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At least 271 records · Page 15Linked to original sources
PubMed2005

Attenuated rabies virus activates, while pathogenic rabies virus evades, the host innate immune responses in the central nervous system.

Rabies virus (RV) induces encephalomyelitis in humans and animals. However, the pathogenic mechanism of rabies is not fully understood. To investigate the host responses to RV infection, we examined and compared the pathology, particularly the inflammatory responses, and the gene expression profiles in the brains of mice infected with wild-type (wt) virus silver-haired bat RV (SHBRV) or laboratory-adapted virus B2C, using a mouse genomic array (Affymetrix). Extensive inflammatory responses were observed in animals infected with the attenuated RV, but little or no inflammatory responses were found in mice infected with wt RV. Furthermore, attenuated RV induced the expression of the genes involved in the innate immune and antiviral responses, especially those related to the alpha/beta interferon (IFN-alpha/beta) signaling pathways and inflammatory chemokines. For the IFN-alpha/beta signaling pathways, many of the interferon regulatory genes, such as the signal transduction activation transducers and interferon regulatory factors, as well as the effector genes, for example, 2'-5'-oligoadenylate synthetase and myxovirus proteins, are highly induced in mice infected with attenuated RV. However, many of these genes were not up-regulated in mice infected with wt SHBRV. The data obtained by microarray analysis were confirmed by real-time PCR. Together, these data suggest that attenuated RV activates, while pathogenic RV evades, the host innate immune and antiviral responses.

Animals↗
PubMed1995

Tick-borne thogoto virus infection in mice is inhibited by the orthomyxovirus resistance gene product Mx1.

We show that tick-transmitted Thogoto virus is sensitive to interferon-induced nuclear Mx1 protein, which is known for its specific antiviral action against orthomyxoviruses. Influenza virus-susceptible BALB/c mice (lacking a functional Mx1 gene) developed severe disease symptoms and died within days after intracerebral or intraperitoneal infection with a lethal challenge dose of Thogoto virus. In contrast, Mx1-positive congenic, influenza virus-resistant BALB.A2G-Mx1 mice remained healthy and survived. Likewise, A2G, congenic B6.A2G-Mx1 and CBA.T9-Mx1 mice (derived from influenza virus-resistant wild mice) as well as Mx1-transgenic 979 mice proved to be resistant. Peritoneal macrophages and interferon-treated embryo cells from resistant mice exhibited the same resistance phenotype in vitro. Moreover, stable lines of transfected mouse 3T3 cells that constitutively express Mx1 protein showed increased resistance to Thogoto virus infection. We conclude that an Mx1-sensitive step has been conserved during evolution of orthomyxoviruses and suggest that the Mx1 gene in rodents may serve to combat infections by influenza virus-like arboviruses.

Animals↗
PubMed2006

Expression kinetics of interferon and interferon-induced genes in Atlantic salmon (Salmo salar) following infection with infectious pancreatic necrosis virus and infectious salmon anaemia virus.

Infectious pancreatic necrosis virus (IPNV) and infectious salmon anaemia virus (ISAV) are economically important pathogens of the salmonid aquaculture industry. Atlantic salmon were challenged by intraperitoneal injection (i.p.) with either virus followed by time-course sampling. Cohabiting fish in the IPNV challenge were also sampled. Kidney tissue was analysed using a TaqMan real-time PCR assay to measure the expression of a range of host immune genes in relation to the endogenous control, elongation factor 1 alpha (ELF). Host genes measured included Mx, type I and type II interferon (IFN), gammaIFN induced protein (gammaIP), interleukin-1 beta (IL-1beta) and tumour necrosis factor alpha (TNF-alpha). Viral levels were also measured. In i.p. injected fish, both viruses greatly induced expression of Mx, gammaIP, type I and type II IFN by day 6 post-infection, however only ISAV caused substantial mortality. Some differences between the expression kinetics produced by both viruses were noted. Infection with ISAV increased IL-1beta expression following day 6, but no effect was seen in fish infected with IPNV. Neither virus induced TNF-alpha expression. This study confirms the presence of both type I and type II IFN responses and their induced genes in Atlantic salmon upon infection with an orthomyxovirus and a birnavirus.

Animals↗
PubMed1973

Quantitative assessment of hemadsorption by myxoviruses: virus hemadsorption assay.

The standardization and quantitative evaluation of an assay for myxoviruses, based on the enumeration of individual infected clone 1-5C-4 cells manifesting hemadsorption within 24 h of infection, are described. Hemadsorption was detectable earlier than immunofluorescence in infected cells or hemagglutinins in culture medium. The relationship between virus concentration and cells exhibiting hemadsorption was linear. The assay was highly precise, sensitive, and reproducible.

Animals↗
PubMed1999

Lack of induction by rhinoviruses of systemic type I interferon production or enhanced MxA protein expression during the common cold.

To study whether MxA protein expression is systemically upregulated during rhinovirus infection, blood specimens were collected from 40 patients with common cold and MxA expression in mononuclear cells analyzed by flow cytometry. None of the patients with a confirmed rhinovirus infection (n = 15) or with an infection of unknown etiology (n = 20) had elevated expression of the MxA protein (median fluorescence intensity, 549 and 582, respectively) when compared to healthy controls (n = 11, median 590). Patients with influenza infections had significantly elevated values (n = 5, median 750), and interferon could be detected only in serum samples from influenza patients. In conclusion, expression of MxA in blood lymphocytes and an apparently systemic type I interferon response is not induced during rhinovirus infection or during most other cases of common cold in young adult patients.

