Increased susceptibility to HIV-1 of peripheral blood lymphocytes in acute infection with Epstein-Barr virus

Epstein-Barr virus (EBV) is an important pathogen in human immunodeficiency virus (HIV)-infected individuals that causes lymphoma and other lymphoproliferative disorders upon disease progression; however, interaction between the two viruses during acute infection is not well known. Expression of CCR5, a major coreceptor for HIV, was enhanced on CD4+ T cells from patients with acute EBV infection. Furthermore, susceptibility of those cells to R5-HIV-1, but not X4-HIV-1, was increased. EBV effects on CCR5 expression on or susceptibility to R5-HIV-1 of CD4+ T cells did not require coinfection of the same cell with the two viruses, because CD4+ T cells from patients with acute EBV infection were not infected with EBV. Considering that both HIV and EBV are transmitted by intimate contact, such possible interaction between the two viruses may have implications for viral transmission and the pathogenesis of HIV disease.     

Restriction endonuclease analysis of varicella-zoster vaccine virus and wild-type DNAs

The DNA from several clinical isolates of varicella-zoster virus (VZV) were compared with the DNA from the vaccine strain VZV using three restriction endonucleases: BamHI, BgII, and HpaI. When electrophoresed through an agarose gel, the vaccine DNA digestion pattern was significantly different from the digestion patterns of the wild-type DNAs. Variations in the digestion pattern of the separate clinical isolates were also observed.     

Dynamics of HIV replication in lymphocytes and the efficacy of protease inhibitors

Using a system that allows transfection of resting peripheral blood lymphocytes (PBLs) two questions were addressed: the kinetics of HIV replication from the state of proviral latency, and the impact of different parameters on the efficacy of protease inhibitors to control HIV replication. PBLs were transfected with an infectious full length HIV-DNA harboring a luciferase reporter gene and activated thereafter. Ritonavir was added at different times at doses ranging from to 0.06 to 1 microM. Viral expression was assessed by quantifying luciferase activity in cell extracts and levels of p24 HIV antigen in culture supernatants. After transfection and cell activation, intracellular expression of HIV proteins, as assessed by luciferase detection, occurred within 2 hr. HIV-gag p24 antigen was detected in culture supernatants between 6 and 8 hr post-activation. Ritonavir was effective in blocking viral replication when given within 4 hr following HIV reactivation, but a delay in ritonavir administration or breaches in ritonavir levels after 6 hr from transfection resulted in viral escape. HIV reactivation from proviral latency in PBLs is an extremely rapid process, faster than estimated from previous models. These data stress the need for maintaining effective antiretroviral concentrations to block completely viral replication.     

临床诊断为非甲～戊型肝炎患者的病原学研究

目的探讨临床诊断为非甲-戊型肝炎患者的病原学。方法 采用巢式PCR（nPCR)检测HBV、TTV、B19、和SENV DNA；用逆转录巢式PCR（RT-nPCR)检测HGV和HCV RNA。结果 60例临床诊断为非甲-戊型肝炎患者中，单独HBVDNA阳性30例（阳性率为50.0%)，HBV和TTVDNA阳性10例（16.7%)，HBV和B19DNA阳性6例（10.0%)，HCVRNA、HBV和SENVDNA阳性1例（1.7%)，单独HCVRNA阳性1例（1.7%)，HCVRNA和B19DNA阳性1例（1.7%),HGVRNA无一例阳性，单独B19DNA阳性2例（3.3%)。单独TTVDNA阳性1例（1.7%)，另8例（13.3%)上述病毒核酸均为阴性。HBV合并感染TTV或B19对其血清学生化指标无影响。结论HBV是临床诊断为非甲-戊型肝炎的主要病原，HGV、TTV、B19和SENV与非甲-戊型肝炎无关。     

Evidence for Presence of Types A and B of Beet Necrotic Yellow Vein Virus (BNYVV) in Iran

Rhizomania a viral disease, caused by beet necrotic yellow vein benyvirus (BNYVV), is now widely spread, throughout the sugar beet growing areas of Iran. Genomes of BNYVV are composed of five RNA molecules with specific functions. In this study sequence analyses were conducted on the major coat protein gene (CP21), and parts of RNA3 and RNA4 of an Iranian strain of BNYVV from the Fars province. Sequence alignments of Iran Fars CP21 with other isolates showed closed similarities at nucleotide and amino acid levels with BNYVV pathotype A isolates; S from Japan, and YU2 from Yugoslavia. These results suggest that Iran-Fars isolate probably originated from Asia or neighboring European countries rather than from Germany or France.     

