Letter from John C. Brewer to Emma Davis. The first part discusses mutual acquaintances, and John's wishes that Emma will not forget their memories together.  The second part, dated for "Wednesday eve", discusses his and Miss Genie's relationship, what Miss Genie thinks of Emma, and Emma not feeling well

Szymula, Agnieszka

Palermo, Richard D

Bayoumy, Amr

Groves, Ian

Ba Abdullah, Mohammed

Holder, Beth

White, Robert E

Brewer, John C.

Portal to Texas History

[Letter from John C. Brewer to Emma Davis, June 4, 1879]

Letter from John C. Brewer to Emma Davis discussing the ending of his relationship with Miss Genie, finding time off to visit Emma, Emma feeling ill, and John's wishes for Emma to make a hair wreath for him

[Letter from John C. Brewer to Emma Davis, June 18, 1879]

The Epstein-Barr virus (EBV) nuclear antigen leader protein (EBNA-LP) is the first viral latency-associated protein produced after EBV infection of resting B cells. Its role in B cell transformation is poorly defined, but it has been reported to enhance gene activation by the EBV protein EBNA2 in vitro. We generated EBNA-LP knockout (LPKO) EBVs containing a STOP codon within each repeat unit of internal repeat 1 (IR1). EBNA-LP-mutant EBVs established lymphoblastoid cell lines (LCLs) from adult B cells at reduced efficiency, but not from umbilical cord B cells, which died approximately two weeks after infection. Adult B cells only established EBNA-LP-null LCLs with a memory (CD27+) phenotype. Quantitative PCR analysis of virus gene expression after infection identified both an altered ratio of the EBNA genes, and a dramatic reduction in transcript levels of both EBNA2-regulated virus genes (LMP1 and LMP2) and the EBNA2-independent EBER genes in the first 2 weeks. By 30 days post infection, LPKO transcription was the same as wild-type EBV. In contrast, EBNA2-regulated cellular genes were induced efficiently by LPKO viruses. Chromatin immunoprecipitation revealed that EBNA2 and the host transcription factors EBF1 and RBPJ were delayed in their recruitment to all viral latency promoters tested, whereas these same factors were recruited efficiently to several host genes, which exhibited increased EBNA2 recruitment. We conclude that EBNA-LP does not simply co-operate with EBNA2 in activating gene transcription, but rather facilitates the recruitment of several transcription factors to the viral genome, to enable transcription of virus latency genes. Additionally, our findings suggest that EBNA-LP is essential for the survival of EBV-infected naïve B cells

Groves, Ian J

Apollo (Cambridge)

English