Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Respirovirus”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed1996

Evaluation of a live attenuated bovine parainfluenza type 3 vaccine in two- to six-month-old infants.

BACKGROUND: A safe and effective parainfluenza type 3 (PIV-3) virus vaccine is needed to prevent serious PIV-3-associated illness in infants younger than 6 months of age. In previous studies a live bovine PIV-3 (BPIV-3) vaccine, which was developed to prevent human PIV-3 (HPIV-3) disease, was shown to be safe, infectious, immunogenic and phenotypically stable in 6- to 36-month-old infants and children. METHODS: The safety, infectivity and immunogenicity of a single dose of the BPIV-3 vaccine was evaluated in a randomized, placebo-controlled, double blinded trial in 19 infants 2 to 5.9 months of age and in 11 additional 6- to 36-month-old subjects. RESULTS: The BPIV-3 vaccine was well-tolerated in both age groups and infected 92% of those younger than 6 months and 89% of those older than 6 months of age. Serum hemagglutination-inhibition (HAI) antibody responses to HPIV-3 and to BPIV-3, respectively, were detected in 42 and 67% of the younger infants, compared with 70 and 85% of the older subjects. In the younger infants we analyzed the rate of antibody response by titer of maternally acquired antibodies; low titer was defined as a preimmunization serum HAI titer < 1:8 and high titer was defined as a preimmunization serum HAI titer > or = 1:8. Young infants with a low titer of maternally acquired antibodies were significantly more likely to respond to the BPIV-3 vaccine that those with a high titer (89% vs. none for serum HAI response to BPIV-3; P = 0.02, Fisher's exact test). CONCLUSIONS: This study demonstrated that the BPIV-3 vaccine was safe and infectious in infants younger than 6 months of age and was also immunogenic in the majority of these young infants. Additional studies are needed to determine whether two or more doses will enhance the immunogenicity of the BPIV-3 vaccine in young infants and to assess its safety and immunogenicity when given simultaneously with routine childhood immunizations.

Antibodies, Viral↗
PubMed2004

National disease burden of respiratory viruses detected in children by polymerase chain reaction.

BACKGROUND: The epidemiology of community-acquired respiratory viruses at the Children's Hospital of Wisconsin between 1996 and 1998 was examined with molecular [multiplex (M) PCR] and standard virologic methods. METHODS AND RESULTS: A total of 3325 patients with lower respiratory infection (LRI) [bronchiolitis (42%), pneumonia (38%) and croup (12%)] were identified. It is estimated that 545,000 LRI hospitalizations occur each year in the United States in children younger than 18 years old (viral, 428,000; pneumonia, 221,000; bronchiolitis, 222,000; croup, 65,000), including a continued increase in bronchiolitis hospitalizations (47.8/1000; <1 year). The most common viruses detected each year in hospitalized children included respiratory syncytial virus (A and B; 117,000), parainfluenza virus (PIV-1 and -2, 48 000; PIV-3, 18,000) and influenza (A and B, 39,000). With multiplex reverse transcription polymerase chain reaction (MPCR), different patient populations demonstrated different LRI epidemiology in relation to specific syndromes and viral causes. At least 21% of LRI hospitalizations were in children with significant medical problems.PIVs were detected much more frequently in immunocompromised children than in previously healthy children (33% vs. 16%). Similarly 15% of respiratory syncytial virus was detected between May and October, mostly in immunocompromised children. Influenza caused 19% of bronchiolitis in previously healthy children, and no virus could be reliably predicted based on clinical presentation, including wheezing. Of children hospitalized for LRI, 40% tested positive for the seven most common respiratory viruses by MPCR. CONCLUSIONS: Work is under way to expand the number of viruses detected by MPCR and to determine whether newly discovered viruses, such as human metapneumovirus, contribute to the burden of pediatric LRI hospitalizations.

Adolescent↗
PubMed1997

Paramyxovirus-induced syncytium cell formation is suppressed by a dominant negative fusion regulatory protein-1 (FRP-1)/CD98 mutated construct: an important role of FRP-1 in virus-induced cell fusion.

