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M Rowe

Publications and source records attributed to M Rowe.

At least 127 records · Page 7Linked to original sources
PubMed1990

Rose hips: a new occupational allergen.

We evaluated 13 workers with respiratory symptoms apparently related to occupational exposure to powdered rose hips. Nine workers had asthma, five had rhinitis, and one worker had urticaria. Seven workers had evidence of IgE specific for rose hips based on positive skin prick tests and positive in vitro tests. Four workers with histories suggestive of asthma related to work exposure underwent bronchopulmonary challenges with rose hips, and two workers had positive challenges with greater than 20% declines in FEV1 measurements. We conclude that rose hips are occupational allergens capable of producing asthma.

Adult↗
PubMed1990

Human cytotoxic T-cell responses against Epstein-Barr virus nuclear antigens demonstrated by using recombinant vaccinia viruses.

The potentially pathogenic effects of infection with Epstein-Barr virus (EBV), a B-lymphotropic agent with cell growth-transforming potential, are contained in healthy virus carriers by virus-specific cytotoxic T-lymphocyte (CTL) surveillance. The target antigens against which such CTL responses are directed are yet undefined, but the antigens probably derived from one or more of the EBV "latent" proteins constitutively expressed in virus-transformed B cells. We have analyzed target specificity of CTL responses from two EBV-immune donors that are preferentially reactive against autologous cells transformed with type A but not with type B virus isolates. Coding sequences for four EBV latent proteins with allelic polymorphism between A and B virus types--namely, the EBV nuclear antigens (EBNAs) EBNA 2, EBNA 3a, EBNA 3c, and EBNA leader protein--have been introduced into vaccinia virus vectors under control of vaccinia promoter P7.5 and used to express relevant EBNA proteins in appropriate target cells. Thus the CTL response from one donor has been mapped to type A EBNA 2 protein and from a second donor to type A EBNA 3a protein. Thereafter, a series of recombinant vaccinia viruses were constructed that carried specific internal deletions within the EBNA 2 type A coding sequence; by using these vectors, the above EBNA 2 type A-specific CTL response was shown to be directed against an epitope within a 100-amino acid fragment near the N terminus of the protein. This work clearly shows human CTL recognition of virus-coded nuclear antigens in the EBV system; moreover, it establishes an experimental approach that can be extended to all EBV latent proteins and to the more common CTL responses that cross-react against type A and type B virus isolates.

Antigens, Viral↗
PubMed1990

Different Epstein-Barr virus-B cell interactions in phenotypically distinct clones of a Burkitt's lymphoma cell line.

Epstein-Barr virus (EBV)-positive Burkitt's lymphoma (BL) biopsy cells and early passage BL cell lines have been reported as showing an unusual type of virus-cell interaction; at least two EBV latent proteins appear not to be expressed. Serial passage of such lines is often accompanied by a broadening of virus latent gene expression and a corresponding change in the cell surface/growth phenotype towards that shown by in vitro transformed lymphoblastoid cell lines (LCLs). The sequence of events, both viral and cellular, involved in this transition needs to be defined properly. In the present work, phenotypically distinct cell clones have been derived from early passage cultures of a BL cell line in phenotypic transition, thereby giving access to relatively stable cell populations through which the different EBV-B cell interactions within the parental line can be studied. Clones retaining the original BL biopsy cell phenotype (CD10/CD77-positive, activation antigen/adhesion molecule-negative) expressed the virus-encoded nuclear antigen EBNA 1 but not any of the other known latent proteins, EBNAs 2, 3a, 3b, 3c, -LP and latent membrane protein (LMP). Other clones which had developed an LCL-like phenotype (CD10/CD77-negative, activation antigen/adhesion molecule-positive) now expressed all the above latent proteins and also contained significant numbers of cells in lytic cycle. Phenotypic change occurring within the parental BL cell line itself was initiated in a small subpopulation of cells in which the virus-encoded proteins EBNA 2 and LMP were transiently induced to an unusually high level of expression; this was accompanied by the first detectable changes in cell surface phenotype, namely the increase of cellular adhesion molecules. Some control over EBNA 2/LMP expression then appeared to be re-imposed since the presumed clonal descendents of these cells stably expressed EBNA 2 and LMP at much reduced levels typical of those seen in conventional LCLs.

Antigens, Surface↗
PubMed1990

Epstein-Barr virus nuclear antigen 2 induces expression of the virus-encoded latent membrane protein.

