EBV - Beatty

Question 1

Left side is positive for what?

Answer 1

EBV - Monospot test (Heterphil test)

Question 2

A patient comes to your clinic with tender lymph nodes, a fever of 102 F, enlarged tonsils, and a dull sound over the Traube’s space and lymphocytosis. Under a microscope, you see atypical lymphocytes that is indented by surrounding RBC’s (looks like a skirt).

What test would you do next?

What would you expect to see?

Answer 2

Patient may have mononucleosis from EBV. Do a heterphil test (monospot).

The left one is positive – red agglutination on a blue backround show presence of infectious mononucleosis heterphile antibodies.

Question 3

In infectious mononucleosis, patients develop an antibody called ___ antibodies. These antibodies are not specific for EBV, but attach to sheet and horse ___s. The test shows the ability of the patients serum to ___ to the horse RBC. What would clumping mean?

Answer 3

Clumping means a posititve monospot test.

Question 4

There are many false negatives in a monospot test. What would do you do if you still believe someone has mono?

What would you expect to see?

Answer 4

You can do a serological test to test for different antibodies.

In acute phase infectious mononucleosis, you can do an a IgM antibody test to measure the presence of viral capdi antigens of EBV (IgM-VCA).

Question 5

VCA-IgM = IgM antibody to viral capsid antigen (__ acute, __ past)

VCA-IgG = IgG antibody to viral capsid antigen (__ acute, ___ past)

EA = Antibody to the EBV early antigen (__ acute, __ past)

EBNA = Antibody to EBV nuclear antigen (__ acute, __ past)

Answer 5

VCA-IgM = IgM antibody to viral capsid antigen (+ acute, - past)

VCA-IgG = IgG antibody to viral capsid antigen (+ acute, - past)

EA = Antibody to the EBV early antigen (+/- acute, - past)

EBNA = Antibody to EBV nuclear antigen (- acute, + past)

Question 6

EBV induces a proliferation of __ in lymphoid tissue. When EBV infects these, they become transformed ___. They become large atypical cells with prominant ___ resembling malignant ___.

EBV ONLY INFECTS _____!!!

Answer 6

EBV induces a proliferation of LYMPHOCYTES in lymphoid tissue. When EBV infects these, they become transformed LYMPHOCYTES. They become large atypical cells with prominant NUCLEOLI resembling malignant LYMPHOCYTES.

EBV ONLY INFECTS B CELLS!!!

Question 7

EBV is a type of HHV-___

Answer 7

4

Question 8

EBV is transmitted by human contact, and frequently by kissing. It is ubiquitous and infects >__% people by age 25.

Answer 8

95%

Question 9

Pathogenesis of EBV:

Initially, it affects the ___ epithelial cells, then spreads to underlying __ tissue (___ and __, where mature __ cells are infected.

EBV binds to the ___ B cell receptor, normally used for the ___ component of complemenet.

Answer 9

Pathogenesis of EBV:

Initially, it affects the oropharyngeal epithelial cells, then spreads to underlying lymphoid tissue (tonsils and adenoids, where mature B cells are infected.

EBV binds to the CD21 B cell receptor, normally used for the c3d component of complement.

Question 10

Infection of B cells may take 1 of 2 forms:

1. ____ - minority of B cells infected lead to viral replication and eventual cell lysis accompanied by release of virions, which may infect other B cells.
2. ____ - majority of B cells during which the virus persists as an extrachromosomal episome.

Answer 10

Infection of B cells may take 1 of 2 forms:

1. Lytic - minority of B cells infected lead to viral replication and eventual cell lysis accompanied by release of virions, which may infect other B cells.
2. Latent - majority of B cells during which the virus persists as an extrachromosomal episome.

Question 11

People who lack B cells like in _____ disease, don’t have get infections of EBV.

Answer 11

X linked Agammaglobulinemia

Question 12

Pathogenesis of EBV latentcy stage:

1. EBNA (ebstein-barr nuclear antigens 1,2) - binds the EBV genome to the host cell chromosome during ___. This inserts viral episomes in every daughter cell when infected cells divide.
2. Latent membrane protein (LMP-1) - drives __ cell activation. Mimics ___, a B cell receptor. Binds TNF receptor associated factors (TRAFs). LMP prevents apoptosis by activating ___.
3. Homologue of IL-10, vIL-10 - ____ cell-mediated responses and inhibits ___, and ___ cells and supresses anti-viral T cell response.

Answer 12

Pathogenesis of EBV latentcy stage:

1. EBNA (ebstein-barr nuclear antigens 1,2) - binds the EBV genome to the host cell chromosome during mitosis. This inserts viral episomes in every daughter cell when infected cells divide.
2. Latent membrane protein (LMP-1) - drives B cell activation. Mimics CD40, a B cell receptor. LMP prevents apoptosis by activating Bcl-2 (anti-apoptosis).
3. Homologue of IL-10, vIL-10 - Supresses cell-mediated responses and inhibits macophages, and dendritic cells and supresses anti-viral T cell response.

