43 results about "Host factors" patented technology

Antibacterial antisense compounds and methods of their use in treating a Mycobacterium tuberculosis infection in a mammalian host are disclosed. The compounds include an antisense oligonucleotide conjugated to a carrier peptide that significantly enhances the antibacterial activity of the oligonucleotide. The antisense oligonucleotides contain 10-20 nucleotide bases and have a targeting nucleic acid sequence complementary to a target sequence containing or within 20 bases, in a downstream direction, of the translational start codon of a bacterial mRNA that encodes a bacterial protein essential for bacterial replication, where the compound binds to a target mRNA with a T_m of between 45° to 60° C. The carrier peptide is an arginine-rich peptide containing between 6 and 14 amino acids. Antisense compounds that target host factor genes that facilitate Mycobacterium tuberculosis infection are also provided, as are methods of using these compounds to treat Mycobacterium tuberculosis infections, alone or in combination with other therapies.

The invention relates to the technical field of biomedicine, in particular to a novel target resistant to Japanese encephalitis virus (JEV) infection and application. Human neuroblastoma cells (SK-N-SH) are taken as target cells, RNA technology is adopted to reduce expression of host protein of the target cells to find host factors capable of effectively inhibiting JEV-infected human neuroblastoma cells (SK-N-SH) so as to protect functions of a nerve system and prevent virus from infecting a central nerve system to cause inflammation. The invention provides application of Cofilin in preventing and treating JEV infection, and experiments find that Cofilin plays an important role in JEV-infected SK-N-SH, and JEV infection can be inhibited remarkably by reducing expression of Cofilin. The invention further provides application of Cofilin in preparing drug for preventing or treating JEV infection.

This application relates to the modulation of host cell factors required for influenza virus replication. The application relates to compounds, including nucleic acid compounds (such as, e.g., small interfering RNAs (siRNAs)) and small molecules, that target human host cell factors involved in influenza virus replication, and the use of such compounds for modulating influenza virus replication and as antiviral agents. The application also relates to methods of treating an influenza virus infection and methods of treating or preventing a symptom or disease associated with influenza virus infection, comprising administering to a subject a composition comprising a compound, such as a nucleic acid compound (e.g., an siRNA) or small molecule, that targets a human host cell factor involved in influenza virus replication.

The invention relates to the biomedical technology field, and provides a new target spot for resisting enterovirus 71-type infection and applications. Human colon cancer cells (Caco-2) are employed as target cells, the RNA interference technology is employed to reduce expression of the target cell host proteins, a host factor capable of inhibiting EV71 infection of human colon cancer cells (Caco-2) effectively is sought and the purpose of cutting off EV71 infection from the source (intestinal tract) effectively is achieved. Experiments show that hepatocyte growth factor-regulated tyropsine kinasesubstrate (HRS) plays an important role in inhibiting EV71 infection of Caco-2, the HRS expression is reduced, and EV71 infection can be inhibited obviously. Applications of HRS in preparation of medicines preventing or treating enterovirus 71-type infection are provided.

The invention provides a method for improving PCR amplification sensitivity by using an integrated host factor. The method comprises the following steps: adding the integrated host factor IHF into a reaction solution containing deoxyribonucleoside triphosphate, DNA polymerase, an oligonucleotide primer and a nucleic acid fragment which serves as a template, carrying out repeated heat circulation according to three steps of unwinding, annealing and extending of the normal PCR, thereby amplifying a target nucleic acid fragment, wherein the mole ratio of a primer to the integrated host factor IHF is 0.005-1. The method is capable of specifically and efficiently amplifying a target nucleic acid sequence.

The invention relates to the technical field of molecular biology, and particularly relates to a method of screening an HIV-1 activity determinative factor based on high-throughput RNAi. Aiming at shRNA libraries of 474 kinases, and through a high-throughput RNAi screening technique, HIV-1 LTR-hRluc/HSVTK-hLuc luciferase double reporter plasmids are stably expressed in HEK293T, and kinase-involved HIV-1 LTR regulatory transcriptional activity is obtained by dividing HIV-1 LTR relative transcriptional activity of hRluc expression fluorescence intensity by hLuc fluorescence intensity. The method aims at human kinase genes, performs functional silence screening, searches HIV replication related host factors, and provides valuable reference basis for further understanding interactions between HIV and hosts and for searching HIV-infection resisting potential treatment targets.