Syncytium formation and subsequent generalized cell fusion have been reported as potentially important mechanisms of virus-induced cytotoxic effects. We tried to clarify the roles of fusion regulatory factor-1 (FRP-1) in virus-induced cell fusion. Two mutated human FRP-1/CD98 proteins [FRP-1/HN, in which the cytoplasmic domain was replaced with the cytoplasmic domain of human parainfluenza virus type 2 (HPIV-2) haemagglutinin-neuraminidase (HN), and FRP-1/330 (serine), in which a cysteine at amino acid 330 was mutated to serine], when expressed stably in L929 cells, were lacking in cell-fusion-enhancing activity stimulated by anti-FRP-1 antibodies. Anti-FRP-1 antibodies enhanced Newcastle disease virus (NDV)-mediated polykaryocyte formation in parent HeLa cells, while anti-FRP-1 antibodies showed no/low effect on polykaryocyte formation in NDV-infected HeLa cells constitutively expressing FRP-1/HN (HeLa-FRP-1/HN cells), indicating that the FRP-1/HN molecule is capable of acting as a dominant negative inhibitor. Furthermore, when HeLa-FRP-1/HN cells were infected with various rubulaviruses (HPIV-2, mumps virus, simian viruses 5 and 41), virus-induced cell fusion was also suppressed, although virus replication was not inhibited in these cells, showing that FRP-1 molecules are required for virus-induced cell fusion. Therefore, FRP-1 is considered to be related to the pathogenesis of paramyxoviruses.

Animals↗
PubMed1999

Long-term CD8+ T cell memory to Sendai virus elicited by DNA vaccination.

The capacity of DNA vaccines to prime CD8+ T cells makes them excellent candidates for vaccines that are designed to emphasize cellular immunity. However, the long-term stability of CD8+ T cell memory induced by DNA vaccination is poorly characterized. Here, the quality of CD8+ T cell recall responses in mice was investigated more than 1 year after DNA vaccination with the Sendai virus nucleoprotein gene. Cytotoxic T lymphocyte (CTL) activity specific for both dominant and subdominant epitopes could be recalled readily 1 year after vaccination and the frequencies of CTL precursors specific for both of these epitopes were relatively high. These CTL responded strongly to subsequent Sendai virus infection in terms of their ability to migrate to the lung and to differentiate into effector cells. In addition, the recall response to virus infection, as determined by CTL activity in the lungs and IFN-gamma responses in the spleen, was both faster and greater in magnitude than that in control-immunized mice. Significantly, virus titres were reduced at least 100-fold in the lungs of mice that were immunized more than 1 year before infection, as compared with control mice. These data demonstrate that CD8+ T cell memory elicited by DNA vaccination is functionally relevant and persists for at least 1 year.

Animals↗
PubMed2003

Isolation and partial characterization of a novel paramyxovirus from the gills of diseased seawater-reared Atlantic salmon (Salmo salar L).

A formerly undescribed virus has been isolated from the gills of farmed Atlantic salmon post-smolts in Norway suffering from gill disease. Cytopathic effects appeared in RTgill-W1 cells 9 weeks post-inoculation with gill tissue material. Virus production continued for an extended period thereafter. Light and electron microscopic examination revealed inclusions and replication in the cytoplasm. The viral nucleocapsid consisted of approximately 17 nm thick filaments in a herringbone pattern. Certain areas of the plasma membrane were thickened by the alignment of nucleocapsids on the internal surface and projections of 10 nm long viral glycoprotein spikes on the external surface. Virus assembly and release was achieved by budding through the modified plasma membrane. Negatively stained virions were spherical and partly pleomorphic with a diameter of 150-300 nm as seen by electron microscopy. The virus was sensitive to chloroform, heat and low and high pH, and replication was not inhibited by Br-dU or IdU indicating an RNA genome. Both haemagglutination and receptor-destroying enzyme activity were associated with the virions and the formation of syncytia in infected cultures indicated fusion activity. The receptor-destroying enzyme was identified as neuraminidase. The virus contained five major structural polypeptides with estimated molecular masses of 70, 62, 60, 48 and 37 kDa. Its buoyant density was 1.18-1.19 g ml(-1) in CsCl gradients. From the observed properties we conclude that this new virus belongs to the Paramyxoviridae and suggest the name Atlantic salmon paramyxovirus (ASPV). Furthermore, replication occurred at 6-21 degrees C, suggesting a host range confined to cold-blooded animals.