Infection of Epstein-Barr virus-negative human B-lymphoma cell lines with the fully transforming B95.8 Epstein-Barr virus strain was associated with complete virus latent gene expression and a change in the cell surface and growth phenotype toward that of in vitro-transformed lymphoblastoid cell lines. In contrast, the cells infected with the P3HR1 Epstein-Barr virus strain, a deletion mutant that cannot encode Epstein-Barr nuclear antigen 2 (EBNA2) or a full-length EBNA-LP, expressed EBNAs1, 3a, 3b, and 3c but were negative for the latent membrane protein (LMP) and showed no change in cellular phenotype. This suggests that EBNA2 and/or EBNA-LP may be required for subsequent expression of LMP in Epstein-Barr virus-infected B cells. Recombinant vectors capable of expressing the B95.8 EBNA2A protein were introduced by electroporation into two P3HR1-converted B-lymphoma cell lines, BL30/P3 and BL41/P3. In both cases, stable expression of EBNA2A was accompanied by activation of LMP expression from the resident P3HR1 genome; control transfectants that did not express the EBNA2A protein never showed induction of LMP. In further experiments, a recombinant vector capable of expressing the full-length B95.8 EBNA-LP was introduced into the same target lines. Strong EBNA-LP expression was consistently observed in the transfected clones but was never accompanied by induction of LMP. The EBNA2A gene transfectants expressing EBNA2A and LMP showed a dramatic change in cell surface and growth phenotype toward a pattern like that of lymphoblastoid cell lines; some but not all of these changes could be reproduced in the absence of EBNA2A by transfection of P3HR1-converted cell lines with a recombinant vector expressing LMP. These studies suggest that EBNA2 plays an important dual role in the process of B-cell activation to the lymphoblastoid phenotype; the protein can have a direct effect upon cellular gene expression and is also involved in activating the expression of a second virus-encoded effector protein, LMP.

Antigens, Viral↗
PubMed1990

Epstein-Barr virus latent membrane protein (LMP1) and nuclear proteins 2 and 3C are effectors of phenotypic changes in B lymphocytes: EBNA-2 and LMP1 cooperatively induce CD23.

Latent Epstein-Barr virus (EBV) infection and growth transformation of B lymphocytes is characterized by EBV nuclear and membrane protein expression (EBV nuclear antigen [EBNA] and latent membrane protein [LMP], respectively). LMP1 is known to be an oncogene in rodent fibroblasts and to induce B-lymphocyte activation and cellular adhesion molecules in the EBV-negative Burkitt's lymphoma cell line Louckes. EBNA-2 is required for EBV-induced growth transformation; it lowers rodent fibroblast serum dependence and specifically induces the B-lymphocyte activation antigen CD23 in Louckes cells. These initial observations are now extended through an expanded study of EBNA- and LMP1-induced phenotypic effects in a different EBV-negative B-lymphoma cell line, BJAB. LMP1 effects were also evaluated in the EBV-negative B-lymphoma cell line BL41 and the EBV-positive Burkitt's lymphoma cell line, Daudi (Daudi is deleted for EBNA-2 and does not express LMP). Previously described EBNA-2- and LMP1-transfected Louckes cells were studied in parallel. EBNA-2, from EBV-1 strains but not EBV-2, induced CD23 and CD21 expression in transfected BJAB cells. In contrast, EBNA-3C induced CD21 but not CD23, while no changes were evident in vector control-, EBNA-1-, or EBNA-LP-transfected clones. EBNAs did not affect CD10, CD30, CD39, CD40, CD44, or cellular adhesion molecules. LMP1 expression in all cell lines induced growth in large clumps and expression of the cellular adhesion molecules ICAM-1, LFA-1, and LFA-3 in those cell lines which constitutively express low levels. LMP1 expression induced marked homotypic adhesion in the BJAB cell line, despite the fact that there was no significant increase in the high constitutive BJAB LFA-1 and ICAM-1 levels, suggesting that LMP1 also induces an associated functional change in these molecules. LMP1 induction of these cellular adhesion molecules was also associated with increased heterotypic adhesion to T lymphocytes. The Burkitt's lymphoma marker, CALLA (CD10), was uniformly down regulated by LMP1 in all cell lines. In contrast, LMP1 induced unique profiles of B-lymphocyte activation antigens in the various cell lines. LMP1 induced CD23 and CD39 in BJAB; CD23 in Louckes; CD39 and CD40 in BL41; and CD21, CD40, and CD44 in Daudi. In BJAB, CD23 surface and mRNA expression were markedly increased by EBNA-2 and LMP1 coexpression, compared with EBNA-2 or LMP1 alone. This cooperative effect was CD23 specific, since no such effect was observed on another marker, CD21.(ABSTRACT TRUNCATED AT 400 WORDS)

Antigens, CD↗
PubMed1990

Frequent fallers. Leading groups to identify psychological factors.

