3.26 RYAN CMV, EBV, and KSHV Flashcards
CMV Pathogenesis
- Not highly contagious
- direct contact with secretions, not by aerosol, primary replication in epithelial cells, followed by spread to lymphoid tissue
- CMV latently infects B-Cells, T-Cells, monocytes and lymphocytes where it causes large, puffed up cells
CMV symptoms
- 80% of adult pop is CMV+
- Neonatal infections can occur un utero; most are asymptomatic, cause result in retardation and deafness
- Most adult infections are also asymptomatic, but mononucleosis accompanied by fever can occur
Immunocompromised
- At high risk
- most organ transplant patients get CMV infection with pneumonitis representing the most life-threatening aspect
- -infect from CMV+ donor or by reactivation of CMV+ recipient
- -prophylactic treatment with CMV ig and ganciclovir (promising)
- AIDS patients are prone to CMV retinitis, colitis and pneumonitis
Diagnosis
-ELISA or PCR detection, shell vial assay
CMV Treatment
Ganciclovir: requires phos by viral kinase for activity, side effects: neutropenia and GI tract bleeding
Epstein-Barr Virus (EBV)
- Adolescence and early adults get mononucleosis
- 90 to 95% of adult pop contains ab to EBV
- can cuase oral hairy leukoplakia in immunocomp
- Posttransplant lymphoproliferative disease (PTLD) in some transplant pts
- associated with Burkitt’s lymphoma and nasopharyngeal carcinoma
EBV pathogenesis
- Spread through saliva
- incubation period 4-7 weeks
- initial replication in oropharyngeal epithelium
- Sperad to lymphocytes and then liver and spleen
- EBV remains latent in throat epithelium and B-cells
- Oral shedding of virus occurs for many weeks
EBV symptoms
Most infections are asymptomatic
- Infectious mononucleosis: sore throat, fever 1-2 weeks, malaise, lymphadenopathy
- Recovery is uneventful
Diagnosis
- at least 50% atypical, large lymphocytes with lobulated nuclei
- diagnosis usually made off symptoms
- Large lymphocytes are T-cells responding to infection, not infected B-cells***
- Monospot test test for EA (early antigen)
Antigenic markers
EBNA-EBV nuclear antigens arise early in primary infection, EBNA1 maintains genome replication in dividing b-cells, conversion to anti-EBNA IgG indicates resolution of primary infection
- VCA: viral capsid antigen,
- -anti-VCA IgM: primary infection
- -anti-VCA IgG w/o anti-EBNA: primary infection
- -antiVCA IgG w/ anti EBNA IgG: past infection
EBV and neoplasms
PTLD: uncontrolled prolifertion of B cells, highest risk in seroneg transplant recipients
–treatment: stop immunosuppression (be careful, watch for rejection)
BURKITT’S: neoplasm of B-cells that affects bones of the jaw (africa and new guinea)
–associated w/ 3 factors: (1) early EBV infection leading to latency (2) activation of c-myc (3) malaria: suppresses typical immune response
NASOPHARYNGEAL CARCINOMA: epithelial cells, ass with EBV worldwide, high frequency in souther CHINA (high salt diet), at best 60% pts survive 10 yrs
QUICK THINK: compare and contrast CMV and EBV
Both can cuase mono and are latent in B cells. Both can cause Post-transplant complications, but presentation is diff.
-CMV is sexually transmitted and a source of congenital infection
-CMV is always heterophile AB neg
(neg mono spot test)
-EBV is a known oncogenic virus
Human herpesvirus-8 (KSHV)
- could cause kaposi’s sarcoma
- B-cell and endothelial latency tropism
- –lining of the lymphatic system, lymph channels fill with blood cells: bluish bruised appearance
KS pts in US
They are AIDS patients
- sexually trans-but no virus in semen and vaginal secretions
- present in saliva: STD not understood
- 10 yr incubation period b/f onset of KS: may be mild, can be life-threatening in immunocomp
HHV-8 B cell abnormalities
Primary effusion lymphoma: non-hodgkin B-cell lymphoma, commonly found in body cavities, mean survival tiem 2-6 months, KSHV found in virtually all tumors of HIV+ pts
CASTLEMAN’S DISEASE: lymph node tumors, not strictly cancer, KSHV found in virtually all tumors of HIV+ pts (nonmetastic)
