Rescued virus from infectious cDNA clone of rabbit hemorrhagic disease virus is adapted to RK13 cells line

RHDV is an extremely pathogenic virus. The mor-tality rate of infected rabbits is almost 99%. The dis-ease caused by RHDV is also called “rabbit plague”, and it has been regarded as one of the most important infection diseases of rabbits. RHDV was desig…     

Evolution and molecular epidemiology of foot-and-mouth disease virus in China

Foot-and-mouth disease (FMD),caused by foot-and-mouth disease virus (FMDV),is considered one of the most important viral diseases of cloven-hoofed animals,causing severe economic losses in affected regions of the world.Three serotypes (A,O,and Asia 1) of FMDV have been identified in China since 1958.In addition,the occurrence of novel subtypes within these serotypes has made the epidemiology of FMDV more complicated over the last few years.In this review,we summarize the history and the current epidemiological situation in China,genetic diversity (e.g.,quasispecies dynamics,antigenic heterogeneity,and functional constraints),intertypic recombination,and the evidence for positive selection of different FMDV serotypes.We also assess these genetic data to understand the origin,evolution,and transmission of FMDV,the findings of which may be useful in developing control measures for future epidemics.     

Chemical basis of antigenic variation in foot-and-mouth disease virus

One of the difficulties in controlling foot and mouth disease by vaccination is the occurrence of the virus as seven distinct serotypes because immunity conferred by vaccination against one serotype leaves the animals susceptible to infection by the other six. Moreover, the antigenic variation, even within a serotype, can be so great that immunity against the homologous strain of virus need not necessarily ensure protection against infection by other viruses within that serotype. Here we report the separation of three natural antigenic variants, distinguishable in cross-neutralization tests from an isolate of foot-and-mouth disease virus (FMDV). The serological differences could also be demonstrated by antisera elicited by synthetic peptides corresponding to residues 141-160 of the capsid polypeptide VP1, showing that this region contains a major immunogenic site of the virus. The results have practical implications for the choice of viruses for vaccine production.     

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.     

Structural and serological evidence for a novel mechanism of antigenic variation in foot-and-mouth disease virus.

Changes resulting in altered antigenic properties of viruses nearly always occur on their surface and have been attributed to the substitution of residues directly involved in binding antibody. To investigate the mechanism of antigenic variation in foot-and-mouth disease virus (FMDV), variants that escape neutralization by a monoclonal antibody have been compared crystallographically and serologically with parental virus. FMDVs form one of the four genera of the Picornaviridae. The unenveloped icosahedral shell comprises 60 copies each of four structural proteins VP1-4. Representatives from each of the genera have similar overall structure, but differences in the external features. For example, human rhinovirus has a pronounced 'canyon' that is proposed to contain the cell attachment site, whereas elements of the attachment site for FMDV, which involves the G-H loop (residues 134-160) and C-terminus (200-213) of VP1, are exposed on the surface. Moreover, this G-H loop, which is a major antigenic site of FMDV, forms a prominent, highly accessible protrusion, a feature not seen in other picornaviruses. It is this loop that is perturbed in the variant viruses that we have studied. The amino acid mutations characterizing the variants are not at positions directly involved in antibody binding, but result in far-reaching perturbations of the surface structure of the virus. Thus, this virus seems to use a novel escape mechanism whereby an induced conformational change in a major antigenic loop destroys the integrity of the epitope.     

Replication of Epstein-Barr virus in human epithelial cells infected in vitro

Epstein-Barr virus (EBV), a member of the herpes group of viruses and the aetiological agent of infectious mononucleosis, is usually thought of as a lymphotrophic virus with the ability to transform B lymphocytes. So the association of EBV with nasopharyngeal carcinoma is puzzling, especially given the lack of success of attempts to infect epithelial cells with EBV in culture and the apparent lack of EBV receptors on epithelial cells. Circumvention of the apparent requirement for membrane receptors by techniques of transfection, microinjection and receptor transplantation has clearly demonstrated that there is no inherent barrier to EBV replication in nonlymphoid cells, including epithelial cell types. Our ability routinely to detect EBV DNA by in situ hybridization in epithelial cells of the oropharynx from persons with acute infectious mononucleosis suggests that, in vivo, EBV regularly gains access to and replicates lytically in epithelial cells. We report here in vitro evidence for direct infection by EBV and replication of the virus in cultured normal human epithelial cells.