The invention relates to the biomedical technology field, and provides a new target spot for resisting Japanese encephalitis virus infection and applications. Human brain microvascular endothelial cells (HBMEC) are employed as target cells, the RNA interference technology is employed to reduce expression of target cell host proteins, a host factor capable of inhibiting Japanese encephalitis virus infection of human brain microvascular endothelial cells (HBMEC) effectively is sought, the function of protecting the blood brain barrier is achieved, viruses are prevented from going through the blood brain barrier and infecting the central nervous system. Applications of N-ethylmaleimide sensitive factor in preventing Japanese encephalitis virus infection are provided. Experiments show that the N-ethylmaleimide sensitive factor (NSF) plays an important role in inhibiting JEV infection of HBMEC, the NSF expression is reduced, and JEV infection can be inhibited obviously. Applications of NSF in preparation of medicines preventing or treating Japanese encephalitis virus infection are provided.

The invention belongs to the technical field of biology, and particularly relates to a preparation method and application of an anti-Epinephelus akaara nervous necrosis virus medaka haploid embryonicstem cell. Medaka haploid embryonic stem cells (HX1 cells) are induced by Ethylmtrosourea (ENU)), and then the anti-Epinephelus akaara nervous necrosis virus medaka haploid embryonic stem cell G1 canbe screened; the anti-Epinephelus akaara nervous necrosis virus medaka haploid embryonic stem cell G1is preserved in china center for type culture collection on January 17 th, 2018, the preservation address is wuhan university in china, and the preservation number is CCTCC NO: C201832. The anti-Epinephelus akaara nervous necrosis virus medaka haploid embryonic stem cell G1 provides an experiment basis and a theoretical basis for further identifying host factors participating in virus infection, and provides a new way for genetic breeding of antiviral fishes.

The invention relates to the technical field of biomedicine, in particular to a novel target resistant to enterovirus 71 infections and application thereof. Brain microvascular endothelial cells (HBMEC) are used as target cells, the expression of host proteins of the target cells are down-regulated by using the RNA interference technology, and thus host factors effective in inhibiting EV71 infections for brain microvascular endothelial cells (HBMEC) are thus found, the blood brain barrier function is protected, and the virus is prevented from penetrating the blood brain barrier to infect the central nervous system. Experiments show that protein tyrosine kinase FYN proto-oncogene (FYN proto-oncogene, Src family tyrosine kinase) molecules play an important role in the HBMEC infection by EV71, and EV71 infections can be significantly inhibited by down-regulating the expression of FYN. The invention provides application of the FYN in the preparation of drugs for preventing or treating enterovirus 71 infections.

The invention belongs to the technical field of biomedicine, and relates to a novel target used for preventing enterovirus 71 infection, and applications thereof. According to the invention, SH-SY5Y is taken as the target cell, and RNA interference technology is adopted for down-regulation of expression of target cell host protein so as to search host factors capable of inhibiting EV71 infection of SH-SY5Y cells effectively and protect the functions of central nervous systems. It is fond by experiments that calcium-and inte-grin-binding protein, CIB1 molecular possesses significant importance in EV71 infection of SH-SY5Y, and down-regulation of expression of CIB1 is capable of inhibiting EV71 infection obviously. The invention also provides applications of CIB1 in preparing drugs used for preventing or treating EV71 infection.

The invention relates to an RNAi (RNA interference) vector construction method and an application thereof in watermelon genetic transformation, relates to the technical field of plant virus control and belongs to the application technology in biological and modern agriculture technique fields. The mediated virus infection function is destroyed by acting on host factors and thus watermelons obtain antiviral activity, which has not been reported yet at present. An RNAi vector is constructed and genetically transformed to watermelons, the constructionmethod is characterized in that watermelon eIF4E and a homological isomer eIF(iso)4E gene thereof are cloned and connected, 4E-iso sense and antisense fragments are obtained and connected to two sides of an intron sequence, and a 4E-iso hairpin structure fragment is obtained; the 4E-iso sense fragment, the 4E-iso antisense fragment and the hairpin structure fragment are inserted into a pCAMBIA1301 vector through T4 connection and homologous recombination, and the RNAi vector is obtained; target gene fragments are transformed into watermelon cotyledon explants through agrobacterium tumefaciens-medicated transformation, and transgenic watermelons with the target gene fragments are obtained through screening cultivation. The method is mainly used for providing a novel material and a novel technology for watermelon virus and disease control.