散发性戊型肝炎病毒感染的诊断

用基因工程重组的戊型肝炎病毒基因结构区第二码框架和第二读码框架具有免疫表位的嵌合抗原，建立了间接酶联免疫法，检测散发性急性肝炎病人血清中抗－ＨＥＶＩｇＧ和ＩｇＭ抗体。在４６例急性肝炎病人中出抗－ＨＥＶＩｇＧ抗体阳性７例，阳性率为１５．２２％，７例ＩｇＧ抗体阳性中，有５例ＩｇＭ抗体也阳性，占７１．４％。     

A patient with hepatic granuloma formation and angiotensin-converting enzyme production by granuloma cells during clinical relapse of hepatitis A

Elevation of the serum angiotensin-converting enzyme (sACE) level and hepatic granulomas were found during a clinical relapse in a 22 year old patient with acute viral hepatitis type A (AVH-A). The serum transaminase level and sACE level remained high for more than 6 months. In the biopsied specimen of the liver, fibrous rings of granulomas composed of collagen types I, III, and V were observed. Furthermore, the localization of ACE was visible in the rough endoplasmic reticulum of epithelioid cells of granulomas in the liver under electron microscopy using the indirect immunoperoxidase method. These results suggest that granuloma cells in the liver caused by hepatitis A may be involved in ACE production. In addition, other diseases associated with the presence of granulomas in the liver, such as lymphoma, cytomegalovirus infection, visceral leishmaniasis, and lupoid hepatitis, were ruled out. However, the hepatic granulomas disappeared with the healing of AVH-A. In this regard, the present case is considered to be one of the very few cases of hepatic sarcoidosis.     

抗SARS病毒N蛋白单克隆抗体的制备和初步应用

目的 制备抗SARS病毒N蛋白的单克隆抗体并研究其初步应用。方法 用基因重组N蛋白免疫小鼠，取免疫后的鼠脾细胞与骨髓瘤细胞融合，筛选分泌抗SAPS病毒N蛋白单克隆抗体细胞株。将阳性细胞株接种小鼠腹腔制备单克隆抗体腹水并对抗体进行纯化，分析纯化抗体的相对亲和力。选择亲和力较高的抗体制备检测SARS病毒抗原的酶联免疫诊断试剂，并对其敏感性和特异性进行分析。结果 共获得11株单克隆抗体细胞株，其中3株单抗与N蛋白具有较高的亲和力，4株纯化单抗与N蛋白反应很弱，其余4株单抗介于两者之间。用亲和力较高的单抗制备检测SARS病毒抗原的诊断试剂，其敏感性可达31PFU／ml，而且与其他呼吸道病毒无交叉反应。结论 该试剂特异性较好，可用于SARS病毒抗原的检测，其敏感性仍需用临床急性期样品进行评价。     

Preaxial acrofacial dysostosis (Nager syndrome) associated with an inherited and apparently balanced X;9 translocation: Prenatal and postnatal late replication studies

We report on an infant with preaxial acrofacial dysostosis (Nager syndrome) who was diagnosed prenatally as having an apparently balanced X/autosome translocation [46,X,t(X;9)(p22.1;q32)mat] inherited from a previously diagnosed mosaic translocation carrier mother [46,XX/46,X,t(X;9)(p22.1;q32)]. Replication studies on amniocytes showed the normal X chromosome to be late replicating while the same studies repeated on the infant's lymphocytes showed the translocated X chromosome to be late replicating in most cells. Late replication studies of the mother's lymphocytes demonstrated that the normal X chromosome was late replicating in most cells. The presence of Nager syndrome in this infant may be the result of critical break-points and/or position effects on chromosome 9, inducing expression of a gene responsible for the syndrome. © 1993 Wiley-Liss, Inc.