Biomedical subjects

J M Routes

Publications and source records attributed to J M Routes.

22 records · Page 2Linked to original sources

PubMed1992

Diffuse pulmonary infiltrates in hypogammaglobulinemia.

This is the first case report of lymphangitic carcinomatosis from adenocarcinoma of the stomach presenting as interstitial lung disease in a patient with CVH. Adenocarcinoma of the stomach occurs with increased frequency and at an earlier age in CVH as compared with the normal population. This diagnosis should be kept in mind during evaluation of patients with CVH. Periodic examinations of stool for occult blood should be performed. Aggressive diagnostic evaluation should be undertaken in any CVH patient with gastric complaints, as well as careful follow-up in patients with pernicious anemia, atrophic gastritis, or achlorhydria with regard to cancer screening.

Adenocarcinoma↗

PubMed1991

Anti-adenovirus type 5 cytotoxic T lymphocytes: immunodominant epitopes are encoded by the E1A gene.

Virus specific, major histocompatibility complex-restricted, cytotoxic T lymphocytes (CTL) generated in Fischer strain rats infected with human adenovirus type 5 (Ad5) were found to recognize antigenic determinants encoded within the Ad5 early region 1A (E1A) gene. Preliminary mapping studies suggest that the E1A CTL epitopes are encoded within the regions between bp 625 to 810 and 916 to 974 in the first exon of this gene. These epitope-coding regions occur within subregions of E1A that are conserved functionally, and to some extent structurally (approximately 50% sequence homology), among adenoviruses of different groups. Nevertheless, Ad5-specific CTL lysed only targets infected with adenoviruses of the same group (group C; e.g., Ad2) and not targets infected with adenoviruses of different groups (groups A, B, and E). These results suggest that virus-specific CTL may limit adenoviral dissemination by destroying virus-infected cells at an early stage in the viral replicative cycle, during E1A gene expression. Expression of other adenovirus genes does not appear to be required to target infected cells for elimination by CTL.

Adenovirus Early Proteins↗

PubMed1990

Resistance of human cells to the adenovirus E3 effect on class I MHC antigen expression. Implications for antiviral immunity.

Group C human adenovirus (Ad) serotypes (e.g., Ad2 and Ad5) cause persistent infections in man. One proposed mechanisms to explain human adenovirus persistence is an ineffective CTL response due to reduced cell surface expression of class I MHC Ag on virally infected cells, an effect mediated by the 19-kDa glycoprotein encoded by Ad early region 3 (E3). In the present study, the generality of this phenomenon was tested by analyzing E3 19-kDa glycoprotein down-regulation of cell surface class 1 MHC Ag on a variety of human cell types. With the exception of the Ad5 early region 1 (E1) transformed cell line, 293, Ad2/5 infection of fibroblastic, epithelial, and lymphoid cells did not cause major decreases in surface class I Ag until the terminal stages of infection when cell death is imminent. Furthermore, newly synthesized class I Ag continued to be surface expressed on most cell types at times when infected cells contained large amounts of Ad E3 19-kDa glycoprotein. These data indicate that most types of human cells are resistant to the E3 19-kDa glycoprotein effect, suggesting that virus-specific CTL recognition and lysis of most Ad2/5-infected human cells should not be limited by E3 19-kDa-mediated reduction in class I MHC Ag expression.

Adenoviridae Infections↗

PubMed1989

Adenovirus persistence in man. Defective E1A gene product targeting of infected cells for elimination by natural killer cells.

Human adenovirus types 2 and 5 (Ad2/5) cause persistent infections in man. Ad2/5 infection of rodent cells induces increased susceptibility to NK lymphocyte-mediated lysis that is dependent on target cell expression of Ad2/5 E1A gene products. In contrast to infected rodent cells, Ad2/5 infection of human fibroblasts and epithelial cells does not result in increased susceptibility to either human or rodent NK cell-mediated killing, despite high levels of E1A protein expression. This functional inactivity of E1A gene products in Ad-infected human cells may contribute to adenoviral persistence by rendering the NK cell response to Ad-infected cells ineffective.

Adenoviridae Infections↗