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Epstein-Barr
virus was discovered during ultrastructural studies of endemic
Burkitt’s lymphoma in Africa.
There is now strong evidence that the virus causes two
cancers endemic Burkitt’s lymphoma in Africa and nasopharyngeal carcinoma, especially in the Orient.
EBV is a
gamma-group herpes virus that causes a benign, self-limited lymphoproliferative disease that is characterized by
fever, generalized
lymphadenopathy, splenomegaly, sore throat and appearance
in the blood of atypical activated T-lymphocytes.
EBV enters the
epithelial cell cytoplasm by directly fusing with the plasma membrane. EBV enters the
B-cell cytoplasm by fusing with the endosomal membranes.
Two EBV
proteins, EBNA2 and LMP-1, are associated with B-cell immortalization,
which may occur in latently infected lymphocytes.
In infectious mononucleosis, the total
white cell count increases to as many as 18,000, 95% of which are
atypical T-lymphocytes with an abundant, finely granular, basophilic
cytoplasm, containing small fenestrations.
The lymph
nodes in the posterior cervical, axillary, and groin regions are enlarged
, show
increased number of T-cells in their paracortical zones and contain
large binucleate cells, Reed-Sternberg-like cells.
With impaired
immunity, infectious mononucleosis may become chronic and transform into B-cell lymphoma.
In Burkitt
lymphoma associated with EBV there is a characteristic 8:14
translocation, in which the c-myc oncogenes is placed into the
immunoglobulin heavy chain expression region.
Pathological features:
The pathologic
changes are prominent in the lymph nodes and spleen because of the
underlying immunologic nature of the illness.
In most patients the lymphadenopathy is symmetrical and most striking in the neck, and the
nodes are movable, discrete, and tender.
On gross examination they are
soft and swollen and the hyperemic (pink) cut surfaces occasionally
display foci of necrosis.
Microscopically, the general architecture is
preserved.
The germinal centers are large and have indistinct margins
because of proliferation of immunoblasts.
They contain frequent
mitoses and scattered nuclear debris, presumably from degenerated B-cells.
The nodes contain occasional large hyperchromatic cells with
polylobated nuclei that resemble Reed-Sternberg cells.
The immunoblastic hyperplasia and consequent architectural distortion, and
the presence of atypical cells, may present diagnostic problems
because of the morphologic similarity to Hodgkin’s disease or
non-Hodgkin’s lymphoma.
The spleen is large and soft owing to
hyperplasia of the red pulp and is susceptible to rupture.
Many immunoblasts are present throughout the pulp and
infiltrate the walls of vessels, the trabeculae, and the capsule.
The
edema and infiltration of the capsule probably account for the
tendency to rupture.
The liver is almost always involved, but the
hepatitis is nonspecific.
The sinusoids contain atypical lymphocytes,
and there are mild lymphocytic infiltrates in the portal tracts.
Most patients
recover completely, although convalescence may be protracted.
Uncommon neurologic complications include diffuse or focal encephalitis
(sometimes involving the cerebellum) and occasionally, aseptic
meningitis.
In the rare fatal cases, meningoencephalitis is the most
common cause of death.
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