Viruses are powerful tools for the study of modern neurosciences. Most of the research on the connection and function of neurons were done by using recombinant viruses, among which neurotropic herpesvirus is one of the most important tools. With the continuous development of genetic engineering and molecular biology techniques, several recombinant neurophilic herpesviruses have been engineered into different viral tools for neuroscience research. This review describes and discusses several common and widely used neurophilic herpesviruses as nerve conduction tracers, viral vectors for neurological diseases, and lytic viruses for neuro-oncology applications, which provides a reference for further exploring the function of neurophilic herpesviruses.
Herpesviridae/genetics* ; Neurosciences ; Genetic Vectors/genetics* ; Genetic Engineering ; Neurons

Cyprinid herpesvirus 3 (CyHV-3) is the causative agent of an extremely contagious and aggressive disease afflicting common corp Cyprinus carpio L. termed koi herpesvirus disease (KHVD). Since it was first reported in 1997, the virus has spread worldwide rapidly, leading to enormous financial losses in industries based on common carp and koi carp. This review summarizes recent advances in CyHV-3 research on the etiology, epidemiology, pathogenesis, diagnosis, prevention, and control of KHVD.
Animals ; Fish Diseases ; diagnosis ; virology ; Fishes ; classification ; virology ; Herpesviridae ; genetics ; isolation & purification ; physiology ; Herpesviridae Infections ; diagnosis ; veterinary ; virology

Herpesviridae is a large family comprising linear, double-stranded DNA viruses. Herpesviridae contains three subfamilies: α-, β- and γ-herpesviruses. The glycoproteins gB, gH and gL of each subfamily form the "core fusion function" in cell-cell fusion. Other herpesviruses also need additional glycoproteins to promote fusion, such as gD of the Herpes simplex virus, gp42 of the Epstein-Barr virus, and gO or UL128-131 of the Human cytomegalovirus. In contrast, glycoproteins gM or gM/gN of herpesvirus inhibit fusion. We describe the molecular mechanisms of glycoprotein-induced fusion and entry of herpesviruses. It will be helpful to further study the pathogenic mechanism of herpesvirus.
Animals ; Cell Fusion ; Glycoproteins ; genetics ; metabolism ; Herpesviridae ; genetics ; metabolism ; Herpesviridae Infections ; physiopathology ; virology ; Humans ; Viral Proteins ; genetics ; metabolism

Recently, avian viral diseases have become one of the main models to study mechanisms of viral infections and pathogenesis. The study of regulatory relationships and mechanisms between viruses and microRNAs has also become the focus. In this review, we briefly summarize the general situations of microRNAs encoded by avian herpesviruses. Also, we analyze the regulatory relationships between tumorigenicity of avian herpesviruses and microRNAs. Additionally, the possible applications for prevention and treatment of viral diseases (such as infectious bursal disease, avian influenza and avian leucosis) using the regulatory mechanisms of microRNAs are also discussed.
Animals ; Avian Leukosis ; Birds ; virology ; Birnaviridae Infections ; Herpesviridae ; genetics ; Influenza in Birds ; MicroRNAs ; genetics

Since Epstein Barr virus was shown to encode microRNAs(miRNAs) in 2004, more than 470 miRNAs have been discovered in α-, β-, and γ-herpesviruses. MiRNAs are small non-coding RNA molecules and generally only have 18-25 nucleotides in length, which can regulate the expression of target genes by targeting its transcripts. Herpesvirus-encoded miRNAs not only target the key genes from latency to lytic replication, but also regulate various host cellular genes. Current data manifest that herpesvirus-encoded miRNAs can regulate viral latent infection and lytic replication, immune recognition, apoptosis, and tumorigenesis. The purpose of this paper is to summarize the targets and their fuction of hepesvirus-encoded miRNAs, in order to provide theoretical support for further analysis herpesviral pathogenesis.
Animals ; Herpesviridae ; genetics ; metabolism ; Herpesviridae Infections ; virology ; Humans ; MicroRNAs ; genetics ; metabolism ; RNA, Viral ; genetics ; metabolism

Glycoprotein N is encoded by glycoprotein N (gN) gene of herpesviruses. The amino acid composition and expression level of this protein vary among difference species of herpesviruses. According to present studies, gN protein is expressed in cytoplasm of host cells, mainly in endoplasmic reticulum. The gN forms a complex with glycoprotein M in host cells. The complex is involved in the processes of viral replication and inter-cellular infection. Moreover, this protein plays a role in immune evasion from host immune system. The study will provide a theoretical basis for further study of herpesvirus gN gene and its encoded protein.
Animals ; Herpesviridae ; genetics ; metabolism ; Herpesviridae Infections ; virology ; Humans ; Viral Envelope Proteins ; genetics ; metabolism

BACKGROUNDThe infection of Kaposi's sarcoma-associated herpes virus (KSHV) is most likely the cause of clinical Kaposi's sarcoma, primary effusion lymphoma, and multi-center Castleman's disease. KSHV infection has very limited epidemiological survey data in China, and its definite mode of transmission remains controversial. This study aimed to determine the infection status and the main transmission route of KSHV in Chinese population.