Adult↗
PubMed1990

Transgenic mice with intracellular immunity to influenza virus.

We have generated transgenic mice that express the intracellular anti-influenza virus protein Mx1 under control of an interferon-responsive regulatory element. Upon infection with influenza virus, mice of a high responder line produce Mx1 protein locally at the sites of initial viral replication, exhibit little viral spread, and survive infection. Mice of a low responder line show more extensive viral spread and survive infection only when virus is given at high doses. To survive low dose infections, these mice require injection of interferon along with virus. The results show that influenza viral pathogenesis is determined by a subtle balance between the dose of the infecting virus and the levels of the antiviral host factor Mx1 and that mice can be rendered resistant to a virulent infection by "intracellular immunization" achieved through germline transformation.

Animals↗
PubMed1999

Human MxA protein protects mice lacking a functional alpha/beta interferon system against La crosse virus and other lethal viral infections.

The human MxA protein is part of the antiviral state induced by alpha/beta interferon (IFN-alpha/beta). MxA inhibits the multiplication of several RNA viruses in cell culture. However, its antiviral potential in vivo has not yet been fully explored. We have generated MxA-transgenic mice that lack a functional IFN system by crossing MxA-transgenic mice constitutively expressing MxA with genetically targeted (knockout) mice lacking the beta subunit of the IFN-alpha/beta receptor (IFNAR-1(-/-) mice). These mice are an ideal animal model to investigate the unique antiviral activity of human MxA in vivo, because they are unable to express other IFN-induced proteins. Here, we show that MxA confers resistance to Thogoto virus, La Crosse virus, and Semliki Forest virus. No Thogoto virus progeny was detectable in MxA-transgenic mice, indicating an efficient block of virus replication at the primary site of infection. In the case of La Crosse virus, MxA restricted invasion of the central nervous system. In contrast, Semliki Forest virus multiplication in the brain was detectable in both MxA-expressing and nonexpressing IFNAR-1(-/-) mice. However, viral titers were clearly reduced in MxA-transgenic mice. Our results demonstrate that MxA does not need the help of other IFN-induced proteins for activity but is a powerful antiviral agent on its own. Moreover, the results suggest that MxA may protect humans from potential fatal infections by La Crosse virus and other viral pathogens.

Alphavirus Infections↗
PubMed1992

[Severe community-acquired pneumopathy. What initial antibiotics to use?].

Even if they represent only a minor percentage of all respiratory infections, acute pulmonary infections are the leading mortality cause from infectious diseases. Epidemiologic data amongst hospitalized patients with acute infections reveal mean mortality figures of 20%. The adequate assessment of severity criteria is fundamental so that patients can be oriented towards suitable hospitalized units. Risks factors to be considered are: other illnesses, age (greater than 60 years), breathing frequency greater than 30/min, diastolic blood pressure less than 60 mmHg, confusion, a PaO2 less than 60 Torr, a leukocytosis greater than 30,000 or less than 4,000/mm3, albuminemia less than 35 g/l and blood urea greater than 7 mmol/l. The association of these factors increases the risk of complications and mortality in a linear way. By contrast, the type of responsible organism is not relevant. Five microorganisms are responsible for 80 to 90% of documented acute pulmonary infections: pneumococci, Mycoplasma pneumoniae, Haemophilus influenzae, Legionella pneumophila, Myxovirus influenzae. However, direct examination of bacteriologic smear allows for a proper identification of the infectious agent in only 15% of cases. The clinician can therefore use epidemiologic, clinical and radiological findings to propose an oriented, though probable, antibiotic treatment. In these conditions, the initial treatment remains the association of an A type penicillin with an inhibitory effect on beta-lactamases and of a macrolide (or, eventually, of a fluoroquinolone) until results of bacteriologic investigations is known. No data is available to suggest the use of new third generation oral cephalosporins in the first intention treatment of acute severe pulmonary infections due to their low and inconsistent effect on pneumococcus.

Acute Disease↗
PubMed1987

Influenza virus resistance of wild mice: wild-type and mutant Mx alleles occur at comparable frequencies.

The laboratory-reared progeny of wild Mus musculus domesticus from several places in Europe and from California were tested for resistance to experimental infection with influenza viruses and for the ability of their explanted macrophages to synthesize Mx protein in response to type I interferon. About 75% of these mice were resistant to influenza viruses and were able to synthesize Mx protein, as expected for mice carrying the influenza virus resistance allele Mx+ in either homozygous or heterozygous form. Resistance of wild mice was inherited as a single autosomal dominant trait which cosegregated with the ability to synthesize Mx protein. About 25% of the randomly bred wild mice failed to synthesize Mx protein and died after infection with influenza virus, very much like inbred mice homozygous for the Mx- allele. We conclude that Mx+ and Mx- alleles occur at roughly equal frequencies in wild mice and that some selective advantage for heterozygous individuals exists in the wild. This finding raises new questions about the physiological role of the Mx locus.

Animals↗