SEARCH FOR HERPES SIMPLEX VIRUS TYPE2（HSV－2）AND HUMAN PAPILLOMAVIRUS（HPV）IN THE NORMAL AND ABNORMAL CERVICAL SAMPLES

ＳＥＡＲＣＨＦＯＲＨＥＲＰＥＳＳＩＭＰＬＥＸＶＩＲＵＳＴＹＰＥ２（ＨＳＶ－２）ＡＮＤＨＵＭＡＮＰＡＰＩＬＬＯＭＡＶＩＲＵＳ（ＨＰＶ）ＩＮＴＨＥＮＯＲＭＡＬＡＮＤＡＢＮＯＲＭＡＬＣＥＲＶＩＣＡＬＳＡＭＰＬＥＳＺｈａｎｇＷｅｉ;张伟;ＪｉｎＳｈｕｎｑｉａ...     

PATHOLOGICAL STUDIES ON THE ANTI－INVASIVE CHARACTER BY RECOMBINANT HUMAN INTERLEUKIN－6 GENE－TRANSFECTED MOUSE LEUKEMIA CELLS

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The Paper Symposium on PLC VIRAL HEPATITIS（HBV AND HCV）BACKGROUND IN CHINESE PATIENTS WITH HEPATOCELLULAR CARCINOMA

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PROMOTION OF IN VITRO GROWTH OF HUMAN MEDULLOBLASTOMA CELLS BY EXOGENEOUS IL－6

ＰＲＯＭＯＴＩＯＮＯＦＩＮＶＩＴＲＯＧＲＯＷＴＨＯＦＨＵＭＡＮＭＥＤＵＬＬＯＢＬＡＳＴＯＭＡＣＥＬＬＳＢＹＥＸＯＧＥＮＥＯＵＳＩＬ－６ＬｉｕＪｉａｉ刘佳；ＬｉＨｏｎｇ李宏；ＨａｍｏｕＭａｒｉｅ－Ｆｒａｎｃｅ；ＮｉｃｏｌａｓｄｅＴｒｉｂｏｌｅｔ（１Ｄｉ...     

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THE CERVIX MULTI－VIRUSES INFECTION AND THE DEVELOPMENT OF CERVICAL CARCINOMAS

ＴＨＥＣＥＲＶＩＸＭＵＬＴＩ－ＶＩＲＵＳＥＳＩＮＦＥＣＴＩＯＮＡＮＤＴＨＥＤＥＶＥＬＯＰＭＥＮＴＯＦＣＥＲＶＩＣＡＬＣＡＲＣＩＮＯＭＡＳＺｈａｎｇＷｅｉ张伟；ＪｉｎＳｎｕｎｑｉａｎ金顺钱；ＬｉｕＢｏｑｉ刘伯齐；ＬｉａｎｓＸｉａｏ梁肖；ＭｉｎｇＬｉｈｕ...     

TWO－STAGE RESECTION FOR ADVANCED HEPATOCELLULAR CARCINOMA─PRELIMINARY RESULTS OF 16 CASES

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ADENOSQUAMOUS CARCINOMA OF THE NASOPHARYNX CONTAININGEB VIRUS，APROPOS OF A CASE

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ＡＤＹＮＡＭＩＣＳＴＵＤＹＯＦＴＨＥＣＹＴＯＴＯＸＩＣＥＦＦＥＣＴＳＯＦＨＹＰＥＲＴＨＥＲＭＩＡＣＯＭＢＩＮＥＤＷＩＴＨＣＩＳ－ＤＩＡＭＩＮＥＤＩＣＨＬＯＲＯＬＰＬＡＴＩＮＵＭ（ＤＤＰ）ＯＮＨＵＭＡＮＧＡＳＴＲＩＣＣＡＮＣＥＲＣＥＬＬＬＩＮＥＳＭＫＮ...     

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A novel natural killer cell line (KHYG-1) from a patient with aggressive natural killer cell leukemia carrying a p53 point mutation.