Animals↗
PubMed1996

Further search for small molecular inactivants capable of eliciting respiratory mucosal immunogenicity by modifying Sendai virus core RNA.

Five groups of 32 chemicals were examined regarding their immunological functions as modifier inactivants to make inactivated Sendai nasal vaccine using a contact exposure experiment, direct immunofluorescent method, and serum HI titer. (1) Five of the nine reactive groups of reactive dyes (2-chloropyridine, 2, 4, 6-trichloropyrimidine, vinylsulfonic acid, epichlorohydrin and beta-chloroethylamine) induced complete or almost complete defense in the entire respiratory tract, and the four other vaccines brought about slight infection in the respiratory tracts. There was no marked rise in serum HI titers post-exposure, despite uneven development. (2) Of the four sizable substituted AS naphthol vaccines, naphthol AS-IRG and AS-G vaccines elicited nearly complete defense, but the two other vaccines, inactivated with more elongated molecules, invited rare and successive infections. The three immune groups produced invariably high serum HI titers. (3) Of the six naphthalene derivative vaccines, two (3-hydroxy-2-naphthoic acid methylester and 2-naphthol-6-sulfonic acid) induced complete or almost complete protection. But two vaccines brought about less protection, and the remaining two vaccines caused heavy infections. (4) Of the six benzene derivative vaccines, both m-nitrobenzenesulfonic acid and isatoic anhydride induced complete protection. Three vaccines permitted slight infections but 2, 4, 6-trinitrobenzenesulfonic acid vaccine caused severe infection. (5) Of the seven food dye vaccines, only orange I induced complete or nearly complete defense, while the other dye vaccines were inferior. In effect, twelve inactivated Sendai nasal vaccines modified the ribose and/or phosphate groups of the virus core RNA through five groups of small-sized molecules with specially fixed side chains, and elicited complete or almost complete respiratory mucosal defense. The viral stabilization requiring the least alteration of the configuration will be involved in the chemical modification.

Administration, Intranasal↗
PubMed1995

Isolation and characterization of paramyxoviruses from snakes and their relationship to avian paramyxoviruses.

Several viruses were isolated from snakes which died during an outbreak of disease in a zoo. The viruses could be cultivated at 28 degrees C on a snake cell line (VH2, ATCC CCL 140). In cell culture they formed syncytia, leading to destruction of the monolayer. The isolates were sensitive to treatment with chloroform but not to growth in the presence of IUDR and revealed haemagglutinating activity with chicken erythrocytes. These results, combined with electron microscopic examination of the infectious supernatant, confirmed the diagnosis of paramyxoviruses (PMV). Haemagglutination inhibition tests with antisera against avian PMV revealed a serological relationship between the snake viruses and the avian PMV serotypes 1 and 7. Tests for thermostability at 56 degrees C showed a marked decrease of the haemagglutination and infectivity titres in contrast to the avian PMV serotype 7. The multiplication of the snake viruses seemed to be restricted to incubation temperatures below 37 degrees C. At 28 degrees C the snake viruses could be cultivated in several cell cultures. Separation of virus proteins using polyacrylamide gel electrophoresis showed differences between the snake isolates and avian PMVs of serotypes 1 and 7.

Animals↗
PubMed1997

Experimental infection of swine and cat central nervous systems by the pig paramyxovirus of the blue eye disease.

