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Knockout of Epstein-Barr virus BPLF1 retards B-cell transformation and lymphoma formation in humanized mice.

Whitehurst CB, Li G, Montgomery SA, Montgomery ND, Su L, Pagano JS - MBio (2015)

Bottom Line: EBV also causes aggressive lymphomas in individuals with acquired and innate immune disorders and is strongly associated with diffuse large B-cell lymphomas, classical Hodgkin lymphoma, Burkitt lymphoma, and nasopharyngeal carcinoma (NPC).Typically, EBV initially infects epithelial cells in the oropharynx, followed by a lifelong persistent latent infection in B-cells, which may develop into lymphomas in immunocompromised individuals.Currently, there is no efficacious treatment for EBV, and therapeutic targeting of BPLF1 may lead to a new path to treatment for immunocompromised individuals or transplant recipients infected with EBV.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA cbwhiteh@med.unc.edu.

No MeSH data available.


Related in: MedlinePlus

Increased proliferation in lymphoma region of spleens of infected mice with tumors. (A) Mice containing tumors showed increased rates of proliferation as determined by staining spleen sections with the proliferation marker Ki67. There were not significant differences between WT and DUB KO virus-infected tissue samples. (B) Ki67-positive cells from the tumor region were counted and graphed as percentages of total cells. The entire sample of negative control 2 was used for Ki67 staining.
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fig7: Increased proliferation in lymphoma region of spleens of infected mice with tumors. (A) Mice containing tumors showed increased rates of proliferation as determined by staining spleen sections with the proliferation marker Ki67. There were not significant differences between WT and DUB KO virus-infected tissue samples. (B) Ki67-positive cells from the tumor region were counted and graphed as percentages of total cells. The entire sample of negative control 2 was used for Ki67 staining.

Mentions: To determine if there were differences in proliferation rates of lymphomas of mice infected with WT or deltaBPLF1 virus, sections of spleen were stained for the proliferation marker Ki67 (Fig. 7A). In contrast to the negative control, cellular proliferation in infected mice is greatly increased in WT4, WT5, and DUB KO3, as expected. Visually, it appeared that DUB KO3 had slightly less Ki67 staining, suggesting that the lymphoma produced by infection with DUB KO virus proliferates more slowly. To see if this were the case, Ki67-positive cells were counted over the entire tumor region. Examination determined that Ki67 staining was relatively constant over the entire tumor area, indicating that tumors formed with DUB KO virus (in this one instance) did not proliferate more slowly than those formed with WT EBV (Fig. 7B). A summary of data from infected mice is provided in Table 1.


Knockout of Epstein-Barr virus BPLF1 retards B-cell transformation and lymphoma formation in humanized mice.

Whitehurst CB, Li G, Montgomery SA, Montgomery ND, Su L, Pagano JS - MBio (2015)

Increased proliferation in lymphoma region of spleens of infected mice with tumors. (A) Mice containing tumors showed increased rates of proliferation as determined by staining spleen sections with the proliferation marker Ki67. There were not significant differences between WT and DUB KO virus-infected tissue samples. (B) Ki67-positive cells from the tumor region were counted and graphed as percentages of total cells. The entire sample of negative control 2 was used for Ki67 staining.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
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getmorefigures.php?uid=PMC4620474&req=5

fig7: Increased proliferation in lymphoma region of spleens of infected mice with tumors. (A) Mice containing tumors showed increased rates of proliferation as determined by staining spleen sections with the proliferation marker Ki67. There were not significant differences between WT and DUB KO virus-infected tissue samples. (B) Ki67-positive cells from the tumor region were counted and graphed as percentages of total cells. The entire sample of negative control 2 was used for Ki67 staining.
Mentions: To determine if there were differences in proliferation rates of lymphomas of mice infected with WT or deltaBPLF1 virus, sections of spleen were stained for the proliferation marker Ki67 (Fig. 7A). In contrast to the negative control, cellular proliferation in infected mice is greatly increased in WT4, WT5, and DUB KO3, as expected. Visually, it appeared that DUB KO3 had slightly less Ki67 staining, suggesting that the lymphoma produced by infection with DUB KO virus proliferates more slowly. To see if this were the case, Ki67-positive cells were counted over the entire tumor region. Examination determined that Ki67 staining was relatively constant over the entire tumor area, indicating that tumors formed with DUB KO virus (in this one instance) did not proliferate more slowly than those formed with WT EBV (Fig. 7B). A summary of data from infected mice is provided in Table 1.

Bottom Line: EBV also causes aggressive lymphomas in individuals with acquired and innate immune disorders and is strongly associated with diffuse large B-cell lymphomas, classical Hodgkin lymphoma, Burkitt lymphoma, and nasopharyngeal carcinoma (NPC).Typically, EBV initially infects epithelial cells in the oropharynx, followed by a lifelong persistent latent infection in B-cells, which may develop into lymphomas in immunocompromised individuals.Currently, there is no efficacious treatment for EBV, and therapeutic targeting of BPLF1 may lead to a new path to treatment for immunocompromised individuals or transplant recipients infected with EBV.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA cbwhiteh@med.unc.edu.

No MeSH data available.


Related in: MedlinePlus