Question 13

EBV promotes __ cell proliferation, drives __ cell activation and prevents ___. It does this because it is living inside of _ cells, but on the other hand, it does not want to be killed by T cells, so it suppresses T cells. During latency phase, B cells divide and all __ cells will have EBV genome.

Answer 13

EBV promotes B cell proliferation, drives B cell activation and prevents apoptosis (via Bcl-2). It does this because it is living inside of B cells, but on the other hand, it does not want to be killed by T cells, so it suppresses T cells. During latency phase, B cells divide and all daughter cells will have EBV genome.

Question 14

Ineffective __ cell response leads to uncontrolled __ cell proliferation and called __ cell malignancies!

Answer 14

Ineffective T cell response leads to uncontrolled B cell proliferation and called B cell malignancies!

Question 15

Clinical findings of EBV in:

1. early childhood?
2. children, adolescents, and young adults?

Answer 15

Clinical findings of EBV in:

1. early childhood –> often asymptomatic
2. children, adolescents, and young adults –> fever, malaise, cervical lymphadenopathy, SPLENOMEGALY, and in rare occasion splenic rupture, myocartidis, pericarditis, mild hepatitis.

Question 16

What type of lymphocytes would you expect to see in a person infected with EBV?

Answer 16

Atypical lymphocytes that look like skirts.

Question 17

Hemotologic findings in EBV:

one of the key features is absolute ___.

Answer 17

Absolute lymphocytosis > 4.0 x 103 mL (Range 10-30 x 103 mL)

Question 18

Patients with EBV tend to have enlarged ___. On a stain, EBV looks ___.

Answer 18

lymphnodes/tonsils

black

Question 19

IM Diagnosis in increasing order of specificity:

•Increasing order of specificity:

1.Atypical _____

•Characteristic ___ lymphocytes in the peripheral blood

2. Positive _____ antibody reaction
3. Rising titer of specific antibodies for EBV antigens

• ____
• ___
• ____

Answer 19

•Increasing order of specificity:

1.Atypical lymphocytosis

•Characteristic atypical lymphocytes in the peripheral blood

2. Positive heterophile antibody reaction
3. Rising titer of specific antibodies for EBV antigens

• Viral capsid antigens (VCA)
• Early antigens (EA)
• Epstein-Barr nuclear antigen (EBNA)

Question 20

HSV 1 + 2 - latency infection

Entry of site? ___ or ___

Causes: ___ ___ lesions

Establishes infections in innervated __ ___.

Replicates where? __ and __ membranes

Clinical presentations of;
HSV-1? ___, ___

HSV 2? ___ herpes

Reactivation may occur repeadetly with or without symptoms.

Answer 20

HSV 1 + 2 - latency infection

Entry of site? oropharynx or genitals

Causes: epidermal vesicular lesions

Establishes infections in innervated sensory neurons.

Replicates where? skin and mucus membranes

Clinical presentations of;
HSV-1? gingivostomatitis, corneal keratitis (blindess)

HSV 2? genital herpes

Reactivation may occur repeadetly with or without symptoms.

Question 21

VZV

Transmitted by ___ aerosols, disseminates ____, causing widepread ___ or localized ____ and epidermal blisters (aka ___). Evades IR and establishs latency in __ ___.

Acute infection - __ __

Reactivation (shingles - herpes zoster)

Answer 21

VZV

Transmitted by respiratory aerosols, disseminates hematogenously, causing widepread POX or localized epidermal blisters (aka shingles). Evades IR and establishs latency in sensory ganglia.

Acute infection - chicken pox, intraepithelial vesicles with intranuclear inclusions

Reactivation (shingles - herpes zoster)

Question 22

___

___ infected cells enhibit ____ of entire cell and nucleus. Typically contains a large inclusion surrounded by a clear halo (OWL’S EYES).

Latently, infects ___ and their bone marrow progenitors.

Reactivated when IS is compromised.

Evades IS by down-modulating MHC I and II molecules

Question 23

Acute transient infections elivist effective immune responses that eliminate the pathogens, limiting the duration of infection. They do/do not go into latency phases.

An example is ___.

Answer 23

Measles

Question 24

Measles are characterized by what kind of cells?

What do they look like and where are the found?

How are measles confirmed?

Answer 24

Warthin-Finkley giant multinucleared cells. They are a grape-like cluster of nuclei found in hyperplastic lymph nodes –> particularly in LUNGS.

Confirmation of measles of rash, WFMC and Koplik spots.

Question 25

Koplik spots are ulcerations found in the ___ __ and are typically seen in __

Answer 25

Koplik spots are ulcerated mucosal lesions in the oral cavity and found in MEASLES

Question 26

What are three examples of an ATVL (Acute Transiet Viral Infection)?

Answer 26

Measles

Mumps

Polio

Question 27

Mumps:

Transmission through ___ ____

Pathogenesis: spreads to local lymphoid tissues, repliacte in activated ___ cells, and spreads through