This study analyses whether the pig paramyxovirus of blue eye disease (PPBED) infects the central nervous system (CNS) utilizing anterograde and retrograde peripheral nerve transport systems. The virus was injected into muscle and skin, and inoculated per nasum. The presence of PPBED was detected by an immunohistochemical method using polyclonal mouse antibodies against the whole inactivated virus, and was revealed with polyclonal rabbit antibodies against mouse immunoglobulin G (IgG) labelled with peroxidase. The PPBED injected into the pig medial gastrocnemius (MG) muscle was detected in a terminal branch innervating the MG muscle, in neural fibres of the sciatic nerve, in fibres of the ventral and dorsal spinal roots and in ventral horn neurones of the spinal cord. When PPBED was injected into the skin area innervated by the sural nerve, it was detected in neural fibres of the sural and sciatic nerves and in spinal cord dorsal horn neurones. The per nasum inoculum rapidly invaded the CNS through the olfactory nerve. The study concluded that, in order to invade the CNS, PPBED was transported retrogradely by peripheral cutaneous and muscular nerves, and anterogradely by the olfactory nerve. No PPBED was detected in either cat peripheral nerves or in cat CNS.

Animals↗
PubMed2001

Reproductive disease and congenital malformations caused by Menangle virus in pigs.

OBJECTIVE: To describe a new syndrome characterised by embryonic mortalities, stillbirths, mummified foetuses and congenital malformations in a herd of intensively farmed pigs. DESIGN: Field observations, laboratory investigations and examination of breeding records. PROCEDURE: Pathology examinations were performed on mummified and congenitally deformed piglets during an outbreak of reproductive disease at a 2600 sow intensive piggery in New South Wales from April to October 1997. Reproductive performance was monitored during the outbreak and breeding records were examined retrospectively. Serum and tissue samples from pigs were tested for evidence of infection with known porcine pathogens and for a new virus, Menangle virus, isolated from stillborn piglets with deformities from the affected piggery in August 1997. RESULTS: Reproductive disease occurred sequentially in all four breeding units at the affected piggery over a period of 21 weeks. The farrowing percentages in each unit decreased from 80 to 82% before the outbreak to 63 to 78% during the outbreak and the number of live piglets per litter declined from a mean of 9.6 to 9.8 before the outbreak to 7.2 to 8.9 during the outbreak. The proportion of affected litters (litters with less than six liveborn piglets) was highest (64%) in the sixth week of the outbreak. Mummified foetuses, stillborn piglets with arthrogryposis, craniofacial deformities and degeneration of the brain and spinal cord, were observed along with occasional abortions. Sera from sows that produced affected litters contained neutralising antibodies against Menangle virus and there was evidence that this virus had been introduced to the piggery in February 1997. CONCLUSIONS: Reproductive disease in pigs due to Menangle virus was characterised by stillbirths, mummification, embryonic death and infertility, along with abortions, skeletal deformities and degeneration of the brain and spinal cord in affected foetuses and stillborn piglets.

Animals↗
PubMed2001

Epidemiology and control of Menangle virus in pigs.

OBJECTIVE: To describe the epidemiology and eradication of Menangle virus infection in pigs. DESIGN: Field observations and interventions, structured and unstructured serological surveys, prospective and cross-sectional serological studies and laboratory investigations. PROCEDURE: Serum samples were collected from pigs at a 2600-sow intensive piggery in New South Wales that experienced an outbreak of reproductive disease in 1997. Serum samples were also collected from piggeries that received pigs from or supplied pigs to the affected piggery and from other piggeries in Australia. Serum and tissue samples were collected from pigs at piggeries experiencing reproductive disease in New South Wales. Sera and faeces were collected from grey-headed flying foxes (Pteropus poliocephalus) in the region of the affected piggery. Serum samples were tested for neutralising antibodies against Menangle virus. Virus isolation was attempted from faeces. RESULTS: Following the outbreak of reproductive disease, sera from 96% of adult pigs at the affected piggery, including sows that produced affected litters, contained neutralising antibodies against Menangle virus. Neutralising antibodies were also detected in sera from 88% of finisher pigs at two piggeries receiving weaned pigs from the affected piggery. No evidence of Menangle virus infection was found in other piggeries in Australia. In cross-sectional studies at the affected piggery, colostral antibodies were undetectable in most pigs by 14 to 15 weeks of age. By slaughter age or entry to the breeding herd, 95% of pigs developed high antibody titres (> or = 128) against Menangle virus in the virus neutralisation test. Menangle virus was eradicated from the affected piggery following a program of serological testing and segregation. Neutralising antibodies against Menangle virus were also detected in P poliocephalus from two colonies in the vicinity of the affected piggery. Two piggery workers were infected with Menangle virus. There was no evidence of infection in cattle, sheep, birds, rodents, feral cats and a dog at the affected piggery. CONCLUSIONS: Serological evidence of infection with Menangle virus was detected in pigs at a piggery that had experienced reproductive disease, in pigs at two associated piggeries and in fruit bats in the region of the piggery. Two humans were infected. The mode of transmission between pigs is unknown, but spread by faecal or urinary excretion is postulated. This virus can be eradicated by the segregation of pigs into discrete age groups.

