Nearly 30 years ago, Fingeroth and her colleagues discovered that this attachment occurs via the CD21 protein, which until now was the only known B cell attachment receptor for EBV. The recent finding that B cells from a patient lacking CD21 can be infected and immortalized by EBV had indicated that an alternative attachment receptor must exist. The identification of this second receptor -- CD35 -- by Fingeroth's team, led by first author Javier Ogembo, PhD, of BIDMC and the University of Massachusetts Medical School, not only underscores an important finding regarding primary infection but also underscores the importance of EBVgp350/220, (the virus protein that has been found to bind to both attachment receptors) for the development of a vaccine against EBV.
"The EBV glycoprotein gp350/220 is the most abundant surface glycoprotein on the virus," notes Fingeroth, adding that these results further suggest the virus fusion apparatus is the same for both receptors. "An EBV vaccine might be able to prevent infection or, alternatively, greatly reduce a person's risk of developing infectious mononucleosis and EBV-associated cancers, without necessarily preventing the EBV infection itself."
Interestingly, she adds, whereas a human has now been identified to be lacking the CD21 receptor, no persons are known to lack CD35.
"CD35 is a latecomer in evolution and in its current form, exists only in humans," says Fingeroth. "We know that it is often targeted in autoimmune diseases and was recently identified as a malaria receptor. Our new discovery may, therefore, reveal new avenues for the exploration of unexplained links between EBV, autoimmune diseases, malaria and cancer."
|Contact: Bonnie Prescott|
Beth Israel Deaconess Medical Center