of latent infection
does primary infection cause immunity?
yes there is absolute immunity to reinfection
how does shingles occur if primary infection causes immunity?
immune to NEW infection but virus can sit latent in sensory ganglia and reactivate
difference in distribution of chicken pox and HSV1/2 lesions
chicken pox mainly on trunk, head, and fewer lesions on extremities
chicken pox in children vs adults vs pregnant ppl
more vicious infection in adults –> more symptoms + more lesions
in pregnant ppl can cause viral pneumonia
difference in distribution of chickenpox and smallpox lesions
smallpox mainly extremities and head, chicken pox mainly torso and head
4 types of ppl that varicella/chicken pox usually occurs in:
- returnees from subsaharan africa
- non-vaccinated children
- non-vaccinated adults
- farm workers
describe the 6 types of spinal nerves
- 12 pairs cranial nerves
- 8 pairs cervical nerves
- 12 pairs thoracic nerves
- 5 pairs sacral nerves
- 5 pairs lumbar nerves
- 1 pair coccygeal nerves
how does shingles latency occur relative to nerves?
occurs unilateral of various nerves
describe shingles at trigeminal nerve + what is trigeminal nerve
trigeminal nerve = cranial nerve that is the main sensory nerve
lesions at one of 3 branches (V1, V2, V3)
how can you diagnose shingles that has very few lesions?
by culturing virus
chicken pox vaccine name?
zostavax
shingles vaccine name?
shingrix
describe CMV infection
very common but inapparent
Canadian city with highest rate of CMV?
Montreal –> 74%
city with highest rate of CMV?
Burkina Faso –> 99.5%
how many infants infected with CMV?
30-50% of infants infected during 1st year of life
how do infants get infected with CMV?
VERTICAL TRANSMISSION - intrauterine and neonatal
bc CMV present in maternal blood and breast milk
how many ppl at reproductive age get infected with CMV?
20-50% infected during 2nd and 3rd decades of life
where is CMV present in ppl of reproductive age?
in saliva and genital secretions
where do ppl asymptomatic for CMV have infectious virus? (7)
- urine
- saliva
- WBC
- semen/vaginal secretions
- breast milk
- CSF
- tissue
why is CMV found in many tissues despite having serum antibodies?
serum antibodies don’t prevent it from replication
who does SYMPTOMATIC CMV infect?
immunocompromised ppl
is symptomatic cmv new infection or reactivation of virus?
can be either!
what 3 symptoms of CMV are common in transplant patients?
- fever
- hepatitis
- pneumonia
what 4 symptoms of CMV are common in AIDS patients?
- retinitis
- pneumonia
- esophagitis
- disseminated infection
what is the fovea?
what is the optic disk?
fovea –> highest concentration of retinal cells
optic disk –> where optic nerve enters retina from brain
what does a pale area in the retina indicate?
retinal necrosis from CMV
how many ppl in North America carry EBV by age 5?
by age 30?
50%
90-95%
proportion of oropharyngeal shedding of virus in seropositive healthy adults?
10-25%
proportion of oropharyngeal shedding of virus in recent transplant recipients?
50-75%
proportion of oropharyngeal shedding of virus in acute infectious mononucleosis?
50-100%
proportion of oropharyngeal shedding of virus in acute leukemia/AIDS?
85-100%
what happens to the mouth with Mono
uvula is engorged, tonsils increased, inflammation everywhere!
describe lymphocytes found in Mono
big and floppy and can get indented by RBCs
what happens to spleen with mono?
can increase in size, can split open and hemorrhage
why should you not engage in contact sports for at 3m after infection?
the main cause of death is hemorrhage!
