Thin-section CT scores correlated with clinical and laboratory parameters in patients after SARS. Although ground-glass opacity and interstitial opacity resolve over time, air trapping persists.

The clinical picture of severe acute respiratory syndrome (SARS) is characterized by pulmonary inflammation and respiratory failure, resembling that of acute respiratory distress syndrome. However, the events that lead to the recruitment of leukocytes are poorly understood. To study the cellular response in the acute phase of SARS coronavirus (SARS-CoV)-host cell interaction, we investigated the induction of chemokines, adhesion molecules, and DC-SIGN (dendritic cell-specific ICAM-3-grabbing nonintegrin) by SARS-CoV. Immunohistochemistry revealed neutrophil, macrophage, and CD8 T-cell infiltration in the lung autopsy of a SARS patient who died during the acute phase of illness. Additionally, pneumocytes and macrophages in the patient's lung expressed P-selectin and DC-SIGN. In in vitro study, we showed that the A549 and THP-1 cell lines were susceptible to SARS-CoV. monocytes, and activated T cells in a chemotaxis assay. We also demonstrated that DC-SIGN was inducible in THP-1 as well as A549 cells after SARS-CoV infection. Our in vitro experiments modeling infection in humans together with the study of a lung biopsy of a patient who died during the early phase of infection demonstrated that SARS-CoV, through a dynamic interaction with lung epithelial cells and monocytic cells, creates an environment conducive for immune cell migration and accumulation that eventually leads to lung injury.Severe acute respiratory syndrome (SARS) in adults causes new pulmonary infiltration, lymphopenia, thrombocytopenia, and high levels of proinflammatory cytokines and chemokines (30) and C-reactive protein (28) in the sera. The clinical picture is characterized by a cascade of immunological events leading to pulmonary inflammation and respiratory failure (9, 17), resembling adult acute respiratory distress syndrome (ARDS) (8). High levels of chemokines and cytokines, triggered by the host immune response to SARS coronavirus (SARS-CoV), are believed to contribute to the progressive pulmonary infiltration of macrophages (16), polymorphonuclear leukocytes (2), and T cells (11) and to eventual diffuse alveolar damage and fibrosis (12). However, it remains to be determined how the cellular response in the early stage of virus-host cell interaction results in the sequence of events that leads to the severe clinical outcome.In situ hybridization and immunohistochemistry revealed that both SARS-CoV nucleic acids and antigens are present within type II pneumocytes (26). Alveolar macrophages are also reported to harbor SARS-CoV (23). Hence, it is important to investigate how the interaction between SARS-CoV and pneumocytes and macrophages influences the subsequent events in the lung.DC-SIGN (dendritic cell-specific ICAM-3-grabbing nonintegrin) is a type II C-type lectin that is naturally expressed in human dendritic cells. It has been reported that DC-SIGN binds SARS-CoV and mediates its entry into myeloid dendritic cells by binding to the spike protein (31). However, the inducibility of DC-SIGN in cells encountering the virus and its si...

The genome of one Taiwanese severe acute respiratory syndrome-associated coronavirus (SARS-CoV) strain (TW1) was 29,729 nt in length. Viral RNA may persist for some time in patients who seroconvert, and some patients may lack an antibody response (immunoglobulin G) to SARS-CoV >21 days after illness onset. An upsurge of antibody response was associated with the aggravation of respiratory failure.

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Metaplastic carcinoma of the breast (MCB) is characterized by the biphasic presence of both a carcinomatous component (CC) and heterogeneous sarcomatous components (HSCs). Although an epithelial or myoepithelial origin of the HSCs has been suggested, molecular evidence for a common origin for the CC and HSCs is limited and the mechanism underlying the sarcomatous or metaplastic change is unknown. The present study investigated the frequency and nature of p53 expression and mutation in 11 biphasic and three monophasic MCBs by immunohistochemistry and either needle-assisted or laser-capture microdissection, followed by PCR and direct sequencing. In all 11 biphasic MBCs, staining for p53 was concordant in the CC and HSCs (8/11 positive and 3/11 negative), consistent with a monoclonal origin of both components. Significantly, whenever a component of carcinoma in situ was present (5/11), the p53 staining was always concordant with that in the CC and HSCs. Screening of the 14 cases for p53 mutation identified four mutants, each in a single case of biphasic MCB with concordant p53 overexpression. Both the CC and each of the HSCs revealed identical p53 mutation in all four cases; in addition, one of the four cases also had an in situ component and the same mutant was found simultaneously in the in situ, invasive, and sarcomatous components. The concordant pattern of p53 alteration (overexpression or mutation) implies that early p53 mutation, occurring prior to invasion, was maintained throughout tumour progression and metaplastic change. The findings therefore support a monoclonal histogenesis of the various components, but are neutral regarding the role of p53 alteration in the development of metaplastic change in MCBs.