Viral inf. Circ, RES, and Lymph + Parasitic of lymph etc.

Question 1

What component does the EBV use for entery into it’s host cells, what are the host cells of EBV?

Answer 1

EBV infects B-cells and does so by using the C3d component of the complement system.
The EBV will remain latent in memory B cells!

Question 2

What specific marker serves as a positive of EBV infection?

Answer 2

Heterophile antibodies!

Remains latent in memory B-cells!

Question 3

What is the Latent Membrane Protein 1 (LMP 1) EBV gene responsible for?

Answer 3

6 transmembrane-spanning domains that act as:
CD40 homologue
Increases the growth and suppressed apoptosis.

Question 4

What is the Latent membrane protein 2 EBV gene responsible for?

Answer 4

This gene is responsible for the increased proliferation of B cells in EBV infection.

Question 5

What is the Epstein Barr Virus Nuclear Antigen 1 gene responsible for in EBV infections?

Answer 5

This gene is responsible for the inhibition of apoptosis and is a transactivator of the EBV transforming genes.

Question 6

A young patient comes in with tender swollen lymph nodes of the neck following a malaria infection, when administered ampicillin he had a widespread rash. What is the pt most likely infected with?

Answer 6

EBV.

The virus forms a possible immune complex with the ampicillin leading to the rash.

Question 7

What can be detected serologically in EBV patients early in the infection?

Late in the infection?

Answer 7

Early anti EA (Early antigen) and Anti VCA (Viral capsid antigen) IgM can be detected.

Late there is a switching to IgG and anti EBNA (Ebstein bar nuclear antigen) can be detected.

Question 8

What does a positive mono spot test show?

Answer 8

Agglutination of IgM to vira capsid antigen (VCA) showing primary EBV infection.

Question 9

Downey cells are indicative of what clinical infection?

Answer 9

Downey cells are atypical T cells with vacuoles, altered nucleus, and indented cell margins.

These are found in patients with EBV infections.

Question 10

What are some of the drugs available to treat EBV oral hairy leukoplakia in HIV patients?

Answer 10

Antiherpetic drugs can be used as active EBV replication is occuring here.
Predophyllin resin

Question 11

How does Burkits lymphoma present and where is it most often seen?

Answer 11

Burkits lymphoma is a complication following EBV presenting as a painful mass in the jaw typically in children. This presentation is known as the Endemic form and resides within B cells.

Question 12

How does Endemic Burkits Lymphoma cause massive proliferation?

Answer 12

Through a translocation between chromosomes 8 and 14 leading to an over expression of the myc gene. This leads to proliferation of cells and protein formation.

Question 13

How does Hodgkins disease present?

Answer 13

This disease has a B cell origin and presents as a non tender, palpable, lymphandnopathy. Or even enlargement of lymph nodes in the chest.

Unlike Burkits, there is no translocation that leads to this health problem.

Question 14

Identifying a multinucleited large Reed-Sternberg cell could be a sign or symptom of what disease?

Answer 14

Hodgkins disease

Question 15

What cell type does Nasopharyngeal Carcinoma originate from and what country is it most prevelant in?

Answer 15

This originates in the nasopharynx epithelial cells.

Most commonly found in Africa.

Question 16

What are some of the cofactors of Nasopharyngeal Carcinoma?

Answer 16

Genetics

Diet

Question 17

What is Post-transplantation Lymphoproliferative Disorder (PTLD) and what serves as a major risk factor for it?

Answer 17

This is an abnormal proliferation of the lymphoid cells after receiving a transplant.

Being infected with EBV at the time of implant increases the risk dramatically.

Question 18

How is Post-transplantation Lymphoproliferative Disorder (PTLD) diagnosed?

Answer 18

This is diagnosed by histological analysis of tissue and detection of EBV genomes.

Question 19

How is Post-transplantation Lymphoproliferative Disorder (PTLD) treated?

Answer 19

Post-transplantation Lymphoproliferative Disorder (PTLD) is treated mostly by reducing immunodeficiency following transplantation.

Rituximab can also be used as it i an anti-CD20 antibody.

Chemotherapy can also be used.

Question 20

Why is timing and multiple sample containment so important to Cytomegalovirus diagnosis?

Answer 20

Because the virus can still be shed in urine or saliva for months to years. Thus multiple tests are needed to determine how new or old the infection is.

Question 21

How does Gancyclovir work and what does it treat?

Answer 21

Gangyclovir is used to treat cytomegalovirus and works by being converted to viral polymerase inhibitor by CMV enzymes.

Question 22

How does Valganciclovir work and what does it treat?

Answer 22

It is converted to gancylclovir within the body and increases bioavailability for CMV treatment.

