Interferon-induced Transmembrane Proteins (IFITMs) were identified through small interference RNA (siRNA) screening method in 1980s. The antiviral properties of the IFITMs were firstly discovered in 1996. Recently, its antiviral effect and mechanism have become a research hotspot. Many studies have shown that IFITM can inhibit the replication of multiple pathogenic viruses, including influenza A virus (IAV), Human Immunodeficiency Virus (HIV-1), hepatitis C virus (HCV), Ebola virus (EBOV), West Nile virus and so on. IFITMs inhibit the replication of virus in the early stage of the viral life cycle, which occurred before the release of viral genomes into the cytosol. Recent studies indicate that IFITM proteins could block viral replication by mediate viral membrane fusion. However, the mechanism is still under investigation. Here we review the discovery and characterization of the IFITM proteins, elucidate their antiviral activities and the potential mechanisms.
Animals ; Humans ; Interferons ; genetics ; immunology ; Membrane Proteins ; genetics ; immunology ; Virus Diseases ; genetics ; immunology ; virology ; Viruses ; genetics ; immunology

Hepatitis B virus (HBV) infection is one of the most serious public health problems. HBV infection could lead to hepatitis B, and even further develop into hepatic cirrhosis and hepatocellular carcinoma. Interferon lambda (IFN-λ) is a member of the interferon (IFN) family and an important cytokine for antiviral defense. There are four members in IFN-λ family, including IFN-λ1, IFN-λ2, IFN-λ3, and IFN-λ4. The genetic polymorphisms in the IFN-λ genes are associated with HBV replication and treatment response of HBV patients. In this review, we summarized the roles of genetic polymorphisms of the IFN-λ genes played in HBV infection, disease progression and treatment, with the aim to better understand their function. This review could serve as a reference for the HBV prevention and treatment of HBV patients, as well as for future clinical usage.
Antiviral Agents/pharmacology* ; Hepatitis B/genetics* ; Hepatitis B virus/genetics* ; Humans ; Interferons/pharmacology* ; Liver Neoplasms ; Polymorphism, Genetic ; Virus Replication/genetics*

OBJECTIVETo study the expression of gene associated with retinoid-interferon-induced mortality-19(GRIM-19) in preimplantation embryo of mice and explore its role in embryonic development.

METHODSThe protein and mRNA expressions of GRIM-19 in 2-cell, 4-cell, 8-cell, morula, and blastocyst phases of mice preimplantation embryo were detected by Western blot analysis and Real-time polymerase chain reaction (PCR).

RESULTSGRIM-19 was continuously expressed in every stage of preimplantation embryo of mice. Western blot analysis and Real-time PCR demonstrated a gradual increase of GRIM-19 expression from 2-cell, which reached a peak in 8-cell phase and then decreased progressively.

CONCLUSIONSThe expression of GRIM-19 in mouse preimplantation embryos changes as at different developmental phases. GRIM-19 may play an important role during embryonic development.

Animals ; Blastocyst ; drug effects ; metabolism ; Female ; Interferons ; pharmacology ; Mice ; NADH, NADPH Oxidoreductases ; genetics ; metabolism ; Pregnancy ; RNA, Messenger ; genetics ; Tretinoin ; pharmacology

Guanylate-binding protein 1 (GBP1) is an interferon induced protein, that belongs to the guany late-binding protein family. GBP1 is widely involved in anti-infection immune responses, anti-tumor activity and various biological reactions. Recent studies have proved that IFN-alpha, IFN-beta, IFN-gamma, IL1alpha, IL1beta, TNF-alpha and LPS can induce GBP1 expression; hence, the diverse biological functions of GBP1 have been gradually deduced and exploited. Many studies have been performed over recent years to understand the exact mechanisms that underlie the anti-infection and anti-tumor properties of GBP1. This review describes the molecular structure, biological activity, anti-infective properties and other functions of GBP1, in order to provide insights into the divergent roles of GBP1 in the regulation of various biological processes.
Animals ; Antineoplastic Agents ; metabolism ; Antiviral Agents ; metabolism ; GTP-Binding Proteins ; chemistry ; genetics ; metabolism ; Humans ; Interferons ; genetics ; metabolism

Amino Acid Sequence ; Hepatitis C, Chronic ; drug therapy ; Humans ; Interferons ; pharmacology ; therapeutic use ; Viral Nonstructural Proteins ; chemistry ; drug effects ; genetics