Hepatitis C Virus (HCV) infects 200 million individuals worldwide. Although several FDA approved drugs targeting the HCV serine protease and polymerase have shown promising results, there is a need for better drugs that are effective in treating a broader range of HCV genotypes and subtypes without being used in combination with interferon and/or ribavirin. Recently, the crystal structure of the core of the HCV E2 protein (E2c) has been determined, providing structural information that can now be used to target the E2 protein and develop drugs that disrupt the early stages of HCV infection by blocking E2's interaction with different host factors. By targeting sites containing conserved E2 amino acids in the CD81 binding site on HCV E2, one might also be able to develop drugs that block HCV infection in a genotype-independent manner. Using the E2c structure as a template, a structural model of the E2 protein core (residues 421-645) was developed that includes the three amino acid segments that are not present in the E2c crystal structure. Blind docking of a diverse library of 1715 small molecules to this model led to the identification of a set of 34 ligands predicted to bind near conserved amino acid residues involved in the HCV E2:CD81 interaction. Surface plasmon resonance was used to screen the ligand set for binding to recombinant E2 protein, and the best binders were subsequently tested to identify compounds that inhibit the infection of hepatocytes by HCV. One compound, 281816, blocked E2 binding to CD81 and inhibited hepatocyte infection by HCV genotypes 1a, 1b, 2a, 2b, 4a and 6a with IC50's ranging from 2.2 μM to 4.6 μM. Methods are described for preventing or treating HCV infection using small molecule inhibitors such as 281816 that target E2 and disrupt its interactions.

The present invention provides an integration-defective lentiviral vector based on a parental lentivirus and related methods, the integration-defective lentiviral vector including one or more of the following: (a) a mutation, deletion or other modification of one or more binding sites for a host factor involved in gene silencing; (b) an addition of one or more binding sites for a transcription activator, which can be natural (such as but not limited to ubiquitous and/or tissue/cell type specific) including but not limited to SP1 NFkB, or synthetic including but not limited to binding sites for tetracycline regulated trans activators tTA, rtTA, tT65, and/or rtT65; (c) one or more nucleic acid sequences from a SV40 genome, wherein the one or more sequences are obtained from a region of the SV40 genome upstream to the SV40 poly-adenylation signal; (d) a shRNA expression cassette, which encodes a shRNA directed to a host gene involved in epigenetic silencing and/or in DNA repair pathways; or (e) any combination of (a), (b), (c) and (d), wherein as compared to the parental lentivirus, the integration-defective lentiviral vector resists gene silencing.

The invention relates to the technical field of biomedicine, and provides a new target for resisting entervirus type 71 infection and application. A human neuroblastoma cell (SH-SY5Y) is taken as a target cell, expression of host protein of the target cell is down-regulated by adopting an RNA interference technique to look for a host factor which can effectively inhibit the EV71-infected human neuroblastoma cell (SH-SY5Y), and therefore the function of a central nervous system is protected. Through experiments, it is found that a dynamin 1 (NDM1) plays an important role on the EV71-infected SH-SY5Y, and EV71 infection can be obviously inhibited by down-regulating expression of the DNM1. The invention provides application of the DNM1 in preparation of medicine for preventing or treating the entervirus type 71 infection.

The present invention discloses one kind of tomato RNA virus host factor and its coding gene and application in antiviral breeding of plant. The tomato RNA virus host factor is protein possessing one of the following amino acid residue sequences: 1) SEQ ID No. 1 in the sequence list; and 2) the amino acid residue sequence of SEQ ID No. 1 in the sequence list and through the substitution, deletion or addition of 1-10 amino acid residues and supporting virus copying protein. Silencing the protein coding gene inside plant body via transgenic antisense gene segment or RNA interfering can obtain antiviral plant. The tomato RNA virus host factor gene ToTOM3 and the method of inhibiting the expression of the gene has practical significance and wide application foreground in culturing and breeding antiviral plant.

The invention discloses an application of a DICER1 gene and siRNA thereof in the influence of PRRSV duplication. si-RNA is used to knock-down DICER1, then the influence of DICER1 on a PRRSV infected host cell is detected by qRT-PCR and TCID50; after the host factor DICER1 is specifically knocked-down, the duplication and proliferation of PRRSV are influenced; the specific siRNA of the host factorDICER1 can be used to develop drugs for preventing and treating PRRSV; and corresponding gene DICER1 can be applied to research on PRRSV transgenic pigs.

The invention relates to the technical field of biomedical science, in particular to a new target for resisting enterovirus 71 type infection, and an application. Human colon cancer cells (Caco-2) areused as target cells, an RNA interference technique is adopted for reducing expression of a target cell membrane receptor, a host factor which can effectively restrain EV71 infected human colon cancer cells is sought, and the purpose of blocking EV71 infection from a source (intestinal tract) is achieved. Through experiment, the inventor of the invention finds that the fibroblast growth factor receptor 1 (FGFR1) exerts important effects in EV71 infected Caco-2 cells, so that when the expression of the FGFR1 is reduced, the EV71 infection can be obviously restrained. The invention provides anapplication of the FGFR1 to preparation of medicines for preventing or treating enterovirus 71 type infection, and a new target and a treatment scheme are provided for clinical prevention and treatment of diseases of hand-foot-mouth diseases, meningitis, brainstem encephalitis or poliomyelitis and the like caused by the EV71 infection.