B cell activation by the nontransforming P3HR‐1 substrain of the Epstein‐Barr virus (EBV)

Hu, Cheng-Po; Åman, Pierre; Masucci, Maria G.; Klein, Eva; Klein, George

doi:10.1002/eji.1830160720

Cited by 17 publications

(9 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Triggering of BCGF responsiveness was observed over a wide range of virus dilutions. The effect was smaller compared to that induced by anti-IgM antibodies (not shown), but comparable to that induced by P3HR1 virus [9] and F(ab')* anti-gpl40 antibodies ~7 1 . that this interaction can provide an inhibitory signal for cell proliferation [33].…”

Section: Bcgf Responsiveness Induced By Uv-inactivated Ebvsupporting

confidence: 43%

See 1 more Smart Citation

Activation of B lymphocytes by Epstein‐Barr virus/CR2 receptor interaction

et al. 1987

Self Cite

View full text Add to dashboard Cite

Epstein-Barr virus (EBV) infects and transforms human B lymphocytes. The virus receptor was shown to be identical to the complement receptor CR2. The consequences of EBV/CR2 receptor interaction on B lymphocyte activation were analyzed by infection of B cells with the transforming (B95-8) and the nontransforming (P3HR1) virus strains and with UV-inactivated B95-8 virus. Similar to mitogens and antibodies against surface IgM and CR2 receptor, transforming and nontransforming EBV induced the release of leukocyte migration inhibitory factor (LIF). LIF production occurred early after infection and was not affected by irradiation of the B95-8 virus with doses of UV-light which prevented the expression of viral functions. B lymphocytes infected with UV-inactivated virus responded to T cell-derived B cell growth factors. The results demonstrate that binding of EBV to the CR2 receptor activates the B cells. Progression of the infected cells in the activation pathway required helper cell-derived factors or signals provided by the intact viral genome. The nontransforming P3HR1 virus induced a low level of RNA synthesis and increase of cell size and major histocompatibility complex class I antigen expression. Only the transforming virus induced expression of EBV nuclear antigens and cellular DNA synthesis.

show abstract

Section: Bcgf Responsiveness Induced By Uv-inactivated Ebvsupporting

confidence: 43%

“…Our results demonstrate that B lymphocyte infected with nontransforrning UV-inactivated B95-8 virus and P3HR1 virus [9] became responsive to T cell-derived growth factors. Mouse B cells, operationally defined as resting on the basis of their small size and low RNA content, were shown to respond to BCGF [41,421.…”

Section: Discussionmentioning

confidence: 90%

Activation of B lymphocytes by Epstein‐Barr virus/CR2 receptor interaction

et al. 1987

Self Cite

View full text Add to dashboard Cite

show abstract

“…Indeed, we have shown previously that simple virus binding to the B cell is sufficient to induce a rapid phenotypic shift away from IgD expression in resting B cells. Irradiated, non‐transforming virions were also effective in bringing about such change 15 …”

Section: Discussionmentioning

confidence: 99%

“…Irradiated, non-transforming virions were also effective in bringing about such change. 15 Thorley-Lawson has suggested that the naõ Ève B cell constitutes the primary target for EBV infection and that the subsequently transformed lymphoblast then follows the normal differentiation pathway engaged during a T-dependent antigen response, eventually becoming a long-lived memory cell. 16 This is partly based on the analysis of different subpopulations isolated from tonsil.…”

Section: Ebv Infects and Establishes Lifelong Latency In B Lymphocytesmentioning

confidence: 99%

B‐lymphocyte subpopulations are equally susceptible to Epstein–Barr virus infection, irrespective of immunoglobulin isotype expression

2003

Self Cite

View full text Add to dashboard Cite

SUMMARYWhile Epstein±Barr virus (EBV) is known to establish latency in the memory B-cell compartment, there is controversy as to whether the memory or the naõ Ève B cell is the initial target for infection. Here we have explored the infectability of the B-cell subsets contained in peripheral blood and tonsils, as distinguished by their surface expression of the immunoglobulin isotypes that help to de®ne naõ Ève and memory pools. First we show that both CD21 and major histocompatibility complex (MHC) class II molecules ± respectively, the major receptor and co-receptor for EBVon B cells ± are expressed at similar levels on blood and tonsillar B cells, irrespective of surface immunoglobulin class, indicating that each of the subsets demonstrate an equal potential, at least for infection. Then, following in vitro infection of total tonsillar B cells, we found that the relative frequencies of immunoglobulin (Ig)M-, IgG-and IgA-positive cells containing EBV-encoded Epstein±Barr virus nuclear antigen 5 (EBNA5) protein at 48 hr were similar to those of the starting population. However, IgD expression was uniformly decreased, probably as a consequence of cellular activation. These data indicate that recirculating B cells have both the potential for, and susceptibility to, initial infection by EBV, irrespective of the immunoglobulin isotype expressed.

show abstract

“…EBNA 2 and 5 may play an important role in the early activation of B cells during primary EBV infection Moss et al, 1986;Dillner et al, 1986;Finke et a/., 1987) and in the transformation of B cells. Virus variants that have deletions in the sequences corresponding to the EBNA 2 gene and part of the EBNA 5 gene can partially activate B cells (Hu et al, 1986) but are incapable of transforming B cells (Menezes et al, 1975;Jones et al, 1984;Ernberg et al, 1986). EBNA 2 has also been implied in the regulation of differentiated B-cell functions Cohen et independent of other EBNAs and that EBNA 1 is the only Wang et al, 1987~).…”

Section: Discussionmentioning

confidence: 99%

Expression of Epstein‐Barr virus‐encoded proteins in nasopharyngeal carcinoma

Fåhræus

Ernberg

et al. 1988

Intl Journal of Cancer

Self Cite

417

246

View full text Add to dashboard Cite

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.

show abstract

B cell activation by the nontransforming P3HR‐1 substrain of the Epstein‐Barr virus (EBV)

Cited by 17 publications

References 35 publications

Activation of B lymphocytes by Epstein‐Barr virus/CR2 receptor interaction

Activation of B lymphocytes by Epstein‐Barr virus/CR2 receptor interaction

B‐lymphocyte subpopulations are equally susceptible to Epstein–Barr virus infection, irrespective of immunoglobulin isotype expression

Expression of Epstein‐Barr virus‐encoded proteins in nasopharyngeal carcinoma

Contact Info

Product

Resources

About