Uirusu

Reviews

TLR family and viral infection

Satoshi Uematsu, Shizuo Akira

Article type: Others
Subject area: Others
2004 Volume 54 Issue 2 Pages 145-151
Published: 2004
Released on J-STAGE: June 17, 2005

DOIhttps://doi.org/10.2222/jsv.54.145

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The immune system has been divided into innate and adaptive component, each of which has different roles and functions in defending the organism against foreign agents, such as bacteria and viruses. An important advance in our understanding of early events in microbial recognition and subsequent development of immune responses was the identification of Toll-like receptors (TLRs) as key molecules of the innate immune systems. The family of TLRs in vertebrates detects conserved structures found in a broad range of pathogens and triggers innate immune responses. At present, 11 members of the TLR family have been identified. A subset of TLRs recognize viral components and induce antiviral responses by producing type I interferons. Recent accumulating evidence has clarified signaling pathways triggered by TLRs in viral infection.

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Recognition of virus infected cells by NK cells

Hisashi Arase, Ikuo Shiratori

Article type: Others
Subject area: Others
2004 Volume 54 Issue 2 Pages 153-160
Published: 2004
Released on J-STAGE: June 17, 2005

DOIhttps://doi.org/10.2222/jsv.54.153

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NK cells show cytotoxicity against virus-infected cells and tumor cells and play an important role in host defense. Although mecheanism of target cell recognition by NK cells have been unclear for a long time, it has recently been elucidated that certain NK cell receptors specifically recognize virus products. Furthermore, expression pattern of NK cell receptors, which consist of activating and inhibitory receptors, determines susceptibility to virus-infection. Here, we review recent progress of mechanism of recognition of virus-infected by NK cells.

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Special Issue 1 : ‘Virus and Interferon’

Virus-induced expression of type I Interferon genes

Mitsutoshi Yoneyama, Takashi Fujita

Article type: Others
Subject area: Others
2004 Volume 54 Issue 2 Pages 161-167
Published: 2004
Released on J-STAGE: June 17, 2005

DOIhttps://doi.org/10.2222/jsv.54.161

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Intracellular double-stranded (ds) RNA is a major sign of replication for many viruses. Host mechanisms detect the dsRNA and provoke antiviral responses. Recently, we identified retinoic acid inducible gene-I (RIG-I), which encodes a DExD/H box RNA helicase containing the caspase recruitment domain (CARD) as a critical regulator for dsRNA-induced signaling. The helicase domain with intact ATPase activity is responsible for recognition of dsRNA, and the CARD transmits downstream signals, resulting in the activation of genes including type I interferons. In this review, we discuss the function of RIG-I in antiviral innate immunity.

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Molecular mechanisms for suppression of interferon signal transduction pathway caused by viral infections

Nobuhiro Fujii, Shin-ichi Yokota, Noriko Yokosawa, Tamaki Okabayashi

Article type: Others
Subject area: Others
2004 Volume 54 Issue 2 Pages 169-178
Published: 2004
Released on J-STAGE: June 17, 2005

DOIhttps://doi.org/10.2222/jsv.54.169

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In order to establish infection to host cells, viruses suppress or escape from the host immune response against microorganisms by various strategies. Interferon (IFN) system is an important contributor of innate immunity. IFN is induced by viral infection, and it promotes antiviral state through induction and/or activation of the effector molecules. Many viruses possess the suppression or inhibition mechanisms for the anti-viral effector molecules, whereas they also perform inhibition of IFN signaling pathway, JAK/STAT pathway. We consider that latter is a most effective strategy counteracting IFN function, because the signaling pathway is an entrance of the system. The strategies counteracting JAK/STAT pathway are varied among virus species. Viruses perform (i) production of IFN-binding protein, (ii) degradation of JAK/STAT components, (iii) suppression of activation (phosphorylation) of the components, (iv) inhibition of nuclear translocation of activated transcription factor, and (v) induction of host JAK/STAT negative regulator. Here, we present these strategies, especially our recent resulta of HSV1, mumps virus, and measles virus. For example, HSV1 induces a host JAK/STAT negative regulator SOCS3 (suppressor of cytokine signaling-3). Mumps virus V protein promotes degradation of both STAT-1 and STAT-3. Measles virus freezes the flexibility of IFN-alpha receptor complex by the action of viral proteins, C and V.

