instruction:
In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.
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Avian infectious bronchitis virus (IBV), a coronavirus, causes infectious bronchitis leading to enormous economic loss in the poultry industry worldwide. Hypericin (HY) is an excellent compound that has been investigated in antiviral, antineoplastic, and antidepressant. To investigate the inhibition effect of HY on IBV infection in chicken embryo kidney (CEK) cells, 3 different experimental designs: pre-treatment of cells prior to IBV infection, direct treatment of IBV-infected cells, and pre-treatment of IBV prior to cell infection were used. Quantitative real-time PCR (qRT-PCR), immunofluorescence assay (IFA), flow cytometry, and fluorescence microscopy were performed and virus titer was determined by TCID 50 . The re-sults revealed that HY had a good anti-IBV effect when HY directly treated the IBV-infected cells, and virus infectivity decreased in a dose-dependent manner. Furthermore, HY inhibited IBV-induced apoptosis in CEK cells, and significantly reduced the mRNA expression levels of Fas, FasL, JNK, Bax, Caspase 3, and Caspase 8, and significantly increased Bcl-2 mRNA expression level in CEK cells. In addition, HY treatment could decrease IBV-induced reactive oxygen species (ROS) generation in CEK cells. These results suggested that HY showed potential antiviral activities against IBV infection involving the inhibition of apoptosis and ROS generation in CEK cells.
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Protective effects of hypericin against infectious bronchitis virus induced apoptosis and reactive oxygen species in chicken embryo kidney cells


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The evolution of viral quasispecies can influence viral pathogenesis and the response to antiviral treatments. Mutant clouds in infected organisms represent the first stage in the genetic and antigenic diversification of RNA viruses, such as foot and mouth disease virus (FMDV), an important animal pathogen. Antigenic variants of FMDV have been classically diagnosed by immunological or RT-PCR-based methods. DNA microarrays are becoming increasingly useful for the analysis of gene expression and single nucleotide polymorphisms (SNPs). Recently, a FMDV microarray was described to detect simultaneously the seven FMDV serotypes. These results encourage the development of new oligonucleotide microarrays to probe the fine genetic and antigenic composition of FMDV for diagnosis, vaccine design, and to gain insight into the molecular epidemiology of this pathogen. A FMDV microarray was designed and optimized to detect SNPs at a major antigenic site of the virus. A screening of point mutants of the genomic region encoding antigenic site A of FMDV C-S8c1 was achieved. The hybridization pattern of a mutant includes specific positive and negative signals as well as crosshybridization signals, which are of different intensity depending on the thermodynamic stability of each probe-target pair. Moreover, an array bioinformatic classification method was developed to evaluate the hybridization signals. This statistical analysis shows that the procedure allows a very accurate classification per variant genome. A specific approach based on a microarray platform aimed at distinguishing point mutants within an important determinant of antigenicity and host cell tropism, namely the G-H loop of capsid protein VP1, was developed. The procedure is of general applicability as a test for specificity and discriminatory power of microarray-based diagnostic procedures using multiple oligonucleotide probes.
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BMC Genomics Microarray-based identification of antigenic variants of foot-and-mouth disease virus: a bioinformatics quality assessment


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as well as sporadic cases in industrialized countries. The life cycle of HEV is still poorly understood and the lack of efficient cell culture systems and animal models are the principal limitations for a detailed study of the viral replication cycle. Here we exhaustively examine all possible intraviral protein-protein interactions (PPIs) of HEV by systematic Yeast two-hybrid (Y2H) and LuMPIS screens, providing a basis for studying the function of these proteins in the viral replication cycle. Key PPIs correlate with the already published HEV 3D structure. Furthermore, we report 20 novel PPIs including the homodimerization of the RNA dependent RNA polymerase (RdRp), the self-interaction of the papain like protease, and ORF3 interactions with the papain-like protease and putative replicase components: RdRp, methylase and helicase. Furthermore, we determined the dissociation constant (K d ) of ORF3 interactions with the viral helicase, papain-like protease and methylase, which suggest a regulatory function for ORF3 in orchestrating the formation of the replicase complex. These interactions may represent new targets for antiviral drugs. Hepatitis E virus (HEV) is the causative pathogen of Hepatitis E disease, a major form of acute viral hepatitis worldwide. Four different genotypes are known in various geographical regions 1 : genotype 1 (Asia), genotype 2 (Africa and Mexico), genotype 3 (Europe and North America) and genotype 4 (Asia). The global burden of genotype 1 and 2 infections is substantial and the number of infections is estimated at 20 million per year, leading to 70,000 deaths and 3,000 stillbirths 2 . The Hepatitis E virus is a single strand plus RNA virus belonging to the family Hepeviridae. Approximately 7,200 nucleotides encode for three open reading frames (Fig. 1 ). ORF1 is a nonstructural, functional poly-protein with several defined functions 3,4 . The first functional domain encodes a methyltransferase (Met), which is required for capping the 5′ end of the HEV RNA. Next, ORF1 contains a so-called Y domain which shows significant similarities to sequences of Rubella virus and Beet necrotic yellow vein virus but whose function in the viral context remains unknown. Further downstream ORF1 contains a papain-like cysteine protease (Plp) domain. The functionality of the protease domain was often questioned but recently the processing of the ORF1 poly-protein and ORF2 capsid protein by the Plp protease has been confirmed 5 . Next, a hypervariable (V) proline-rich region is located between the putative protease domain and the subsequent so-called X domain (X). For the proline-rich domain an important role in the fine tuning of viral replication through protein-protein interactions (PPIs) has been postulated 6 . The above mentioned X domain is also known as macro-domain or ADP-Ribose binding domain and has been exclusively associated with viral protease domains in other viruses. Towards the 3′ end, ORF1 encodes for the well characterized helicase
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The Hepatitis E virus intraviral interactome