Adult ; Blood Donors ; Hepacivirus ; drug effects ; genetics ; Hepatitis C, Chronic ; virology ; Humans ; Interferons ; pharmacology ; Middle Aged ; Viral Load

To investigate whether HIV-1 infection affects expression of interferon-stimulated gene 15 (ISG15) and determine the antiviral effect of ISG15 in vitro, ISG15 expression at transcription and protein level and supernatant p24 of HIV-1 was detected in various HIV-1 infected or transfected cell lines, respec tively. HIV-1 molecular clone pNL4-3 was used to transfect 293T, TZM-bl and HeLa cells while HIV-1 pseudo-typed virus was used to infect Jurkat, MT-1 and THP-1 cells. After twenty-four hours post infection or transfection, cells were harvested for extraction of total RNAs and subsequently used in real time PCR for quantification of ISG15 transcriptional expression. After forty-eight hours post infection or transfection, cells were harvested for extraction of total proteins to detect ISG15 protein expression. A significant up-regulation of ISG15 at transcription level was observed in HIV-1 infected or transfected cell lines, particulaly in THP-1 and TZM-bl cells. Up-regulation of ISG15 protein was observed only in TZM-bl cell. Cotransfection of ISG15 and HIV-1 indicated that ISG15 inhibited production of HIV-1 progeny virus in a dose and time depend manner in 293T cell but not TZM-bl cell. These results revealed upregulating ISG15 expression in transcriptional level and potential antagonistic mechanism against ISG15 by HIV-1 infection, simultanelusly.
Base Sequence ; Cell Line ; Cytokines ; genetics ; metabolism ; HIV Infections ; genetics ; metabolism ; virology ; HIV-1 ; physiology ; Humans ; Interferons ; metabolism ; Molecular Sequence Data ; Ubiquitins ; genetics ; metabolism ; Up-Regulation

OBJECTIVETo screen the mi-RNA expression profile after interferon treatment in cells infected with hepatitis C virus (HCV).

METHODSHuh-7.5.1 cells was infected with HCV by in vitro transcription and cultured with interferon. The mi-RNA microarray was used to measure the mi-RNA expression in the control group, HCV transcription group and interference group. Intra-group differences were analyzed by the 2 ((-delt delt CT)) method.

RESULTSWith mi-RNA expressed in normal Huh-7.5.1 cells as a benchmark, expressions of 13 kinds of mi-RNAs were up-regulated after HCV infection and then down-regulated following interferon treatment; 7 were down-regulated after HCV infection and then up-regulated following interferon treatment.

CONCLUSIONmi-RNA10a, mi-RNA21, mi-RNA149, mi-RNA152 and mi-RNA210 may be related to hepatitis C virus replication and transcription.

Cell Line, Tumor ; Gene Expression Profiling ; Hepacivirus ; genetics ; Humans ; Interferon-alpha ; pharmacology ; Interferons ; pharmacology ; MicroRNAs ; drug effects ; genetics ; RNA, Viral ; genetics ; Transfection

Interferon response is the first line of host defense against virus infection. Recent years have witnessed tremendous progress in understanding of fish innate response to virus infection, especially in fish interferon antiviral response. A line of fish genes involved in interferon antiviral response have been identified and functional studies further reveal that fish possess an IFN antiviral system similar to mammals. However, fish virus-induced interferon genes contain introns similar to mammalian type III interferon genes although they encode proteins similar to type I interferons, which makes it hard to understand the evolution of vertebrate interferon genes directly resulting in a debate on nomenclature of fish interferon genes. Actually, fish display some unique mechanisms underlying interferon antiviral response. This review documents the recent progress on fish interferon response and its molecular mechanism.
Animals ; Fish Diseases ; immunology ; virology ; Fish Proteins ; genetics ; metabolism ; Fishes ; immunology ; virology ; Gene Expression Regulation ; Interferons ; genetics ; immunology ; STAT1 Transcription Factor ; metabolism ; Virus Diseases ; immunology ; veterinary

Animals ; Antiviral Agents ; pharmacology ; Disease Models, Animal ; Hepacivirus ; drug effects ; genetics ; metabolism ; Hepatitis C ; virology ; Interferons ; pharmacology ; Mice ; MicroRNAs ; Replicon ; Signal Transduction ; Viral Proteins ; genetics ; Virus Replication