METHODSAn enzyme-linked immunosorbent assay (ELISA) utilizing KSHV ORF65 recombinant protein was employed to analyze the antibody response to KSHV ORF65 in sera from 122 healthy physical examination people, 107 intravenous drug users, 135 non-intravenous drug users, 211 hepatitis B (HBV) patients infected via blood transmission, 107 kidney transplant recipients, and 72 female sex workers in Zhejiang Province in Southeast China.

RESULTSKSHV infection occurred relatively common (13.1%) in healthy population in Zhejiang, China. Infection rate was 16.7% in female sex workers, but significantly elevated in intravenous drug addicts (58.9%), blood-transmitted HBV patients (28.0%) and kidney transplant patients (41.1%).

CONCLUSIONBlood borne transmission of KSHV is probably the main route of infection in Zhejiang Province.

Enzyme-Linked Immunosorbent Assay ; Herpesviridae Infections ; epidemiology ; transmission ; Herpesvirus 8, Human ; genetics ; isolation & purification ; pathogenicity ; Humans ; Open Reading Frames ; genetics

In the last decade, substantial progress has been made in understanding the molecular mechanisms involved in the initial host responses to viral infections. Herpesviral infections can provoke an inflammatory cytokine response, however, the innate pathogen-sensing mechanisms that transduce the signal for this response are poorly understood. In recent years, it has become increasingly evident that the Toll-like receptors (TLRs), which are germline-encoded pattern recognition receptors (PRRs), function as potent sensors for infection. TLRs can induce the activation of the innate immunity by recruiting specific intracellular adaptor proteins to initiate signaling pathways, which then culminating in activation of the nuclear factor kappa B (NF-κB) and interferon-regulatory factors (IRFs) that control the transcription of genes encoding type I interferon (IFN I) and other inflammatory cytokines. Furthermore, activation of innate immunity is critical for mounting adaptive immune responses. In parallel, common mechanisms used by viruses to counteract TLR-mediated responses or to actively subvert these pathways that block recognition and signaling through TLRs for their own benefit are emerging. Recent findings have demonstrated that TLR2 plays a crucial role in initiating the inflammatory process, and surprisingly that the response TLR2 triggers might be overzealous in its attempt to counter the attack by the virus. In this review, we summarize and discuss the recent advances about the specific role of TLR2 in triggering inflammatory responses in herpesvirus infection and the consequences of the alarms raised in the host that they are assigned to protect.
Adaptive Immunity ; Gene Expression Regulation ; immunology ; Herpesviridae ; physiology ; Herpesviridae Infections ; genetics ; immunology ; virology ; Host-Pathogen Interactions ; Humans ; Immune Evasion ; Immunity, Innate ; Interferon Regulatory Factors ; genetics ; metabolism ; Interferon Type I ; biosynthesis ; immunology ; NF-kappa B ; genetics ; metabolism ; Signal Transduction ; genetics ; immunology ; Toll-Like Receptor 2 ; genetics ; immunology

OBJECTIVETo investigate whether allitridin could interfere with the effects of murine cytomegalovirus (MCMV) infection on the transcription, expression and function of IL-12 genes in order to further explore the mechanism of allitridin against MCMV.

METHODSixty mice were randomly divided into allitridin treated group, placebo and blank controls. Allitridin was intra-peritoneal injected to mice in treated group once a day with general dosage (25 mg x kg(-1)) at 24 hours after MCMV infection, and the same dosage of physiological saline were given to placebo and blank groups. Four experimental mice were sacrificed at 3, 5, 7, 10, 14 days after treatment (n = 4 per time point), respectively. The expression of IL-12 p70 and IFN-gamma in supernatant of spleen cell cultures were measured by double-antibody sandwich ELISA, and IL-12 p35 and p40 mRNAs in spleen cells were analyzed by RT-PCR.

RESULTIn systemic infection mice, the expression of both IL-12 p70 protein and p35 mRNA significantly increased on day 3 post-infection (pi); then rapidly and markedly decreased on day 5 pi and later. The level of IFN-gamma reached the peak on day 3 pi, then gradually dropped and returned to normal levels during the period of day 10 to 14 pi, and IL-12 p40 mRNA level was persistently and significantly higher after infection. In allitridin treated mice, the levels of IL-12 p70 protein, IL-12 p35 and p40 mRNAs reached the peak on day 3 after treatment (P < 0.05), and then rapidly dropped to the normal levels during the period of 5-14 days. Level of IFN-gamma was also reached the peak on day 3 after treatment; however, it dropped a little on day 5 and then gradually increased and was much higher than those of both placebo and bland controls during the period of day 7 to 14 after treatment (P < 0.01).

CONCLUSIONAllitridin could completely correct the disturbance of expression of IL-12 gene caused by MCMV and persistently promote IFN-gamma expression, which was useful for enhancing the specific cellular immune reactions against CMV and clearance of CMV viruses from host. The result suggests another mechanism of allitridin against CMV.

Allyl Compounds ; therapeutic use ; Animals ; Antiviral Agents ; therapeutic use ; Enzyme-Linked Immunosorbent Assay ; Female ; Herpesviridae Infections ; drug therapy ; metabolism ; Interleukin-12 ; genetics ; metabolism ; Mice ; Mice, Inbred BALB C ; Muromegalovirus ; drug effects ; pathogenicity ; Reverse Transcriptase Polymerase Chain Reaction ; Sulfides ; therapeutic use

Animals ; Herpesviridae ; genetics ; metabolism ; Humans ; Viral Proteins ; chemistry ; genetics ; metabolism