Epstein–Barr virus in the pathogenesis of oral cancers

Epstein–Barr virus (EBV) is a ubiquitous gamma‐herpesvirus that establishes a lifelong persistent infection in the oral cavity and is intermittently shed in the saliva. EBV exhibits a biphasic life cycle, supported by its dual tropism for B lymphocytes and epithelial cells, which allows the virus to be transmitted within oral lymphoid tissues. While infection is often benign, EBV is associated with a number of lymphomas and carcinomas that arise in the oral cavity and at other anatomical sites. Incomplete association of EBV in cancer has questioned if EBV is merely a passenger or a driver of the tumorigenic process. However, the ability of EBV to immortalize B cells and its prevalence in a subset of cancers has implicated EBV as a carcinogenic cofactor in cellular contexts where the viral life cycle is altered. In many cases, EBV likely acts as an agent of tumor progression rather than tumor initiation, conferring malignant phenotypes observed in EBV‐positive cancers. Given that the oral cavity serves as the main site of EBV residence and transmission, here we review the prevalence of EBV in oral malignancies and the mechanisms by which EBV acts as an agent of tumor progression.     

Bone marrow disorders: characterization with quantitative MR imaging

Thirty patients with various hematologic disorders and 15 healthy control subjects underwent quantitative magnetic resonance (MR) imaging of the lumbar spine with spin-echo techniques. Images of patients with infiltrative bone marrow disorders showed significantly more prolonged T1 times than those of control subjects (P less than .001). It was not possible to distinguish different diffuse infiltrative bone marrow disorders on the basis of T1 values. Aplastic anemia could be distinguished from normality because of significantly shortened T1 (P less than .001). A significant correlation was seen between T1 and bone marrow cellularity (r = .74, P less than .001). T2 was of no value in the characterization of bone marrow disorders. Quantitative MR imaging dose not improve the diagnostic potential of bone marrow imaging in the detection of diffuse marrow infiltrates.     

A CD18 monoclonal antibody increases the incidence and severity of subcutaneous abscess formation after high-dose Staphylococcus aureus injection in rabbits.

Monoclonal antibody (MAb) 60.3 blocks CD18-dependent polymorphonuclear neutrophil adherence to endothelium and has been shown to be of benefit in preventing tissue injury in a variety of inflammatory conditions. However, concern exists that interference with normal polymorphonuclear neutrophil host-defense functions may increase susceptibility to bacterial infection. We compared the development of subcutaneous Staphylococcus aureus abscesses in rabbits pretreated with MAb 60.3 to those pretreated with saline placebo. Bacterial inoculation with 10(6) or 10(7) colony-forming units (CFU) did not result in abscess formation in either control or antibody-treated groups. However, inoculation with 10(8) CFU resulted in more frequent and larger abscesses in antibody-treated rabbits than in controls. Abscess incidence was similar for inoculation with 10(9) CFU, although antibody-treated rabbits developed larger abscesses than did controls. The difference in abscess development is due to delayed leukocyte migration into inoculated tissue. The results of these experiments suggest that subjects treated with MAb 60.3 and exposed to massive S. aureus inocula may be at serious risk of infection. However, despite inhibited leukocyte adhesion, inocula of up to 10(7) CFU were well tolerated in this model. Whether these findings are clinically important remains to be determined, although exposure to bacterial concentrations of 10(8) CFU or greater occurs only rarely in clinical practice.