Question 23

How does Cidofovir work and what is it used to treat?

Answer 23

Cidofovir works by being converted to viral polymerase inhibitor by cellular enzymes and is more toxic than its gancyclovir counterpart.

Used to treat cytomegalovirus

Question 24

How does Foscarnet work and what is it used to treat?

Answer 24

This is a direct inhibitor of the CMV polymerase and has renal toxicity.

Used to treat cytomegalovirus.

Question 25

What would a immunocompetent pt present with following CMV infection?

What is the key to diagnoses when comparing it to a similar presentation?

Answer 25

Mononucleosis-like Illness with an incubation period of 20-60 days and symptoms lasting 2-6 weeks.

Key to diagnosis is NO HETEROPHILE ANTIBODY PRODUCTION WILL BE FOUND.

Question 26

When would you see a case of cytomegalic inclusion body disease?

Answer 26

This is most often observed in Babies of CMV seronegative mothers.

Children present with hepatosplenomegaly, Jaundice, and Petechiae/Rash.

Question 27

What is the most common congenital viral infection in the US?

Answer 27

Cytomegalovirus infections of neonates.

Has 33% chance of CMV transfer to baby in seronegative mothers.

Question 28

How does CMV present in immunosupressed patients?

Answer 28

Presents in organ transplants and HIV patients with a spiking fever, CMV pneumonitis, or GI tract problems.

Can also show up as Graft vs Host disease.

Question 29

What are the most common viral infections known to cause myocarditis?

Answer 29

Adenoviruses 2 and 5
Enteroviruses: Coxsakie B
Parvovirus B-19
HHV 6

Question 30

What viral family does Mumps come from?

Answer 30

Paramyxoviridae family -ssRNA genome with an incubation period of 14-18 days

Question 31

How is the Mumps virus prevented?

Answer 31

The virus can be prevented by use of a live attenuarted MMR or MMRV vaccine combination through intramuscular injection.
The first dose : 12-15 months
2nd dose: 4-6 years.

Question 32

Raised pink, purple, brown tumor lesions with a spindle morphology are indicitive of what sort of infection?

Answer 32

This is indicitive of Kaposis Sarcoma.

Question 33

What classifies Kapossis Sarcoma as “Classical”

Answer 33

Found in the Middle eastern Mediteranean descent

Shows very few lesions and is very rarely ever life threatening.

Question 34

What characteristics does Endemic Kaposkis Sarcoma have?

Answer 34

Endemic KS is found in equatorial Africa and has two forms presenting as either Classical Sarcoma or the aggressive form in pre-pubescent children often fatal within 3 years.

Question 35

What characteristics does Transplant Related Kaposi Sarcoma have?

Answer 35

Occurs in individuals whos immune system has been dropped for an organ transplant and is often resolved when immunosupressive therapy is haltered.

Question 36

What characteristics does AIDS related KS have?

Answer 36

Often causes widespread lesions of KS over the entire body with lymph swelling and fever/ weight loss. Often fatal if lungs become involved.

Question 37

Human Herpes Virus 8 is also known as what?

Answer 37

Also known as Kaposis sarcoma-associated herpes virus contains many homologous genes.

Question 38

HHV-8 gene vGPCR and vFlip, and LANA do what?

Answer 38

vGPCR: IL-8 homologue.
vFLIP: Flip homologue involved in apoptosis protection
LANA: Maintains viral latency and binds to p53.

Question 39

How is HHV-8 reated?

Answer 39

This viral infection is treated mostly by taking into consideration the immunodeficiency.
Herpes antivirals are not effective here as herpes is in the latent phase.
Must use retroviral therapies.

Question 40

Flower cells are a sign of what sort of infection?

Answer 40

Flower cells are seen in Adult T-cell lymphoma (ATL)

Clinically this disease presents with hypercalcemia amongst other symptoms similar to KS.

Question 41

Where is Adult T-cll lymphoma most commonly found?

Answer 41

Most commonly found in Japan, Caribbean, and Central Africa in patients around 55 years of age. Most patients will only survive 7 months or so following diagnosis.

Question 42

How is Adult T-Cell lymphoma most commonly diagnoses?

Answer 42

Diagnosed by the detection of antibodies to Human T-cell leukemia virus 1 (HTLV-1)

Question 43

What is HTLV-1 Associated Myelopathy?

Answer 43

HAM is caused by HTLV-1 and is the demylenation of neurons within the spinal cord. This is likely an autoimmune disease with its highest incidence in adult women.

Question 44

What type of virus is HTLV-1 and what cell types does it primarily infect?

Answer 44

This is an enveloped retrovirus +ssRNA that typically infects CD4 and CD8 cells.