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         Dr. Joseph Ahearn hired me as a technician upon my immigration to the US.  His lab was studying the molecular basis of infection of human cells by Epstein-Barr virus (EBV).  To enter B-lymphocytes EBV uses human complement receptor type II (CR2) (2,3).   An extracellular portion of the CR2 molecule consists of the 16 short consensus repeats (SCRs).  EBV was found to have narrow tropism and is capable of infecting only human B cells but not mouse B lymphocytes (1).  Ahearn's lab used this EBV property to map CR2 domains that are responsible for EBV binding.  We have constructed multiple human-mouse chimerical CR2 molecules and expressed them in COS cells to assess their ability to bind EBV.  EBV binding to COS cells was detected by incubating transient trasformants with EBV and then with mouse anti-gp350 MAb and DTAF-conjugated goat anti-mouse antibodies.
I was responsible for constructing the human-mouse chimerical molecules.  Don Martin was using two-step PCR technique to make fusion proteins and I was screening for recombinant clones and their confirmation by sequence analysis.  I have also constructed several chimerical CR2 molecules by conventional subcloning from previously made chimeras and did several COS cell transfection experiments.  As a result of this effort we demonstrated that the first two N-terminal SCRs of the human CR2 were necessary and sufficient for EBV binding.  Remarkably, the same SCRs are necessary and sufficient for binding to C3dg, which is the natural CR2 ligand 1.  Since human CR2 can bind mouse C3dg as well, it was possible to predict from homology analysis between human and mouse SCRs the individual aminoacids in human CR2 sequence that are responsible for EBV binding.
 

REFERENCES
1. Sugden, B. An intricate route to immortality. Cell, 57:5, 1989
2. Fingeroth, J.D. et al.  Epstein-Barr virus receptor of human B-lymphocytes is the C3d receptor CR2. PNAS, 81:4510, 1984
3. Nemerow G.R., Identification and characterization of the EBV receptor on human B-lymphocytes and its relationship to the C3d receptor (CR2). J. Virol., 55:347



 
 
 

Two-step PCR
        One part of the chimerical molecule is made in the first step by PCR using human CR2 as a template.  The upstream PCR primer has a unique XmaI site.  The second part of the chimera is made by using the amplified human fragment from the first step as an upstream primer for PCR using mouse CR2 as a template and the downstream primer with XhoI restriction site.  Then XmaI-XhoI PCR fragments were recloned intothe  mouse or human complete cDNA and used for the EBV binding studies.
 

1.     From reviewing the literature it becomes clear that most receptors bind  ligands by their N-terminal domains.  The simple reason is that probably only N-terminal of the receptors are readily exposed and other parts are buried by glycosilation and neighboring protein molecules.  (back to main reading)

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