Animals↗
PubMed1987

Efficiency of immunofluorescence for rapid detection of common respiratory viruses.

Rapid immunofluorescence (FA) methods for the detection of common respiratory viruses were compared with culture results over a 3-year period to assess the relative efficiency of FA in a clinical laboratory setting. For respiratory syncytial virus, efficiencies were high (sensitivity, 90 to 95%; specificity, 92 to 95%). The sensitivity of FA for detection of parainfluenza virus type 1, parainfluenza virus type 3, influenza A virus, and adenoviruses ranged from 28 to 63%, but specificities for these viruses were uniformly 98 to 100%. The observations form a basis for consideration of selective reduction of routine culture procedures for specimens with initial positive rapid FA results; however, the possibility of dual viral infection in some situations must also be considered.

Adenoviridae Infections↗
PubMed1997

Inflammatory infiltration of the upper airway epithelium during Sendai virus infection: involvement of epithelial dendritic cells.

We undertook the present study to determine the nature of the cellular inflammatory response within the epithelial lining of the rat trachea during a Sendai virus infection. In particular, we aimed to investigate changes in the resident population of epithelial dendritic cells. Rats were infected with Sendai virus, and tracheal tissue was examined immunohistochemically at various times with a panel of cell-specific monoclonal antibodies. We found that Sendai virus infection was restricted to only the lumenal layer of epithelial cells and that virus nucleoprotein was present from days 2 to 5 postinfection. Starting around day 2 or 3, there was a large cellular influx consisting of macrophages, neutrophils, NK cells, and T cells; this coincided with expression of high levels of ICAM-1 on the basal (uninfected) layers of the epithelium. The T cells were mostly alphabeta T-cell receptor positive; however, a smaller influx of gammadelta T cells also took place. The number of resident dendritic cells increased markedly during infection, with numbers peaking around day 5 and remaining elevated 14 days later. The peak of the inflammatory response occurred on day 5 and declined thereafter, with the exception of dendritic cell and alphabeta T-cell numbers, which remained elevated. Starting around day 3, the tracheal epithelial cells expressed increasing levels of major histocompatibility complex class II antigen. This expression was maximal at day 5 and declined rapidly thereafter. In vitro culture of tracheal segments demonstrated that viral infection was not per se responsible for the upregulation of class II expression and that when cultured in the presence of gamma interferon, class II antigen was induced on epithelial cells.

Animals↗
PubMed1997

Protection of mice from respiratory Sendai virus infections by recombinant vaccinia viruses.