CNAs might be good leaders for groups of frequent fallers for several reasons, two of which are that they provide hands-on care and they know the residents well. Residents who fall frequently do not see themselves as persons who fall; they slip, trip, or slide. Single fallers explore ways to prevent another fall. Residents attempting to "do for themselves" and thus maintain their highly-prized independence is a factor contributing to falls. Preservation of autonomy and self-esteem are co-factors. Denial and independence in the faller need to be identified, supported as strengths, and incorporated into a resident's plan of care.

Accident Proneness↗
PubMed1990

Sjögren's syndrome after infection by Epstein-Barr virus.

We describe a case in which infection with Epstein-Barr virus in a middle aged woman was followed by the development of Sjögren's syndrome with systemic features and high titers of antinuclear antibodies. Humoral and cell mediated immune responses to the virus appeared normal. It is suggested that in this case, Sjögren's syndrome resulted from a failure to control these initially appropriate responses.

Antibodies, Antinuclear↗
PubMed1989

The Epstein-Barr virus:host balance in acute infectious mononucleosis patients receiving acyclovir anti-viral therapy.

This report describes the first of 2 investigations studying mechanisms of Epstein-Barr virus (EBV) persistence in the infected host; specifically, we wish to determine the extent to which virus carriage within the B-cell system is dependent upon continued replication of the virus in permissive oropharyngeal epithelium. Levels of EBV infection at these 2 sites have been monitored in 21 acute infectious mononucleosis (IM) patients before, during and after treatment with high doses of acyclovir (ACV). Twelve patients received oral ACV for 10 days and 9 patients received i.v. ACV for 5 days before the 10-day oral course; all were followed prospectively for 28 days. Infectious EBV, detectable at high initial levels in the patients' throat washings, disappeared almost completely during ACV treatment, then returned again to high levels post treatment. In contrast, levels of virus-infected B cells in the blood showed no reduction linked to the period of ACV treatment nor any increase with resumption of EBV shedding. During IM, therefore, maintenance of high levels of virus carriage within the B-cell pool is not dependent upon the continual recruitment of newly infected B cells. This might reflect an inability of the immune T-cell response in acute IM patients to prevent continued expansion of the existing EBV-infected B-cell pool. Alternatively, it raises the possibility that EBV carriage in B cells in vivo is maintained through a virus:cell interaction which is not sensitive to virus-specific T-cell surveillance.

Acyclovir↗
PubMed1989

Epstein-Barr virus-infected B cells persist in the circulation of acyclovir-treated virus carriers.

In this study, infectious Epstein-Barr virus (EBV) shedding in the oropharynx and numbers of virus-infected B cells in the blood have been monitored in long-term virus carriers receiving acyclovir (ACV) therapy for herpes zoster. Eleven patients on oral ACV were followed prospectively before, during and for 2 weeks after treatment. As expected, the low levels of EBV shedding in these virus carriers (measured as cord-blood lymphocyte transforming activity in throat washings) were eliminated during the period of ACV treatment and returned at later times. Over the same period, however, the frequency of virus-infected B cells in the blood (measured by spontaneous transformation in limiting dilution assay) remained completely unchanged. Regression assays showed that these same patients had normal levels of EBV-specific cytotoxic T-cell immunity, so that the in vivo persistence of virus-infected B cells could not be ascribed to a defect in T-cell surveillance. We infer that the in vivo half-life of the virus-infected B-cell pool in long-term virus carriers is measured in months rather than days. We further suggest that such persistence requires a novel form of virus:B-cell interaction distinct from the type of "latent" infection displayed by in vitro-transformed cells.

Acyclovir↗
PubMed1989

Distinction between Epstein-Barr virus type A (EBNA 2A) and type B (EBNA 2B) isolates extends to the EBNA 3 family of nuclear proteins.

