The respiratory syncytial virus SH protein is incorporated into infectious virus particles that form on virus-infected cells.

The association of the SH protein with respiratory syncytial virus (RSV) particles was examined in HEp2 cells and human ciliated nasal epithelial cells. Imaging of infected cells demonstrated the presence of the SH protein in virus filaments, and analysis of purified RSV particles revealed a SH protein species whose size was consistent with the glycosylated SH protein. Although the SH protein was detected in virus filaments it was not required for virus filament formation. Analysis of RSV-infected ciliated cells also revealed that the SH protein was trafficked into the cilia, and this correlated with reduced cilia density on these cells. Reduced cilia loss was not observed on ciliated cells infected with a RSV isolate that failed to express the SH protein. These data provide direct evidence that the SH protein is trafficked into virus particles, and suggests that the SH protein may also promote cilia dysfunction on nasal epithelial cells.

A sustained antiviral host response in respiratory syncytial virus infected human nasal epithelium does not prevent progeny virus production.

Respiratory syncytial virus infection was examined using a human nasal epithelial cell model. Maximum levels of shed-virus were produced at between 3 and 5 days post-infection (dpi), and the infectivity of the shed-virus was stable up to 10 dpi. The highest levels of interferon signalling were recorded at 2dpi, and infection induced a widespread antivirus response in the nasal epithelium, involving both infected cells and non-infected cells. Although these cellular responses were associated with reduced levels of progeny virus production and restricted virus spread, they did not inhibit the infectivity virus that is shed early in infection. In the clinical context these data suggest that although the host cell response in the nasal epithelium may restrict the levels of progeny virus particles produced, the stability of the shed-virus in the nasal mucosa may be an important factor in both disease progression and virus transmission.

[Acute leukemia relapse of donor origin in two cases after haploidentical bone marrow transplantation].

To investigate the leukemia relapse of AL patients after HLA haploidentical bone marrow transplantation (HLA HBMT), 2 relapsed leukemia patients received HLA HBMT were studied, peripheral blood simples and bone marrow smear were examined, morphologic change of bone marrow cells was observed, while the HLA genotype and chromosome karyotye were analyzed by PCR and routine G-banding methods, respectively. The results indicated that the two cases were diagnosed primarily as acute lymphocytic leukemia (common cell subtype) and acute megakaryocytic leukemia, in which chromosome abnormalities or activation of protooncogene in leukemic cells were observed. The complete hematopuietie reconstitution of donor origin was obtained in these 2 cases after HLA HBMT, but the leukemic cells in these 2 leukemia patients were confirmed to be donor origin after relapse, their blood groups and HLA genotype were found to be originated from donor. These 2 relapsed leukemia patients were diagnosed as acute lymphocytic leukemia (B cell subtype) and acute megakaryocytic leukemia. It is suggested that high-dose of immunosuppressive agents used in transplantation may contribute to leukemia relapse of donor origin in these patients. Abnormalities in hematopoietic microenvironment may be also involved in the leukemia development. Donor-cell leukemia after allogeneic hematopoietic stem cell transplantation can be an ideal model to investigate the related events in human leukemogenesis.