I don't understand this at all, but this paragraph interests me...can anyone explain?

To address these unanswered questions, we cloned and expressed the bat R. pearsonii ACE2 gene and examined the abilities of ACE2 proteins from human, palm civet, and R. pearsonii to support infection by HIV-based pseudoviruses containing different S protein constructs. Our results indicated that the bat SL-CoV (Rp3) S protein is unable to use ACE2 for cell entry regardless of the origin of the ACE2 molecule. We also demonstrated that the human SARS-CoV S cannot use bat RpACE2 as a functional receptor. On the other hand, we demonstrated that after replacement of a small segment (aa 310 to 518) of Rp3-S by the cognate sequence of BJ01-S, the CS protein mimics the function of BJ01-S in regard to receptor usage in the HIV pseudovirus assay system. Although we currently have no way of confirming that the Rp3-S protein is functional in binding its cognate receptor due to the lack of a horseshoe bat cell line, our chimeric-construct analysis suggests that the Rp3-S gene was intact and would be functional if an appropriate receptor was identified. It is also worth noting that, although we have no experimental data to demonstrate direct binding of different S proteins to huACE2 on the HeLa cell surface, we did confirm that either anti-huACE2 or anti-SARS-CoV polyclonal antibodies were able to neutralize infection by different pseudoviruses (data not shown)

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