The Epstein-Barr virus (EBV) nuclear antigens EBNA 3a, 3b, and 3c have recently been mapped to adjacent reading frames in the BamHI L and E fragments of the B95.8 EBV genome. We studied by immunoblotting the expression of the family of EBNA 3 proteins in a panel of 20 EBV-transformed lymphoblastoid cell lines (LCLs) carrying either type A (EBNA 2A-encoding) or type B (EBNA 2B-encoding) virus isolates. Certain human sera from donors naturally infected with type A isolates detected the EBNA 3a, 3b, and 3c proteins in all type A virus-transformed LCLs (with a single exception in which EBNA 3b was not detected) but detected only EBNA 3a in LCLs carrying type B isolates. These results were confirmed with human and murine antibodies with specific reactivity against sequences of the type A EBNA 3a, 3b, or 3c expressed in bacterial fusion proteins. Conversely, selected human sera from donors naturally infected with type B strains of EBV identified the EBNA 3a encoded by both types of isolates plus two novel EBNAs present only in type B, and not in type A, virus-transformed LCLs; these novel proteins appear to be the type B homologs of EBNA 3b and 3c. The distinction between type A and type B EBV isolates therefore extends beyond the EBNA 2 gene to the EBNA 3 family of proteins. This has important implications with respect to the evolutionary origin of these two EBV types and also places in a new light recent studies which identified differences between type A and type B transformants in terms of growth phenotype (A. B. Rickinson, L. S. Young, and M. Rowe, J. Virol. 61:1310-1317, 1987) and of detection by EBV-specific cytotoxic T cells (D. J. Moss, I. S. Misko, S. R. Burrows, K. Burman, R. McCarthy, and T. B. Sculley, Nature [London] 331:719-721, 1988).

Antibodies, Monoclonal↗
PubMed1989

Multivisceral intestinal transplantation: surgical pathology.

We report the diagnostic surgical pathology of two children who underwent multivisceral abdominal transplantation and survived for 1 month and 6 months. There is little relevant literature, and diagnostic criteria for the various clinical possibilities are not established; this is made more complicated by the simultaneous occurrence of more than one process. We based our interpretations on conventional histology, augmented with immunohistology, including HLA staining that distinguished graft from host cells in situ. In some instances functional analysis of T cells propagated from the same biopsies was available and was used to corroborate morphological interpretations. A wide spectrum of changes was encountered. Graft-versus-host disease, a prime concern before surgery, was not seen. Rejection was severe in 1 patient, not present in the other, and both had evidence of lymphoproliferative disease, which was related to Epstein-Barr virus. Bacterial translocation through the gut wall was also a feature in both children. This paper documents and illustrates the various diagnostic possibilities.

Antigens, Viral↗
PubMed1988

Expression of Epstein-Barr virus-encoded proteins in nasopharyngeal carcinoma.

Expression of the Epstein-Barr virus (EBV) encoded nuclear antigens (EBNA 1 to 6) and membrane-associated protein (LMP) was investigated by immunoblotting in 83 nasopharyngeal carcinoma (NPC) biopsies and 25 other tumor and normal tissue specimens from the head and neck region. Fifty-eight of the 83 NPC biopsies were large enough to yield parallel data on virus DNA and viral expression. All 16 cases of clinically diagnosed and histologically confirmed NPCs from North Africa contained EBV DNA and expressed EBNA-1. Of 31 clinically diagnosed NPCs from China, 29 contained EBV DNA and 25 of these expressed EBNA-1. One control tissue biopsy from the oropharynx of NPC patients contained EBV DNA, but none expressed EBNA-1. The latent membrane protein (LMP) was detected in 22/31 of the Chinese and in 10/16 of the North African NPC biopsies. None of the NPC biopsies or control tissues expressed detectable amounts of EBNA 2 or any of the other 4 nuclear antigens which are invariably expressed in EBV-transformed B cells. A smaller number of tumors from Malaysia and East Africa exhibited a similar pattern of expression. EBV was rescued from a nude-mouse-passaged North African NPC tumor by co-cultivation of the tumor cells with umbilical cord blood lymphocytes. The tumor expressed EBNA 1 and LMP, but not EBNA 2 or the other 4 EBNAs. The resulting LCLs expressed all 6 nuclear antigens, EBNA 1 to 6 and LMP. Our data suggest that expression of the EBV genome is regulated in a tissue-specific fashion.

Animals↗
PubMed1988

Isolation of a normal B cell subset with a Burkitt-like phenotype and transformation in vitro with Epstein-Barr virus.

