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Micro (virology) > Herpes > Flashcards

Herpes Flashcards

1
Q

Pathogenesis of VZV

A

infection, incubation, replication, spread and reactivation/ secondary infection

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2
Q

what happens after primary infection of VZV?

A
  • Virus remain latent in dorsal root gangly
  • later in life, after 60, virus is reactivated and risk increases with age.
  • onset of shingle more common AND severe in immunocompromised
  • VZV vaccine available for 50+ y/o to prevent shingle
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3
Q

According to the CDC, what precautionary measures should you take to prevent spreadingVZV?

A
  • Keep rash covered
  • don’t touch or scratch
  • Frequent hand washing
  • until rash develops crust, avoid contact with pregnant women you have never had chicken pox or varicella vaccine, premature or low birth weight babies, and/or immunocompromised patients
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4
Q

CMV

infection

A

Infection is usually through mom to fetus or newborn. also get via sex in adulthood.
usually only a problem for immunosuppressed or very young

neonate contract by transplacental transmission, intrauterine, and/or cervical secretions

baby/child contracts by breast milk, saliva, tears, and/or urine

adult contracts by sexual transmission (semen), blood transaction, or bone graft

causes mental retardation, deafness, neuropathy, pneumonia, retinitis and microcephaly

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5
Q

CMV

A

cytomegalovirus (HSV-5).
most are infected by middle adulthood
primary infection can result in mono like symptoms
may account for 1/5 of “mono” cases
most common viral congenital infection
4000/yr show symptoms of in utero infection

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6
Q

CMV latency

A

Established latent infection in many cells, including immune cells- lymphocytes and macrophages.

Virus can be shed in saliva due to chronic replication in salivary glands, for month and even up to 2 years after acute infection

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7
Q

CMV and the immune system

A

CMV is held in check by our immune system unless there is immunosuppression.
i.e. HIV infection- CMV is the leading cause of death
People on immunosuppressant and receiving organ transplants

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8
Q

EBV

A

Epstein Barr (HSV-4)
causes most infection cases of mono (79%)
common infection worldwide
frequently seen in high school and college students
“kissing disease”
most people become infected at some point in life
in developing areas in Africa, EBV infection is associated with Burkett’s lymphoma and nasopharyngeal carcinoma

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9
Q

what is infected in EBV?

A

infection of anti-body producing B cells and makes them hyperproliferate
the infected cells will produce IgM which is detected in the blood (heterophiles lab)

elicit T cell responses that are against the B cells. this causes spleen inflammation and fatigue

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10
Q

Mononucleosis symtoms

A

Caused by an aggressive T cell response due to the infection and hyper proliferation of the infected B cells

  • sore throat
  • fever
  • swollen lymph glands
  • malaise
  • sometimes an enlarged spleen or liver
  • heart problems (rare)
  • CNS problems (rare)

symptoms usually resolve within 1-2 months

remains latent in the throat and blood for the rest of a person’s life

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11
Q

Diagnosis of EBV

A

patient feels like they have mono
elevated mononuclear WBC count
Heterophiles Ab test: the antibodies that bind non-EBV antigens but are induced by EBV infection.
Staining of cells for viral antigens.

N.B. if a patient has hairy leukoplakia, there is a loss of cytotoxic T cell responses to EBV which leads to a viral re-emergence

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12
Q

Differential Diagnosis between EBV and CMV

A

CMV is a heterophile negative cause of infectious mono that is most likely confused with EBV infectious mono but usually not accompanied by posterior cervical adenopathy

the CMV infection mono is characterized by its prolonged course of prominent liver involvement.

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13
Q

HHV-6

A

spread by saliva
present in nearly everyone by adulthood
associated with various neurological problems like MS
possible molecular mimicry of myelin basic protein may stimulate T cell responses that destroy neuron function

Roseola/Exanthema subitum (aka 6th disease) is a rash condition usually occurring in children. Roseola also seen in HHV-7

seems to be linked to Alzheimer’s and infertility

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14
Q

HHV-8

A

aka Kaposi’s sarcoma associated herpesvirus (KSHV)

causes Kaposi’s sarkoms in people with AIDS
most likely requires immunosuppression

inactivates Rb

HIV Tat protein contributes to development of KS

Formerly a rare cancer found almost exclusively in Mediterranean and sub-Saharan men

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15
Q 
HSV-1
HSV-2
VZV
EBV
(H)CMV
HHV-6
HHV-7
HHV-8
A 
herpes simplex virus 1
herpes simplex virus 2
varicella zoster virus
Epstein-Barr Virus
human cytomegalovirus
Human herpes virus 6
human herpes virus 7
human herpes virus 8 aka Kaposi's Sarcoma virus
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16
Q

how does the herpetic lesion spread?

