计算机网络病毒的安全防治策略

通过对几种网络病毒的系统介绍，揭示其对社会及网络用户的危害，提出了预防计算机网络病毒的整体策略。     

木马病毒入侵原理与防范

简要介绍了木马病毒的危害性、发展趋势及特点,分析了木马病毒的主要原理,提出了一些防范木马病毒的建议。     

浅谈计算机病毒及其防治

文章从计算机的病毒分类谈起，进一步分析了如何预防和查杀病毒及其后期的处理。     

牙鲆贫血症病毒分离株的特性

用CHSE－214细胞，从患贫血症的牙鲆肾脏组织分离出一株病毒。电镜揭示为无囊膜、6面体、粒子直径约60nm；理化特性表明：病毒复制不受IUdR、BVdU的影响，对氯仿、乙醚不敏感性，热（60℃，30min）、酸（pH3．0，3h）中稳定；可被抗IPNV－Sp、Ab和VR－299株血清中和，其中抗Sp株血清的ND50为1:2560;病毒能在5～30℃增殖，最适为15～25℃；在盐度0．8～2．0％的培养液中，生长无明显差别；在16种鲑科和非鲑科鱼类细胞上，15℃培养1～4d出现CPE；感染细胞丫啶橙染色显示为黄绿色；用BirnavirusYAV株引物，PCR检出该病毒。结果提示该病毒株应属dsRNA的Birnavirus。     

几种 IP 地址共享方式的分析与应用

对ＴＣＰ／ＩＰ网上ＩＰ地址共享的几种常见方式（代理ＡＲＰ、ＩＰ伪装和代理服务器）在网络协议、适用范围、对客户端及服务器端程序的要求、内网可访问性、对防火墙的支持等方面的不同特点进行了分析和比较．给出了在Ｌｉｎｕｘ和Ｗｉｎｄｏｗｓ操作系统下上述几种技术的具体应用实例．     

口蹄疫病毒持续感染的研究进展

口蹄疫病毒(foot-and-mouth disease virus,FMDV)能引起偶蹄动物患一种名为口蹄疫(foot-and-mouth disease,FMD)的高度接触性、发热性、急性的传染病.FMD的大规模爆发会导致整个国家或地区的动物和动物相关制品产量降低、贸易受限,造成巨大的经济损失.FMDV持续感染是造成FMDV容易蔓延并难以根除的重要原因.该文综述了FMDV持续感染期间病毒在体内的存在位置与感染特性,并以病毒与宿主细胞、宿主免疫系统之间的相互作用为重点,介绍了持续感染相关机制研究进展,总结了疫情防控相关策略,以期为解决FMDV持续感染问题提供参考.     

ARP病毒的原理与防范措施

ARP病毒具有很大危害性,它能够发送大量的伪造数据包,占用网络带宽。ARP病毒会通过伪造网关,造成全网段计算机无法正常上网;还可以通过截取网关数据包方式,盗取用户账户和密码等信息。本文对ARP协议工作原理和ARP病毒工作原理进行分析,并结合具体工作实践,提出了一套切实有效的防范措施,对防止ARP病毒有很好的效果。     

贵州南方菜豆花叶病毒的ELISA检疫

采用ELISA间接法对分布于贵州几个地区的菜豆进行南方菜豆花叶病毒的检测 ,结果表明 :在所采集到的样品中 ,仅贵阳地区的菜豆感染有南方菜豆花叶病毒。其检测的灵敏度和最佳反应稀释度分别为 80 6ng/mL和 1∶5 0 0稀释度。     

H2株甲肝减毒活疫苗K7的核苷酸全序列分析

应用ＲＴ－ＰＣＲ获取Ｈ２株甲肝减毒活疫苗（Ｋ７）的ｃＤＮＡ片段，经末端终止测序ＰＣＲ试剂盒和全自动测序仪（ＡＢＩ３７７）作序列测定，用Ｍａｘｔｒｉｇｅｎｅ软件进行计算机分析，Ｋ７疫苗病毒的核苷酸全长含７４４３个碱基．Ｋ７对比其亲代Ｈ２株，减毒的ＨＭ１７５株以及ＨＭ１７５野毒株，同源性分别为９９．７５％，９９．９５％和９９．６１％；彼此间在Ｐ１和Ｐ２连接区１６８个碱基的同源性为９９．４％～１００％，均为ⅠＢ基因亚型．前三者在５’非编码区均有１３１～１３４位和２０３位５个碱基缺失，且结构蛋白基因区序列完全一致．本文用分子病毒学方法证实了Ｋ７疫苗的优异纯毒水平，也为开展甲型肝炎分子流行病学工作提供了基础资料     

Thymidine kinase gene mutation leads to reduced virulence of pseudorabies virus

To explore correlation between the tk gene structure of pseudorabies virus (PRV) and its virulence, to study the effect of the gene mutation on PRV biological properties, and to investigate mechinism of reduced virulence, thymidine kinase (TK)-deficient mutant of pseudorabies virus strain Hubei (PRV HB) was isolated by selection for resistance to 5-bromodeoxyuridine. The tk genes of PRV HB and its TK^― mutant were cloned and sequenced. 1587 base pairs of the tk gene and flanking regions of wild-type (wt) virus were sequenced, which included an open reading frame (ORF) of 1098 bp encoding a protein of 366 amino acids. The ORF contained two 137-bp repeated sequences, which were connected by an adenosine. 1458 bp of the tk and flanking regions of TK^― mutant were sequenced. Analysis of the tk gene sequence of TK^― mutant indicated that one of 137 bp repeated sequence and the connecting adenosine in the tk gene of the wt virus was deleted and a repeated sequence of 8 nucleotides (GCGCGCC) was inserted. All other nucleotides of TK^―mutant were identical to that of wt virus. Deletion and insertion of the nucleotide sequence resulted in a frameshift and a premature chain termination, and the resultant TK protein was not active. Analysis of the amino acid sequence revealed that TK protein of PRV HB contained the conserved consensus sequence of herpesviral TKs and an additional conserved-DHR-motif. The results of this work also indicated that TK^― mutant was genetically stable. Compared to PRV HB, virulence of TK^― mutant was greatly decreased. Mice vaccinated with TK^― mutant were completely protected against a lethal challenge with virulent PRV (HB).