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HEV infections in human and pigs have been reported in many countries; however, the precise distribution and multiplication of this virus in the host remains poorly understood. In this study, we examined the distribution and multiplication of HEV genotype 3 in two piglets at the early phase of intravenous infection, and also examined the virus distribution in a naturally infected pig. We developed real-time RT-PCR to determine copy numbers of the HEV genome in the sera, feces and organs. HEV-RNA was detected in serum from a pig transiently for 7 days post-inoculation (dpi). The HEV copy numbers in the feces appearing 7 dpi were increased to 3.4x106 copies/g at 14 dpi. In contrast, the higher copy numbers of HEV were widely distributed in the tissue organs from naturally HEV-infected pig. The study showed that intravenously inoculated HEV was distributed in several restricted tissues, such as in the liver and intestine.

A CD4 peptide of amino acid residues 68-130 [CD4(68-130)], which had the capacities to inhibit HIV-1 replication and HIV-1-induced syncytium formation, was used as an immunogen for the preparation of mAb. The mAbs prepared were classified into at least five types (I-V) in terms of their recognition sites by ELISA using various kinds of smaller CD4 peptides. Among them, the type I mAb no. 35 recognizing amino acid residues 72-84, which lies just before the region corresponding to an immunoglobulin third complementarity-determining region (CDR3), showed the strongest effects in reducing both HIV-1 infection and HIV-1-induced syncytium formation, although a large amount of no. 35 mAb was necessary to reduce such HIV-1 activities compared with those of anti-Leu-3a and OKT4A mAbs which recognize CD4 epitopes near a portion corresponding to an immunoglobulin CDR2. Western blot analysis showed that the reactivities of CD4 molecule in CD4-positive cells or sCD4 molecule with types I-V mAbs were stronger than that with anti-Leu-3a mAb. Flow cytometry showed that no. 35 mAb was faintly reactive with native CD4 molecule on cell surface at the concn showing the inhibitory effects on HIV-1 infection and syncytium formation. In addition, a smaller peptide CD4(66-92), one of the good epitope peptides for no. 35 mAb, also showed strong inhibitory effect on HIV-1 infection as well as a weaker inhibitory effect on syncytium formation. These results suggest that, in addition to the CD4 CDR2-related region, the pre-CDR3-related region is also involved in the early events of the interactions between the host cell and HIV-1.