17. Herpesvirus 1 Flashcards by Zara Jalil

when did publications about herpesvirus start to increase?

1960s

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what type of genome does herpesvirus have? size?

dsDNA –> 125,000-229,000 bp

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shape of herpesvirus capsid?

icosahedral

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is herpesvirus enveloped or naked?

enveloped

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where does herpesvirus envelope come from?

come from nuclear membrane from budding

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how many capsomeres are there?

162

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what surrounds the capsid?

tegument

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is herpesvirus a complex virus?

yes –> over 100 transcripts and over 70 ORFs

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all human herpesviruses have identical ___________

all human herpesviruses have identical EM morphology

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are herpesviruses ubiquitous or rare?

ubiquitous –> infect a majority of all humans

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can herpesviruses be latent?

yes, ALL remain latent lifelong and may reactivate

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8 human herpesviruses:

HSV1 (HHV1)
HSV2 (HHV2)
Varicella-zoster virus (HHV3)
EBV (HHV4)
Cytomegalovirus (CMV, HHV5)
HHV6
HHV7
Kaposi sarcoma-associated virus (KSHV, HHV8)

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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

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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

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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

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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

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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

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what type of people are infected with cytomegalovirus/HHV5?

immunocompromised people
(ex. AIDS patients)

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what 2 type of disease does cytomegalovirus cause in immunocompromised ppl?

hematologic disease and solid organ cancer

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4 locations of CMV infections in immunocompromised ppl

Brain –> encephalitis
Eye –> retinitis
Lung –> pneumonia
Stomach/intestines –> gastroenteritis

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treatment for CMV infection? and most common type

treat with biologic modifying infections, most commonly Mab

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downside of Mab?

all have complications –> relative immunosuppression, infections, etc.

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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

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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

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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?

1. concurrent infection, fever 2. 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

1. Varicella --> chicken pox 2. 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:

1. returnees from subsaharan africa 2. non-vaccinated children 3. non-vaccinated adults 4. farm workers

describe the 6 types of spinal nerves

1. 12 pairs cranial nerves 2. 8 pairs cervical nerves 3. 12 pairs thoracic nerves 4. 5 pairs sacral nerves 5. 5 pairs lumbar nerves 6. 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)

1. urine 2. saliva 3. WBC 4. semen/vaginal secretions 5. breast milk 6. CSF 7. 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?

1. fever 2. hepatitis 3. pneumonia

what 4 symptoms of CMV are common in AIDS patients?

1. retinitis 2. pneumonia 3. esophagitis 4. 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!