Identification of conserved residues in the E2 envelope glycoprotein of the hepatitis C virus that are critical for CD81 binding.

Hepatitis C virus (HCV) cell entry involves interaction between the viral envelope glycoprotein E2 and the cell surface receptor CD81. Knowledge of conserved E2 determinants important for successful binding will facilitate development of entry inhibitors designed to block this interaction. Previous studies have assigned the CD81 binding function to a number of discontinuous regions of E2.

Successful treatment of invasive cavernous sinus aspergillosis with oral itraconazole monotherapy.

An 83-year-old woman receiving long-term prednisolone treatment presented with a right optic neuropathy and right third, fourth, fifth, and sixth cranial nerve palsies secondary to sino-orbital aspergillosis with cavernous sinus involvement. Because the patient refused conventional treatment, she was given a two-year course of oral itraconazole 200 mg/day, leading to a complete imaging resolution of the lesion. Three years after completing treatment, there is no clinical or imaging evidence of disease recurrence.

Characterization of the hepatitis C virus E2 epitope defined by the broadly neutralizing monoclonal antibody AP33.

The mouse monoclonal antibody (MAb) AP33, recognizing a 12 amino acid linear epitope in the hepatitis C virus (HCV) E2 glycoprotein, potently neutralizes retroviral pseudoparticles (HCVpp) carrying genetically diverse HCV envelope glycoproteins. Consequently, this antibody and its epitope are highly relevant to vaccine design and immunotherapeutic development. The rational design of immunogens capable of inducing antibodies that target the AP33 epitope will benefit from a better understanding of this region.

Tonsillar homing of Epstein-Barr virus-specific CD8+ T cells and the virus-host balance.

Patients with infectious mononucleosis (IM) undergoing primary EBV infection show large expansions of EBV-specific CD8+ T cells in the blood. While latent infection of the B cell pool is quickly controlled, virus shedding from lytically infected cells in the oropharynx remains high for several months. We therefore studied how responses localize to the tonsil, a major target site for EBV, during primary infection and persistence.

Target cells of Epstein-Barr-virus (EBV)-positive post-transplant lymphoproliferative disease: similarities to EBV-positive Hodgkin's lymphoma.

Background: Epstein-Barr virus (EBV)-associated post-transplant lymphoproliferative disease (PTLD) encompasses a histologically broad range of lesions, arising from the expanded pool of EBV-infected B cells in the immunocompromised host. Identification of the precise cellular origin of these tumours could clarify their pathogenesis.

Methods: Of 13 cases of EBV-positive cases of PTLD characterised by histological analysis, pattern of EBV gene expression, and clinical course, 11 had monoclonal or biclonal lesions in which we determined the progenitor B cell by immunoglobulin heavy chain (IgH) genotyping.