We present the establishment of a natural killer (NK) leukemia cell line, designated KHYG-1, from the blood of a patient with aggressive NK leukemia, which both possessed the same p53 point mutation. The immunophenotype of the primary leukemia cells was CD2+, surface CD3-, cytoplasmic CD3epsilon+, CD7+, CD8alphaalpha+, CD16+, CD56+, CD57+ and HLA-DR+. A new cell line (KHYG-1) was established by culturing peripheral leukemia cells with 100 units of recombinant interleukin (IL)-2. The KHYG-1 cells showed LGL morphology with a large nucleus, coarse chromatin, conspicuous nucleoli, and abundant basophilic cytoplasm with many azurophilic granules. The immunophenotype of KHYG-1 cells was CD1-, CD2+, surface CD3-, cytoplasmic CD3epsilon+, CD7+, CD8alphaalpha+, CD16-, CD25-, CD33+, CD34-, CD56+, CD57-, CD122+, CD132+, and TdT-. Southern blot analysis of these cells revealed a normal germline configuration for the beta, delta, and gamma chains of the T cell receptor and the immunoglobulin heavy-chain genes. Moreover, the KHYG-1 cells displayed NK cell activity and IL-2-dependent proliferation in vitro, suggesting that they are of NK cell origin. Epstein-Barr virus (EBV) DNA was not detected in KHYG-1 cells by Southern blot analysis with a terminal repeat probe from an EBV genome. A point mutation in exon 7 of the p53 gene was detected in the KHYG-1 cells by PCR/SSCP analysis, and direct sequencing revealed the conversion of C to T at nucleotide 877 in codon 248. The primary leukemia cells also carried the same point mutation. Although the precise role of the p53 point mutation in leukemogenesis remains to be clarified, the establishment of an NK leukemia cell line with a p53 point mutation could be valuable in the study of leukemogenesis.     

Transformation of large granular lymphocytic leukemia during the course of a reactivated human herpesvirus-6 infection.

A patient with CD3+ large granular lymphocytic (LGL) leukemia developed transformation (TF). The phenotype of the leukemic cells was CD3+, CD4+ and CD8-. The leukemic cell count increased rapidly; the cells became large and the nuclear outline, which had been reniform, became lobulated. Anti-HTLV-1 and anti-HIV antibodies were negative in the serum of the patient and no HTLV-1 specific sequences were detected in the cDNA of the leukemic cells by polymerase chain reaction (PCR). Comparison of the karyotype abnormality of the leukemic cells before and after TF revealed an abnormality of the 21 trisomy in 90% of mitotic cells of the patient. Analysis of the cell cycle revealed that 13.7% of the leukemic cells were in DNA synthesis phase which was not previously found. The titer of anti-human herpesvirus-6 (HHV-6) immunoglobulin G which had been high at chronic phase (1:1640 compared to normal titer of less than 1:160), became 1:20,000 at TF. The titer of anti-HHV-6 immunoglobulin M also increased from less than 1:4 at the chronic phase to 1:120 at TF (normal value less than 1:4). A HHV-6-specific DNA sequence was detected by PCR in the peripheral mononuclear cells collected at TF but not at the chronic phase. These data suggests that TF occurs not only in CD3-negative but also in CD3-positive LGL leukemia. HHV-6 reactivation is therefore a possible cause in immunocompromised hosts whose general conditions are deteriorated.     

Lymphokine-activated killer (LAK) cells discriminate between Epstein-Barr virus (EBV)-positive Burkitt's lymphoma cells

We have generated in vitro lymphokine-activated killer (LAK) cells from healthy donors by stimulating their mononuclear leukocytes with recombinant interleukin-2 (rIL-2) (100 U/ml). After 6 days in culture, the lytic properties of the LAK cells were analyzed in the 51Cr-release assay by utilizing a target panel of 6 paired lines consisting of an Epstein-Barr virus (EBV)-positive Burkitt's lymphoma (BL) cell line and an EBV-transformed lymphoblastoid cell line (LCL) from the same donor, the Raji BL line and the natural killer (NK) cell-sensitive K562 line. The patterns of lysis showed that the LAK cells discriminated between two categories of BL cell lines. Group I/II BL tumor cells which expressed the common acute lymphoblastic leukemia antigen (CALLA), the BL-associated glycolipid antigen (BLA) and phenotypically resembled biopsy cells were strongly lysed whereas group III BL cells which had assumed an LCL-like phenotype during culture and lacked the CALLA and BLA surface markers were only poorly lysed. The LCL targets were generally resistant to lysis but the K562 cell line was particularly sensitive. The outcome of cell depletion and monoclonal antibody (MAb) studies indicated that the LAK cell populations were phenotypically and functionally heterogeneous and consisted of at least 2 subpopulations of effector cells; a tumor-specific component and an NK-cell-mediated component.     

