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Articles: Anne K. Junker Epstein-Barr Virus Pediatrics in Review 2005; 26: 79-85 [Full text] [PDF]

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response to Dr. Kamal

anne k junker   (13 April 2005)

The EBV infection

Khalid Kamal   (13 April 2005)

response to Dr. Kamal 13 April 2005
anne k junker, physician author Send letter to journal: Re: response to Dr. Kamal sydney_sutherland{at}urmc.rochester.edu anne k junker	Dr. Junker replies to Dr. Khalid Kamal: Regarding EBV-associated neutropenia, there are a number of mechanisms. These cells can be more rapidly cleared in the peripheral circulation via autoantibodies; FAS-mediated "death"; and potentially, by hemophagocytosing macrophages. Production by bone marrow precursor cells can be impaired by direct virus infection, disease-response cytokines, and activated (cytotoxic or suppressor) T cells. EBV-induced polyclonal activation of B lymphocytes can result in anti-neutrophil antibody production. The FAS system is an important immune regulatory pathway. During EBV infection, neutrophils up-regulate expression of the FAS receptor and serum levels of the FAS ligand are increased. Receptor- ligand interaction activates the apoptosis (death) pathway. In one of the extreme complications of EBV infection - virus-associated hemophagocytic syndrome - neutrophils are ingested by activated macrophages and this can be visualized on blood smears and bone marrow specimens. In short, neutropenia can arise from direct infection of the cell, but is more frequently a consequence of the potent impact this virus has on the host immune system. Regarding the protective role of maternal antibodies, infants born to seropositive mothers do not get EBV infection until later in infancy, some months after disappearance of transplacental-derived antibodies. That maternal antibody appears to protect infants from EBV infection was first demonstrated by R. J. Biggar et al in Ghanaese infants in 1978. With respect to gastric carcinoma and the respective roles H. pylori and Epstein-Barr virus, much work needs to be done to elucidate the mechanisms involved. Finally, the practice implications of cross-reacting antibodies will depend upon the clinical circumstances (how necessary is it to confirm the viral diagnosis?); and the health care system (ie. cost and availability of other tests). Equivocal serologic results can be confirmed by other techniques - many are available - but need to take into account other clinical and biological observations. If the patient has signs of classic infectious mononucleosis and other tests show a positive heterophil antibody ("positive Monospot") and characteristic hematological findings (absolute and atypical lymphocytosis), one can be comfortable they are dealing with EBV-related disease. Further studies would not be indicated. CMV-EBV co-infections are rare outside the immunocompromised population. CMV infection should be determined by direct means -- virus culture, PCR, or antigen detection. In situations where the clinical presentation is not typical EBV-mononucleosis, and/or there are serious complications, EBV infection can be confirmed by virus load in serum.
The EBV infection 13 April 2005
Khalid Kamal, Pediatrician Children's Hospital of Michigan Send letter to journal: Re: The EBV infection saharfarida{at}aol.com Khalid Kamal	Your excellent article is very interesting and informative. The following questions came to my mind: What is the mechanism of neutropenia? EB infection in the first months after birth is associated with Burkitt Lymphoma. Do the maternal antibodies provide any protection? Why is the coinfection with H pylori associated with a low risk for gastric carcinoma? What are the practice implications of diagnostic antibodies that cross react with CMV? Should we routinely check for CMV as well in classical cases of mononucleosis?