Mechanisms of protection of mice from Sendai virus, which is exclusively pneumotropic and causes a typical respiratory disease, by immunization with recombinant vaccinia viruses (RVVs) were investigated. Although the RVV carrying a hemagglutinin-neuraminidase gene of Sendai virus (Vac-HN) propagated in the noses and lungs of mice by either intranasal (i.n.) or intraperitoneal (i.p.) inoculation, no vaccinia virus antigens were detected in the mucosal layer of upper and lower airways of the i.p.-inoculated mice. The mice immunized i.n. with Vac-HN or Vac-F (the RVV carrying a fusion protein gene of Sendai virus) demonstrated the strong resistance to Sendai virus challenge both in the lung and in the nose, whereas the i.p.-immunized mice showed almost no resistance in the nose but showed a partial resistance in the lung. Titration of Sendai virus-specific antibodies in the nasal wash (NW), bronchoalveolar lavage (BAL), and serum collected from the Vac-F-immunized mice showed that the NW from the i.n.-immunized mice contained immunoglobulin A (IgA) antibodies but no IgG and the BAL from the mice contained both IgA and IgG antibodies. On the other hand, neither IgA nor IgG antibodies were detected in the NW from the i.p.-immunized mice and only IgG antibodies were detected in the BAL, although both i.n.- and i.p.-immunized mice exhibited similar levels of serum IgG, IgA, and neutralizing antibodies. The resistance to Sendai virus in the noses of i.n.-immunized mice could be abrogated by the intranasal instillation of anti-mouse IgA but not of anti-IgG antiserum, while the resistance in the lung was not significantly abrogated by such treatments. These results demonstrate that IgA is a major mediator for the immunity against Sendai virus induced by the RVVs and IgG is a supplementary one, especially in the lung, and that the RVV should be intranasally inoculated to induce an efficient mucosal immunity even if it has a pantropic nature.

Administration, Intranasal↗
PubMed1997

Importance of the cysteine-rich carboxyl-terminal half of V protein for Sendai virus pathogenesis.

The Sendai virus V protein is a nonstructural trans-frame protein whose cysteine-rich C-terminal half is fused to the acidic N-terminal half of the P protein via mRNA editing. We recently created a mutant by disrupting the editing motif, which is devoid of mRNA editing and hence unable to produce the V protein, and demonstrated that this V(-) virus replicated normally or even faster with augmented gene expression and cytopathogenicity in cells in vitro, but was strongly attenuated in pathogenicity for mice (A. Kato, K. Kiyotani, Y. Sakai, T. Yoshida, and Y. Nagai, EMBO J. 16:578-587, 1997). Thus, although categorized as a nonessential protein, the V protein appeared to encode a luxury function required for the viral in vivo pathogenesis. Here, we created another version of a V-deficient mutant, VdeltaC, encoding only the N-terminal half but not the V-specific C-terminal half, by introducing a stop codon in the trans-V frame, and then we compared its in vitro and in vivo phenotypes with those of the V(-) and wild-type viruses. The VdeltaC virus was found to be similar to the wild-type virus in vitro with no augmented gene expression and cytopathogenicity, but in vivo, it resembled the V(-) virus, displaying a similarly attenuated phenotype. Thus, the pathogenicity determinant in the V protein was mapped to the C-terminal half. The N-terminal half was likely sufficient to confer normal (wild-type) in vitro phenotypes.

Amino Acid Sequence↗
PubMed1997

The cytotoxic T-lymphocyte response to Sendai virus is unimpaired in the absence of gamma interferon.

Sendai virus is eliminated from the respiratory tract of gamma interferon (IFN-gamma) -/- BALB/c mice with normal kinetics. The level of virus-specific cytotoxic T-lymphocyte (CTL) activity in the cell population recovered by bronchoalveolar lavage is unimpaired, the prevalence of interleukin-4 (IL-4)-producing cells is increased, and the titers of virus-specific immunoglobulins IgG1 and IgG2b are higher in the IFN-gamma -/- mice. The emergence of this T-helper 2 response profile in both lymphoid tissue and the pneumonic lung has no obvious deleterious consequences. Virus clearance is slightly delayed following depletion of the CD4+ subset, with the effect being similar in magnitude for IFN-gamma -/- and +/+ mice. However, the generation of CTL precursors (CTLp) is diminished in the IFN-gamma -/- (but not +/+) mice in the absence of concurrent CD4+ T help. Apparently the clonal expansion of the CTLp population can be promoted either by a cytokine (perhaps IL-2) produced by the IFN-gamma -/- CD4+ T cells or by IFN-gamma made by other cell types in the +/+ mice.

Animals↗