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Sendai virus proteins counteracting for the host innate immunity

Atsushi Kato

Article type: Others
Subject area: Others
2004 Volume 54 Issue 2 Pages 179-188
Published: 2004
Released on J-STAGE: June 17, 2005

DOIhttps://doi.org/10.2222/jsv.54.179

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The nucleotide sequence of Sendai virus (SeV) genome was determined in the 1980's. During the analysis of its cDNA, two mRNAs were found to be transcribed from the P gene; one encoding P protein, the other encoding V protein. In addition, C protein was found to be translated from both mRNAs. Though the function of V and C proteins was being unknown for a while, the reverse-genetic technique of paramyxoviruses developed at the latter half of the 1990's gave the light on studying them. The V or C protein-knockout-SeV can be made successfully, indicating that the V and C proteins are nonessential for virus growth, However, V knockout-SeV was cleared from the mouse lungs at the one day post inoculation, and C knockout-SeV was cleared immediately after the inoculation. Both V and C proteins were thus appeared to be important for counteracting host innate immunity generated in the early phase of viral infection.

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Expression of Host Genes in Influenza Virus Infected cells

Kazufumi Shimizu, Kazumichi Kuroda

Article type: Others
Subject area: Others
2004 Volume 54 Issue 2 Pages 189-196
Published: 2004
Released on J-STAGE: June 17, 2005

DOIhttps://doi.org/10.2222/jsv.54.189

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The NS1 protein of influenza virus shuts off host gene expression by inhibiting the polyadenylation-site cleavage of host pre-mRNAs, resulting in a general decline in cellular protein synthesis. On the other hand, an activation of several host genes related to host antiviral defense such as interferon-α/β, MxA, 2', 5'-oligoadenylate synthetase, and Fas occures upon infection. Therefore, balance of the shut-off and the activation of cellular genes during virus growth may be crucial in determining the outcome of infection. To obtain a comprehensive view of the global effects of influenza virus infection on human respiratory epithelial cells at the cytoplasmic mRNA level, we performed oligo DNA microarray analysis using GeneChip arrays (Affymetrix). In NCI-H292 cells infected with A/Udorn/72 virus, more than 4-fold increase of expression level was observed for 164 genes at 12 h pi. Approximately 60% of the virus-stimulated genes (VSGs) were also stimulated with interferon-β treatment and contained the genes known to possess antiviral activity. Interestingly, majority of the VSGs were stimulated before induction of interferons, suggesting that the stimulation of the VSGs during early phase of infection is not mediated by interferons, but it is triggered from within by the virus infection.

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Mechanism of persistence in HCV infection

MICHINORI KOHARA, KAZUAKI INOUE

Article type: Others
Subject area: Others
2004 Volume 54 Issue 2 Pages 197-204
Published: 2004
Released on J-STAGE: June 17, 2005

DOIhttps://doi.org/10.2222/jsv.54.197

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One of the prominent features of hepatitis C virus (HCV) is persistent infection, which is assumed to be a crucial event as a result of evading host defense system. Type I interferon beta (IFN-β) system is induced rapidly after viral infection and plays a central role in innate immunity. Upon immediate induction of type I IFN as host first defense line, interferon regulatory factor-3 (IRF-3) is phosphorylated, formed of homodimer and translocates to nucleus. IFN-β induction due to new castle disease virus (NDV) was significantly decreasd after the expression of full HCV genome (HCR6-Rz). Similar modification was observed in cell line expressing core to the NS2 protein region (HCR6-Fse). However, this decreasing was not observed in cell line expressing NS2 to the NS5B region (HCR6-Age). IRF-3 dimer formation induced by NDV infection was also suppressed after the expression of HCR6-Rz and HCR6-Fse, but not HCR6-Age. We further analyzed using transiently expressed HCV core, E1 or E2 in HepG2 cells. The suppression of IRF-3 dimer formation was caused by HCV core protein alone. These results indicated that a new crucial biological function of HCV core protein that may be related to persistence and pathogenesis of HCV.

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Molecular mechanism of tissue-specific infection of poliovirus

Satoshi Koike

Article type: Others
Subject area: Others
2004 Volume 54 Issue 2 Pages 205-212
Published: 2004
Released on J-STAGE: June 17, 2005

DOIhttps://doi.org/10.2222/jsv.54.205

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Poliovirus is the causative agent of an acute disease of the central nervous system, poliomyelitis. Poliovirus will be eradicated in the near future by a world-wide vaccination program. Poliovirus is a neurotropic virus that produces severe lesions selectively in the CNS. However, a basic question why poliovirus exhibits neurotropic property has not been elucidated. Poliovirus receptor and host factors involved in the translation initiation of viral protein, which are required for virus replication, play important roles in determining tissue tropism. We found that type I interferon response is also an important determinant of poliovirus tissue tropism. Type I interferon inhibits viral replication in the non-target tissues. The tissue tropism of poliovirus may be determined based on the balance of these mechanisms.