A

“creep or crawl”

got it’s names from the way it spreads

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17
Q

how long has herpes virus been around

A

centuries

one of the most common viruses found in humans

18
Q

Herpes infection

A

once an individual has become infected it will remain in the body FOR LIFE

it isn’t always active- it can establish a latent state in an immunocompetent host

19
Q

herpes structure

A 
enveloped
icosohedral capsid/ nucleocapsid
dsDNA linear (125-230 kb)
pleomorphic
tegument
20
Q

Tegument

A

in herpes, the tegument is between the envelope and capsid. it contains viral protein that assist viral replication

21
Q

herpesvirus replication

A

infect non-replicating cells like neurons
it will replicate in the cell’s nucleus

transcription of viral genome by cellular DNA-dependent RNA polymerase

regulated by viral-encoded and cellular nuclear factors

this interplay will determine is the virus is active or latent

encode their own DNA polymerase and thymidine kinase

22
Q

what happens when infection is symptomatic?

A

HSV and VZV replicate in a lytic manner. that is, the cells die and then skin lesions form

23
Q

what happens when the infection is latent?

A

it is in specific cells types
only a small number of viral genes are expressed

it can then be reactivated

in latency, the immune system cannot see the virus if noRNA or proteins are being made

24
Q

what happens when the virus is reactivated

A

reactivation and visions made

lytic replication results with attendant symptoms

25
Q

what is thymidine kinase

A

it is encoded by herpes (along with their own DNA polymerase)
TK will increase nucleotide levels in cells
TK assists in the replication of viral genome in non-replicating cells such as neurons
the target of antiviral drugs

26
Q

how is it spread?

A

via cell to cell contact

evades antibodies

27
Q

what is the immune response that herpes illicit

A

T cell responses are primarily responsible for resolving initial infection
Antibodies can protect form acquiring infection (VZV vaccine)
The course of disease is often very different in the immune compromised

28
Q

HSV-1 vs HSV-2

A

have similar structures and replication
have about 80 genes

primary infection by mucosa to mucosa contact
childbirth (HSV-2)

subclinical infection is frequent

recurrent disease

preference for the mouth, pharynx and genitals

both cause latent infections

HSV-1 reactivation occurs most frequently above the waits and HSV-2 below the waist.
Lesions of HSV-1 and 2 look similar

29
Q

where does HSV-1 and 2 replicate

A

1 at the trigeminal ganglia

2 at the sacral ganglia

30
Q

HSV disease mechanism

A

initiation of infection by direct contact between mucosal surfaces. cell to cell spread allows for antibody neutralization

replication causes cytopathic effects on the epithelial cells this forms a syncytia

the cell-mediated immunopathological effects contribute to symptoms

HSV established latency in neurons

31
Q

syncytia

A

fusion between infected and uninfected cells

32
Q

HSV reactivation and triggers

A

from a latent state by various factors

cell mediated immunity is required for resolution of symptoms with a limited role for antibody

-stress, fatigue
-temperature changes
-UV light/sun
=menstruation
-immunosuppression

33
Q

-Herpes Labialis

A
  • cold sores, most common recurrent HSV infection
    Patches of localized vesicles, muccocutaneous junction around the mouth. Painful, annoying, resolve, reappear at the same time

dentists are at risk: lesions in patents not always evident
Virus in saliva of 5% and 2% in adults

34
Q

-Encephalitis

A
  • if virus gets to CNA (very rare and deadly)
35
Q

-Keratoconjunctiva

A

-ocular herpes: affinity for corneal tissue, painful ulcer, recurrences may lead to blindness, immunocompromised susceptible (esp HIV+)

36
Q

-Herpes gladiastorum

A

-found in wrestlers and other engaged in contact sports

37
Q

-Eczema herpeticum

A

-generalized cutaneous infection of a person with eczema- numerous skin vesicles

38
Q

Prevention and treatment of HSV infection

A

prevention- no vaccine: no specific form of prevention. avoid contact with lesions: oral and genital

treatment: acyclovir
ACV is also used for shingles

39
Q

Acyclovir

A

nucleoside (guanosine)analog
converted to acyclo-GMP by viral thymidine kinase
Then converted to acyclovir GTP by cellular kinase. Then incorporated into viral genome and DNA synthesizes stopped because new nucleotides cannot be added (chain termination)

40
Q

lab diagnostic tests

A

Tzank smear: scrape skin off lesion
looking for syncytial cells= giant cells that are multinuclearted, swollen cytoplasm intranuclear bodies
Viral antigen assays test antibody reactivity
PCR for viral nucleic acid provides definitive diagnosis

41
Q

HSV-2

A

Virus can be shed even during asymptomatic periods
practice safe sex
cycler can reduce transmission
pregnant women with active HSV-2 disease is life threatening in children
the cellular immune system is underdeveloped in children
50% mortality
45% of the rest have cognitive impairment

Micro (virology) (7 decks)

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