Epstein-Barr virus (EBV) is causally linked with endemic Burkitt's lymphoma (BL), a tumor whose homogeneous cell surface phenotype suggests derivation from a particular subset of activated germinal centre B cells in vivo. Endemic BL also shows an unusual form of EBV infection with down-regulation of certain of the virus latent proteins which are constitutively expressed when EBV infects and transforms normal resting B cells in vitro. Here we question whether this virus:cell interaction is unique to malignant BL cells or whether it might be reproduced by in vitro infection of those particular germinal centre cells displaying the BL-like phenotype. Firstly, we show by biochemical means that a subset of normal tonsillar B cells does indeed express the globotriaosylceramide glycolipid BLA and the common acute lymphoblastic leukaemia antigen CALLA, 2 important markers of the BL phenotype. Secondly, using 2-colour immunofluorescence labelling with anti-BLA and anti-CALLA monoclonal antibodies (MAbs), 4 subsets of low buoyant density tonsillar B cells (BLA+ CALLA+, BLA+ CALLA-, BLA- CALLA+, BLA- CALLA-) have been separated by means of a FACS and tested for their susceptibility to EBV-induced growth transformation in a limiting dilution assay. The BLA+ CALLA+ (i.e., BL-like) subset contained the highest proportion of cells already actively in cycle in vivo and gave the lowest yield of transformants, perhaps reflecting the greater efficiency with which EBV transforms resting target cells. Of the cell lines established from the BLA+ CALLA+ population, a significant number retained BLA expression but CALLA was always lost. In 2 further respects, these lines resembled conventional in vitro transformants rather than lines of BL type; thus the cells expressed cellular "activation" antigens (CD23, CD39, CD30, Ki-24) characteristic of the lymphoblastoid phenotype and contained the full spectrum of EBV latent proteins.

Antigens, Differentiation↗
PubMed1988

The application of immunoassays and fluorometry to the detection of polycyclic hydrocarbon-macromolecular adducts and anti-adduct antibodies in humans.

The metabolic activation of polycyclic aromatic hydrocarbons (PAH) to chemical species that form covalent adducts with cellular macromolecules (DNA and protein) is central to theories of carcinogenesis. Assays are currently being developed that will accurately reflect human macromolecular exposure to these carcinogens. Immunoassays are capable of detecting low levels of PAH-DNA adducts and antibodies directed against these adducts in humans and HPLC/spectrophotofluorimetry allows the detection of carcinogen-DNA or carcinogen-protein adducts in human peripheral blood. Both types of method have inherent advantages and disadvantages, and the use of more than one type of corroborative assay is a feature in our work. Simplified but highly specific synchronous fluorescence spectra have been obtained for BP-tetrols after mild acid hydrolysis and HPLC of sample materials. When using a wavelength difference of 34 nm to drive the excitation and emission monochromators simultaneously, the pyrene fluorophore, when present, has a signature peak at 345 nm (excitation). The results of immunoassays demonstrate human exposure to PAH as a class of carcinogen, since serological cross-reactivity of antibodies does not limit detection in this system to a single chemical compound. In addition the formation in humans of anti-PAH-DNA antibodies has been shown, presumably in response to both past and present exposure to the parent compounds. In summary the results of each assay can indicate human exposure to PAH and have the potential for molecular dosimetry of this exposure.

Antibodies↗
PubMed1988

Characterization of the serological response in man to the latent membrane protein and the six nuclear antigens encoded by Epstein-Barr virus.

A total of 116 sera from healthy individuals and from patients with Burkitt's lymphoma (BL), nasopharyngeal carcinoma (NPC) or rheumatoid arthritis (RA) were studied with respect to antibody responses to each of the seven known transformation-associated Epstein-Barr virus (EBV)-encoded antigens [latent membrane protein (LMP) and six nuclear proteins (EBNAs 1 to 6)]. The antibodies were detected using modified standard immunoblotting techniques. Antibodies to LMP were detected for the first time in sera from 6/27 (22%) healthy, EBV-immune individuals (seropositive for the viral capsid antigens). An increased incidence of anti-LMP antibodies was found in EBV-immune sera from patients with BL (17/24 positive; 71%), NPC (21/33; 64%), and RA (16/21; 76%). Antibodies to EBNA 1 were detected in all EBV-immune sera at a standard 1:20 dilution. Antibodies to the other EBNAs were detected in only a proportion of these sera (20 to 95%) at the same dilution. Only minor disease-associated differences in the incidence of these antibodies were observed, the most consistent being that RA sera had a higher incidence of antibodies to EBNAs 2 to 6 compared with healthy controls. Testing of the sera at a 1:100 dilution suggested that there were some disease-related differences in the titres of anti-EBNA antibodies. At this serum dilution, a reduced incidence of antibodies to EBNA 2 was seen in NPC (6/31) compared with RA (18/19) and healthy EBV-seropositives (16/26); antibodies to EBNA 3 were detected at an increased incidence in BL (8/15) and NPC (16/31) compared with control sera (7/26); antibodies to EBNA 4 were detected at increased incidence in BL (5/15) and RA (6/19) compared with control sera (1/26); and antibodies to EBNA 6 were detected at increased incidence in NPC (19/31) and RA (7/19) compared with control sera (3/26).