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Special Issue 2 : ‘Notable virus Infectim around Japan’

Rabies and other lyssavirusess

Nobuyuki Minamoto

Article type: Others
Subject area: Others
2004 Volume 54 Issue 2 Pages 213-222
Published: 2004
Released on J-STAGE: June 17, 2005

DOIhttps://doi.org/10.2222/jsv.54.213

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Since rabies has not been reported in Japan for nearly the past 50 years, it has been relegated to the status of a forgotten infectious disease in this country. However, in the neighboring Asian countries, Africa, America, the number of rabies cases had not decrease but on the contrary, seen an increasing trend. In Russia and the former Soviet Union countries (CIS countries), the number of information. Between 30, 000∼20, 000 fatal cases of rabies in both humans and animals had been reported yearly butit was thought that the number might run up to hundred of thousands. japan, Taiwan, UK, Australia and New Zealand are rabies-free countries and should be considered the exception rather than the norm. Due to the long Lull in which rabies has not occurred in Japan, people tend to forget that the disease can infect all mammals including humans, with a mortality rate of 100% after manifestation of debilitating nervous symptoms and that is one of the most dangerous zoonotic viral diseases on earth.

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Crimean-Congo hemorrhagic fever

Masayuki Saijo, Shigeru Moriikawa, Ichiro Kurane

Article type: Others
Subject area: Others
2004 Volume 54 Issue 2 Pages 223-227
Published: 2004
Released on J-STAGE: June 17, 2005

DOIhttps://doi.org/10.2222/jsv.54.223

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Crimean-Congo hemorrhagic fever (CCHF) is an acute infectious disease caused by CCHF virus (CCHFV), a member of the family Bunyaviridae, genus Nairovirus. The case fatality rate of CCHF ranges from 10-40%. Because CCHF is not present in Japan, many Japanese virologists and clinicians are not very familiar with this disease. However, there remains the possibility of an introduction of CCHFV or other hemorrhagic fever viruses into Japan from surrounding endemic areas. Development of diagnostic laboratory capacity for viral hemorrhagic fevers is necessary even in countries without these diseases. At the National Institute of Infectious Diseases, Tokyo, Japan, laboratory-based systems such as recombinant protein-based antibody detection, antigen-capture and pathological examination have been developed. In this review article, epidemiologic and clinical data on CCHF in the Xinjiang Uygur Autonomous Region, compiled through field investigations and diagnostic testing utilizing the aforementioned laboratory systems, are presented. CCHFV infections are closely associated with the environmental conditions, life styles, religion, occupation, and human economic activities. Based on these data, preventive measures for CCHFV infections are also discussed.

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Rift Valley fever virus

Tetsuro Ikegami, Shinji Makino

Article type: Others
Subject area: Others
2004 Volume 54 Issue 2 Pages 229-235
Published: 2004
Released on J-STAGE: June 17, 2005

DOIhttps://doi.org/10.2222/jsv.54.229

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Rift Valley fever virus (RVFV) causes massive mosquito-borne epidemics among humans and decimates ruminants in which the mortality rate is about 1% and 10-30%, respectively. Morbidity in RVFV-infected humans is high largely due to the effects of hemorrhagic fever and encephalitis. This virus is native to sub-Saharan Africa; yet if this virus is introduced into the environment, virus transmission appears to occur whenever sheep and cattle are present with abundant mosquito populations. RVFV is a negative-strand RNA virus which belongs to the family Bunyaviridae, genus Phlebovirus, and contains tripartite-segmented genomes (S, M, and L). S-segment is the ambisense genome, where N and NSs genes are coded in an antiviral-sense and viral sense S-segment, respectively. The inhibition of host mRNA synthesis, which is induced by the binding of NSs protein to RNA polymerase II transcription factor TFIIH, is the primary reason for the host-protein shut-off in RVFV-infected cells. Development of a RVFV reverse genetics system, which has not been accomplished yet, is important for the study of viral replication mechanisms, host virus interaction, viral pathogenicity as well as vaccine evaluation and development.

