Kaposi's sarcoma-associated herpesvirus encodes two proteins that block cell surface display of MHC class I chains by enhancing their endocytosis

Abstract

CorrectionsMICROBIOLOGY. For the article ''Kaposi's sarcoma-associated herpesvirus encodes two proteins that block cell surface display of MHC class I chains by enhancing their endocytosis'' by Laurent Coscoy and Don Ganem, which appeared in number 14, July 5, 2000, of Proc. Natl. Acad. Sci. USA (97, 8051-8056; First Published June 20, 2000; 10.1073͞pnas.140129797), the authors note that in Fig. 3A, images of the identical gel were inadvertently reproduced twice, once in the control row and once in the experimental row. The error occurred during figure preparation and reflects the fact that in both the control and the experimental cell lines, MHC-I chains are processed identically, generating images that are very similar. The corrected Fig. 3A and its legend are printed below. No conclusions of the paper are affected.MEDICAL SCIENCES. For the article ''Human lung cancer and p53: The interplay between mutagenesis and selection'' by Sergei N. Rodin and Andrew S. Rodin, which appeared in number 22, October 24, 2000, of Proc. Natl. Acad. Sci. USA (97, 12244-12249; First Published October 17, 2000; 10.1073͞pnas.180320897), the authors note the following correction. Fig. 2 shows erroneous spectra that do not correspond to the test result (0.979 P value as described in the text) because the lung cancer spectrum in smokers was constructed when erroneous repeats were not removed from the IARC p53 mutational database (April 1999). Also, some mutations were assigned to the wrong cancer type classes because of a spreadsheet macro programming error during the building of the chart. Fig. 2 is repeated here with the correct spectra. These corrections do not change the results or the conclusions reported in the paper. were metabolically labeled for 20 min and chased for the indicated time periods. After being lysed in 1% Nonidet P-40, lysates were divided into three aliquots. Two were kept on ice and one was incubated at 37°C for 1 h. Heterodimeric MHC I molecules were immunoprecipitated with mAb W6͞32 and treated with endo H where indicated. Fig. 2.Comparison of the p53 spectra of G3 T transversions from lung cancer (cases related to radon and other occupational exposures excluded) of ever smokers and cancers in non-lung tissues least accessible to smoke (see Table 1). The size of the bars represents the G3 T frequency at the corresponding guanine. Hot-and ''warm''-spot codons are indicated. A major arm of host immunity to viral infection is the cytotoxic T lymphocyte (CTL), which recognizes viral antigens presented as peptides bound to class I MHC (MHC I) molecules on the surface of infected cells. CTL recognition of such cells can lead to direct cytolysis as well as the release of cytokines that can contribute further to antiviral action and host immune mobilization. Therefore, evasion of CTL recognition is thought to play a key role in the establishment of a systemic viral infection. Consistent with this view, many viruses have evolved complex strategies for such evasion, usually centering on the down-regulation of cell ...

Inhibition of MHC Class II Expression and Immune Responses by c-MIR

“…MIR family proteins bind to the membrane through their hydrophobic domains located at the center and possess two intracellular regions. The initially discovered MIR family proteins are viral E3s: MIR1 and MIR2 of Kaposi's sarcoma-associated herpesvirus (KSHV), mK3 of murine ␥-herpesvirus 68, and m153R of myxomavirus (3,(5)(6)(7)(8)(9). Each molecule targets a different set of Ag presentation-related molecules: CD1d and MHC class I (MHC I) for MIR1; B7-2, ICAM-1, CD1d, and MHC I for MIR2; MHC I for mK3; MHC I, CD4, and Fas for m153R (3, 5, 9 -12).…”

AIDS-associated Kaposi's sarcoma: Is there still a role for interferon alfa?

“…Many of the proteins encoded by HHV-8 may also inhibit immune responses to the virus. For example, vFLIP blocks cytotoxic T-cell killing of HHV-8-infected cells by inhibiting Fas activation [43]; vMIP-II may restrict recruitment of Th1 lymphocytes to HHV-8-infected cells [44]; K1 may prevent class 2 MHC-mediated T cell activation by HHV-8 [45]; and K3 and K5 block cell surface display of class 1 MHC molecules on the cell surface [46]. Although the majority of cells within KS lesions show latent infection, a small subset expresses lytic cycle genes [47] and produce viral progeny [48].…”

The pleiotropic effects of Kaposi's sarcoma herpesvirus

“…The vIRF1 protein has not been detected in KS lesions by immunohistochemistry thus far [62], but this may be due to antibody sensitivity. As assessed by in situ hybridization, expressed viral genes include the major capsid protein encoded by orf 25 [114]; the viral homologue of a G-protein coupled receptor, vGCR [115]; orf K3/MIR1, encoding a membrane protein involved in the down-regulation of MHC class I molecules from the surface of infected cells [116,117]; as well as orf K8/kbZIP, which inhibits entry into S-phase by stabilizing p21 CIP1 [118]. In addition, the non-coding nuclear T1.1 transcript is expressed in cells undergoing lytic replication [114,115].…”