AIDS-Related Complex↗
PubMed1988

Epstein-Barr virus-specific cytotoxic T-cell recognition of transfectants expressing the virus-coded latent membrane protein LMP.

Cytotoxic T cells from Epstein-Barr virus (EBV)-immune individuals specifically kill EBV-transformed B cells from HLA class I antigen-matched donors even though the latently infected cells express only a restricted set of virus genes. The virus-induced target antigens recognized by these immune T cells have not been identified. In our experiments, EBV DNA sequences encoding the virus latent gene products Epstein-Barr nuclear antigen (EBNA)1, EBNA 2, and EBNA-LP and the latent membrane protein (LMP) were individually expressed in a virus-negative human B-lymphoma cell line, Louckes. Transfected clones expressing LMP were killed by EBV-specific cytotoxic T-cell preparations from each of three virus-immune donors HLA matched with Louckes through HLA-A2, B44 antigens; control transfectants or clones expressing one of the EBNA proteins were not recognized. Expression of LMP in a second virus-negative B-cell line, BL41, sensitized these cells to EBV-specific cytolysis restricted through the HLA-A11 antigen. To distinguish between the viral protein and an induced human B-cell activation antigen as the target for T-cell recognition, LMP was then expressed in a murine mastocytoma cell line, P815-A11-restricted human T cells. The LMP-expressing P815-A11 transfectants were susceptible to lysis by EBV-specific cytotoxic T cells from three HLA-A11-positive individuals. Both Louckes and P815-A11 cells were also transfected with constructs capable of encoding a truncated form of LMP (Tr-LMP) which lacks the N-terminal 128 amino acids of the full-length protein. Tr-LMP-expressing transfectants were not recognized by the above T-cell preparations. The results suggest that LMP, and, in particular, epitopes derived from the N-terminal region of the protein, provides one of the target antigens for the EBV-induced human cytotoxic T-cell response.

Animals↗
PubMed1988

Different patterns of Epstein-Barr virus gene expression and of cytotoxic T-cell recognition in B-cell lines infected with transforming (B95.8) or nontransforming (P3HR1) virus strains.

Epstein-Barr virus (EBV)-negative Burkitt's lymphoma (BL) cell lines have been converted to EBV genome positivity by in vitro infection with the transforming EBV strain B95.8 and with the nontransforming mutant strain P3HR1, which has a deletion in the gene encoding the nuclear antigen EBNA2. These B95.8- and P3HR1-converted lines have been compared for their patterns of expression of EBV latent genes (i.e., those viral genes constitutively expressed in all EBV-transformed lines of normal B-cell origin) and for their recognition by EBV-specific cytotoxic T lymphocytes (CTLs), in an effort to identify which latent gene products provide target antigens for the T-cell response. B95.8-converted lines on several different EBV-negative BL-cell backgrounds all showed detectable expression of the nuclear antigens EBNA1, EBNA2, and EBNA3 and of the latent membrane protein (LMP); such converts were also clearly recognized by EBV-specific CTL preparations with restriction through selected human leukocyte antigen (HLA) class I antigens on the target cell surface. The corresponding P3HR1-converted lines (lacking an EBNA2 gene) expressed EBNA1 and EBNA3 but, surprisingly, showed no detectable LMP; furthermore, these converts were not recognized by EBV-specific CTLs. Such differences in T-cell recognition were not due to any differences in expression of the relevant HLA-restricting determinants between the two types of convert, as shown by binding of specific monoclonal antibodies and by the susceptibility of both B95.8 and P3HR1 converts to allospecific CTLs directed against these same HLA molecules. The results suggest that in the normal infectious cycle, EBNA2 may be required for subsequent expression of LMP and that both EBNA2 and LMP (but not EBNA1 or EBNA3) may provide target antigens for the EBV-specific T-cell response.

Antigens, Viral↗