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Nipah Virus Infection

Yoshihiro Katu

Article type: Others
Subject area: Others
2004 Volume 54 Issue 2 Pages 237-242
Published: 2004
Released on J-STAGE: June 17, 2005

DOIhttps://doi.org/10.2222/jsv.54.237

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Nipah virus (NiV), emerged in Peninsular Malaysia, caused an outbreak of severe febrile encephalitis in humans and respiratory diseases in pigs between 1998 and 1999. By May of 1999, the death of 105 humans and the culling of about 1.1 million pigs were reported. Fruitbats of Pteropid species were identified as the natural reservoir hosts. The epidemiological studies suggested that NiV was introduced into pig farms by fruitbats, and was than transmitted to humans (mainly pig farmers) and other animals such as dogs, cats and horses. In 2004, NiV reappeared in Bangladesh with greater lethality. In contrast to the Malaysia case, epidemiologic characteristics of this outbreak suggested the possibility of fruitbats-to-person, or person-to-person transmission. In this article, the epidemiological comparison between two outbreaks in Malaysia and Bangladesh, and the new-trends of virological studies of NiV will be discussed.

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Topics

Recent Topics on Hepatitis E Virus : Emerging, Zoonotic, Animal-to-Human Transmission in Japan

Shunji MISHIRO

Article type: Others
Subject area: Others
2004 Volume 54 Issue 2 Pages 243-248
Published: 2004
Released on J-STAGE: June 17, 2005

DOIhttps://doi.org/10.2222/jsv.54.243

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Hepatitis E is undoubtedly a zoonosis. Recent observations suggest that the zoonotic food-borne mode of transmission has played an important role in the spread of hepatitis E virus (HEV) among Japanese people (who in general likes eating everything uncooked or undercooked : Sushi, Sashimi, Tataki, Namagimo, Shabu-shabu, etc). Moreover, the situation seems to be worsening. Wild boar (and deer also) has recently been increasing in its number, becoming a more potent HEV reservoir to humans than before. Pork, replacing beef in people's recent fear of BSE, is being consumed increasingly, particularly in Hokkaido. It may be Japanese people that an effective HEV vaccine is most longed for by.

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Amendment of the Infectious Diseases Control Law

Nobuhiko Okabe

Article type: Others
Subject area: Others
2004 Volume 54 Issue 2 Pages 249-254
Published: 2004
Released on J-STAGE: June 17, 2005

DOIhttps://doi.org/10.2222/jsv.54.249

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The Law Concerning the Prevention of Infectious Diseases and Medical Care for Patients of Infections (the Infectious Diseases Control Law) enacted on April 1, 1999, accompanies an additional rule for reconsideration in five years after putting the law in operation and for taking necessary steps when needed. The responses against bioterrorism involving anthrax and smallpox after the terrorist attacks on September 11, 2001, in the United States of America (a notice on October 11, 2001 by the Tuberculosis and Infectious Diseases Control Division, MHLW) and the response to severe acute respiratory syndrome (SARS), an emerging infectious disease upon which a Global Alert was issued on March 12, 2003, by WHO, were discussed. On November 5, 2003, partial amendment of the Infectious Diseases Control Law and the Quarantine Law was approved and put into operation on.
In the present amendment, the following three points were principally reconsidered : 1. strengthening infectious disease control in an emergency, particularly the role of national government, 2. reviewing control strategy of infectious diseases of animal origin, and 3. reviewing target diseases of the Infectious Diseases Control Law and categories of infectious diseases.

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BAC system : A novel method for manipulation of herpesvirus genomes based on the bacterial genetics

Yasushi Kawaguchi, Michiko Tanaka

Article type: Others
Subject area: Others
2004 Volume 54 Issue 2 Pages 255-264
Published: 2004
Released on J-STAGE: June 17, 2005

DOIhttps://doi.org/10.2222/jsv.54.255

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Although methods for reverse genetics of herpesviruses have been established in early 1980s, the steps are laborious and time-consuming. In 1997, Dr. Koszinwski's group reported a novel approach for the construction of herpesvirus mutants, based on cloning the viral genome as a bacterial artificial chromosome (BAC) in E. coli. This technique allows the maintenance of viral genomes as plasmid in E. coli and the reconstitution of viral progeny by transfection of the BAC plasmid into eukaryotic cells. Any genetics modification of the viral genome in E. coli using bacterial genetics is possible, thereby facilitating the introduction of mutagenesis into herpesvirus genome. This ‘BAC system’ has opened new avenues for reverse and forward genetics of herpesviruses in basic research and in vector development for human therapy. Here we describe the principle of the ‘BAC system’ in herpesvirus researches.

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