Micro 6 Ex 2

Front 1

Varicellar-Zoster Virus (VZV) genome

Back 1

A double stranded DNA virus of 125 Kb, with 69 genes

Front 2

Varicellar-Zoster Virus (VZV) is responsible for 2 diseases

Back 2

(chickenpox)-moreprevalent and zoster (shingles)

VZV transmits through respiratory secretions, and disseminates via lymphatics and bloodstream

Front 3

Varicellar-Zoster Virus has 2 stages

Back 3

lytic and latent

Front 4

varicella (chickenpox) occurs mostly before

Back 4

90% cases occur before age of 10.
Vesicular rash appears on the face, neck and trunk.
A vaccine is available to prevent chickenpox.

Front 5

Reactivation of the latent virus in ganglia results

Back 5

in zoster.
It occurs in adults previously infected with VZV.
Vesicular eruptions in skin over affected nerves.
Lesions last for two weeks, but pain may persist for longer period.

Front 6

Varicellar-Zoster Virus diagnosed?

Back 6

Cytplogy, cell culture and immnuno-assays.

Front 7

Whats the Varicellar-Zoster tx?

Back 7

Acyclovir, famciclovir, valacylcovir, and immunoglobin

Front 8

Varicellar-Zoster prevention

Back 8

A live attenuated vaccine has been proved. 70-90% effective in normal children.

Front 9

Cytomegalovirus
genome

Back 9

a ds DNA molecule
of 240 Kb.

Front 10

Cytomegalovirus replicates in

Back 10

human fibroblasts, epithelial cells, macrophages and other cells. The infection progress slowly in cell culture.

Front 11

Cytomegalovirus achieves latency in which cells

Back 11

leukocytes (neutrophils and lymphocytes).

Front 12

Cytomegalovirus infection is ubiquitous meaning

Back 12

seropositive in >80% of the adult population ).

Front 13

how is Cytomegalovirus transmitted?

Back 13

transplacental, blood transfusion, and all secretions (urine, saliva, semen, and tears).

Front 14

The most prevalent viral cause of congenital disease

Back 14

Cytomegalovirus. . Affected newborns often exhibit hearing loss
and mental retardation.
CMV causes serious disease in an immunosuppressed or
Immunodeficient person

Front 15

Cytomegalovirus samples for diagnosis can be obtained from

Back 15

throat washings, urine or leukocyte

Front 16

Cytomegalovirus tx

Back 16

: Gagncyclovir , valganciclovir, cidofovir, and foscarnet

Front 17

Human Herpesvirus 8 (HHV 8) genome

Back 17

: a ds DNA molecule of 145 Kb, consisting of at least 87 genes.
Both latent and lytic replication have been observed in infected cells or tissues

Front 18

in what type of cells does HHV 8 replicate?

Back 18

in B cells and endothelial cells.

Front 19

HHV 8 Genes involved in cell growth

Back 19

v-Cyclin, Kaposin, K1, and LANA

Front 20

HHV 8 Genes for apoptosis

Back 20

vBCL2 and v-FLIP

Front 21

HHV 8 production of tumors

Back 21

Immunity---v-interleukin 6, v-interferon regulatory factors
v-GPCR (chemokine receptor), v-interleukin 8 receptor and v
MIP (ckemokine)

Front 22

HHV 8 primary Clinical Manifestation

Back 22

Acute febrile illness with a rash

Front 23

HHV8 is associated with which cancers?

Back 23

Kaposis sarcoma (KS)
Primary effusion lymphoma (PEL)
Multicentric Castleman’s disease (MCD

Front 24

what population suffers more from Human Herpesvirus 8

Back 24

African regions

Front 25

Epidemiologic studies suggest two modes of HHV 8 transmission:

Back 25

- Sexual contact: the most common route of infection in the developed countries.
- Nonsexual routes: predominant in endemic African regions

Front 26

HHV 8 DNA is invariably detected in

Back 26

Karposis sarcoma which is more common in AIDS patients

Front 27

HHV 8 antibodies are more frequently found in

Back 27

group at risk of
KS lesions (HIV infection).

Front 28

HHV 8 seroconversion precedes

Back 28

KS development.

Front 29

HHV 8 causes KS, given

Back 29

sufficient
dose and enough time.

incompetent immune system is
needed.

HHV 8 causes KS via direct interaction
with HIV (Tat protein or cytokine
production).
Latency stage increases KS chances of happening

Front 30

Epstein-Barr Virus (EBV)genome

Back 30

a double stranded DNA molecule of 170 Kb

Front 31

Epstein-Barr Virus (EBV) as tropism for what cells

Back 31

Epithelial cells
B-lymphocyte
Epithelial cell is the initial site of infection. Latency occurs in
B-lymphocytes

Front 32

EBV infection is ubiquitous meaning

Back 32

90% adults have EBV antibody

Front 33

Epstein-Barr Virus (EBV) transmission

Back 33

through infected secretions such as saliva .

Front 34

A young guy comes and complains of fever, enlarged lymph nodes and spleen, fatigue and sore throat.

Back 34

Infectious Mononucleosis. Heterophile antibodies develop

Front 35

Heterophile antibodies are good signal of

Back 35

acute infection

antibody specific and nonspecific to viruses

Front 36

Many of the symptoms of Epstein-Barr Virus (EBV) including Infectious Mononucleosis develop because

Back 36

of activation of T cell response to infection.

Front 37

Primarily a childhood tumor in areas of equatorial Africa and New guinea
Predilection for jaw and abdominal viscera

Back 37

African Burkitt’s Lymphoma

Front 38

African Burkitt’s Lymphoma chromosome translocation

Back 38

(8:14) containing
the proto-oncogene c-myc.

Front 39

African Burkitt’s Lymphoma relation to EBV?

Back 39

Every tumor cell contains EBV DNA and antigens
All patients have antibodies to viral capsid antigens with levels of 8-10
times greater than normal.
Very high levels of antibody months before tumor development

Front 40

High frequency carcinoma in southern China. Diet may be a cofactor.

Back 40

Nasopharyngeal Carcinoma (NPC)

Front 41

Nasopharyngeal Carcinoma (NPC) association to EBV?

Back 41

Carcinoma cells carry the EBV genome and express EBV nuclear antigen.

EBV antibody titers elevated 10 times in cancer patients versus controls.

Front 42

EBV diagnosis

Back 42

Heterophile antibody test
Immunoflourescence test for EBV specific antibodies

Front 43

EBV tx

Back 43

Supportive measures