Effects of Phorbol Esters and Cytokines (Interleukin-2,-4, and -6) on the Proliferation and Surface Phenotype of Epstein-Barr Virus Immortalised Human B Lymphocytes

Epstein-Barr virus (EBV)-induced in vitro infection of peripheral blood mononuclear cells (PBMCs) leads to a polyclonal proliferation and immortalisation of B lymphocytes. In the present study we determined the effects of three different cytokines, interleukin-2 (IL-2), interleukin-4 (IL-4) and interleukin-6 (IL-6), and the tumour promoting phorbol ester 12-0-tetradecanoyl-phorbol-13-acetate (TPA) on EBV-immortalised B lymphocytes. These factors have known activities on normal B cells. IL-4 and IL-6 increased significantly EBV-B cell proliferation after 3 and 5 days of culture, where IL-2 had no effect. The effect of IL-4 and IL-6 on EBV-B cells was abolished after pre-incubation with anti-IL-4 and anti-IL-6 neutralising antisera, respectively. TPA induced a dose dependent inhibition of proliferation both in serum free and 10% fetal calf serum (FCS) supplemented culture medium. Combinations of TPA and interleukins did not restore lymphoblastoid cell proliferation to background levels. All possible combinations of the three cytokines showed no synergistic or antagonistic effect on proliferation. TPA induced significant phenotypic changes of EBV immortalised B lymphocytes, by increasing IL-2 receptor (IL-2R) expression and decreasing CD20 and CD23 antigen expression. Other B cell differentiation antigens; HLA-DR, CD19, and transferrin receptor (CD71), did not demonstrate significant changes. A dose dependent inhibition of CD21 and increase in CD22 expression was observed in 2 out of 3 lymphoblastoid cell lines tested.     

Persistent long-term human herpesvirus 6 (HHV-6) infection in a patient with langerhans cell histiocytosis

Langerhans cell histiocytosis (eosinophilic granuloma) was first diagnosed in the adolescence of a male patient presented. Several years later persisting human herpesvirus 6 (HHV-6) infection was recognized. The HHV-6 infection could be verified retrospectively in his historical histological samples; the continuous presence of HHV-6 could be established through 17 years of disease course. The patient was operated several times during this period for painful relapses, and developed diabetes insipidus. At variable time points during the clinical course, Varicella zoster (VZV), Epstein-Barr virus (EBV) and human herpesvirus 8 (HHV-8) infections were temporarily detected from blood samples and biopsy specimens. HHV-6 was the only virus continuously identified throughout the entire follow-up period. Antiviral therapy effectively cleared EBV and HHV-8, but HHV-6 remained detectable throughout the disease course. Since DNA sequences of HHV-6 could be detected in the pathologic histiocytes of eosinophilic granuloma, and from other samples taken later on, it is suggested that long-term HHV-6 infection may be associated with development or progression of Langerhans cell histiocytosis.     

HHV-6感染在鼻咽癌发病中的意义

目的：探计鼻咽癌组织中人疱疹病毒6型(HHV—6)在鼻咽癌(Nasopharyngeal carcinoma，NPC)发病中的意义。方法：PCR检测27例正常鼻咽组织、21例异型增生及42例鼻咽癌组织中HHV一6DNA和EB病毒(Epstein—barr vims，EBV)DNA存在状况，用免疫组化检测36例NPC组织中EBVLMPl蛋白的表达及40例NPC组织中p53基因的表达。结果：异型增生和NPC组织中HHV一6 DNA的阳性率分别为4．7％和26．2％，EBV DNA分别为4．6％和95．2％；正常鼻咽组织不存在HHV一6DNA，EBVDNA为25．9％。NPC组织中EBV—LMPl蛋白阳性率为47．2％，HHV一6阳性NPC中LMN表达阳性率(81．8％)显著高于HHV一6阴性者(32．0％)。HHV一6阳性与阴性的NPC中p53表达的阳性率无显著性差异，但HHV—6阳性的NPC中p53表达强度显著性增高。结论：NPC组织中存在HHV—6的感染，与EBV—LMP1蛋白表达上调呈正相关。提示在NPC的发生中HHV—6可能直接参与和(或)通过上调EBV—LMP1的表达而起作用，并可能参与鼻咽癌发病中p53过表达的调控。     

人浆细胞分化抗原SI4和SI6特性研究

研究人浆细胞分化抗原SI_4和SI_6的组织分布特征和分子特性的结果表明:SI_6主要表达在人正常和恶性浆细胞表面。SI_6抗原分子量为210kD(非还原状态)或180/32kD(还原状态)。该抗原从B淋巴母细胞阶段起弱表达,至浆细胞阶段显著增强。SI_4从静止B细胞阶段起弱表达,至浆细胞阶段亦显著增强。SI_4抗原分子量为180kD(还原状态)的单肽链结构。本文结果对于研究人正常和恶性浆细胞的分化、发育、生物学特性和多发性骨髓瘤的诊断、分类及生物学治疗具有意义。