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PubMed1981

[Syncytial sprouts and intervillous bridges in human placenta (author's transl)].

In general syncytial sprouts and intervillous bridges are artifacts. Complete series of histological sections reveal that sprouts and bridges are caused by tangential sections through the syncytiotrophoblast. These observations are supported by scanning electron microscopy, graphical reconstructions and model experiments. However, it cannot be decided unequivocally whether short syncytial sprouts are artifacts or true differentiations of the syncytiotrophoblast.

Chorionic Villi↗
PubMedDate not supplied

Diagnosis of syncytial (lacunar cell-predominant) nodular sclerosing Hodgkin's disease by fine needle aspiration. A case report.

We report a case of syncytial nodular sclerosing Hodgkin's disease diagnosed by fine needle aspiration biopsy. To our knowledge, the cytologic findings of this unusual histologic variant have not been reported previously. We believe this entity represents a serious potential pitfall to the aspiration cytologist who targets lymph nodes. This report describes the cytologic features of syncytial nodular sclerosing Hodgkin's disease and emphasizes the need in general for moderate conservatism in fine needle aspiration biopsy interpretation in patients without a previously documented malignancy. It also demonstrates the superiority of tissue sampling with fine needle aspiration biopsy when compared to incisional biopsy.

Adult↗
PubMed1976

[Role of bovine respiratory syncytial virus in the aetiology of viruspneumonia in calves and yearlings ("pinkengriep") (author's transl)].

The clinical picture of "pinkengriep", an enzootic form of bronchopneumonia in young cattle, is described. In addition to cough, conjunctivitis and a soporous state, accelerated respiration initially is an outstanding clinical symptom. In some cases, symptoms of fog fever appear during the second stage of the disease. In the autumn of 1973 and that of 1974, a total number of 292 animals with "pinkengriep" were serologically examined for known respiratory virus infections and Chlamydia. Complement fixation tests showed that there was significant increase in antibodies to respiratory syncytial virus in 76 per cent of the animals studied. In the case of para-influenza virus 3, virus diarrhoea virus, the adenoviruses of the antigen groups 1, 2 and 3, those of the antigen groups 4 to 10 inclusive and Chlamydia, these proportions were 48, 13, 12, 11 en 10 per cent respectively. On the other hand, symptoms of infection with infectious bovine rhinotracheitis virus were absent in the herds studied. These findings suggest a possible role of bovine respiratory syncytial virus in "pinkengriep".

Animals↗
PubMed2004

Role of complement in neutralization of respiratory syncytial virus.

Serum neutralizing antibody titers to respiratory syncytial virus (RSV) are higher when assayed with guinea pig complement. A number of different mechanisms have been suggested for enhancement of neutralization by complement. The most straightforward is that complement-antibody complexes present a greater steric hindrance to viral entry than with antibody alone. To define the implications of measuring serum neutralizing antibody with and without complement, sera from adults, young children, infants, and cord bloods were run in plaque neutralization assays with representative viruses of the RSV A and B subgroups. Although titers of neutralizing antibody were higher in the presence of complement, the addition of complement did not increase the ability to detect antibody rises after natural infection. Some of the complement effect may be attributable to an inhibition of RSV replication by complement alone. While these observations do not address the role for complement in the pathogenesis of RSV infection, they suggest that neutralization assays performed without complement may be most reflective of physiologic conditions in the respiratory tract.

Adult↗
PubMed2025

Whole-Genome Conservation Analysis for the Specific and Accurate Detection of Influenza A and B Viruses and Respiratory Syncytial Virus by Quadruplex RT-qPCR.

Influenza virus (Flu) and respiratory syncytial virus (RSV) are the primary pathogens responsible for acute respiratory infections. Both viruses are prone to mutations due to the seasonal epidemic, leading to an increasing rate of false-negative results. In this study, comprehensive meta-analyses of the genomes focusing on most conserved fragments have been performed for the four seasonal influenza viruses (two subtypes of Flu A: H1N1 and H3N2; two subtypes of Flu B: Yamagata and Victoria) and the two types of RSV: RSVA and RSVB), respectively. The most conserved sequences of 200 bp were identified as targets of the designed primer/probe sets for RT-qPCR were screened and optimized. Good sensitivities of the optimized primer/probe sets were obtained with the limits of detections of 2.95, 2.82, 1.57, 2.8, 1.19, and 2.12 copies/reaction for H1N1, H3N2, Yamagata, Victoria, RSVA and RSVB, respectively. Eventually, quadruplex qPCR using the four designed primer/probe sets can achieve simultaneous screening of the four viruses at a single tube. Furthermore, the assay's good performance in detecting target viruses from clinical throat swab samples demonstrated its potential for diagnosis of these viruses. The method, based on the identified conserved sequences and primer/probe sets, can effectively reduce false-negative results and rapidly respond to these viruses during respiratory disease outbreaks, or even before their widespread emergence, which aid in preventing outbreaks and guiding clinical treatment.

Humans↗
PubMed2025

Development and Validation of Amplicon-Based Protocol for Sequencing of Respiratory Syncytial Virus Genome.

The most prevalent cause of severe respiratory infections in children is the human respiratory syncytial virus (RSV). The advent of next-generation sequencing (NGS) has made it possible to incorporate this technology into pathogen monitoring and surveillance. Whole-genome sequencing (WGS) of RSV has now become a relatively widely used method for tracking viral evolution. Here we report an improved high-throughput RSV-WGS assay performed directly on clinical samples that is suitable for short-read sequencing platforms. A total of 100 RSV-positive samples collected between November 2022 and March 2024 fulfilled the inclusion cycle quantification criteria and were randomly included in the validation process. The WGS protocol was designed to amplify three distinct amplicons to cover the entire RSV genome. The protocol described here can be successfully replicated in several instances (approximately 95%) in samples with a relatively low viral load, typically corresponding to cycle of quantification values of 27-32. The amplicon-based protocol produced meaningful sequencing results in terms of median depth of coverage (more than 12000×) and median of mapped reads (> 1 × 106 reads). The sequences that had passed the filters showed a coverage of at least 98% across the entire genome, with cycle quantification values of 32. Based on the obtained data resulting in an easy-to-perform protocol helpful for the molecular epidemiology surveillance of RSV.

Humans↗
PubMedDate not supplied

New drugs and treatment for respiratory syncytial virus.

The respiratory syncytial virus (RSV) is a global health problem affecting infants and the elderly and claiming more lives than AIDS in many parts of the world. Only two antibody drugs are approved for its prevention, and ribavarin, a relatively nonspecific antiviral, is used for treatment. In the mid-1990s, a number of pharmaceutical and biotech companies initiated research programs against RSV. Together, the academic and the industrial R&D covered the whole spectrum of antibodies, vaccines, synthetic small molecule antiviral and antisense technology, and at one point, accounted for at least 25 active R&D programs. However, coincident to the marketing of the monoclonal antibody palivizumab (Synagis) in 1998, a sharp decline in such projects ensued. Many companies recently cancelled RSV projects during a prioritisation of their R&D portfolios although the continuing medical need, large market size and sales projections clearly indicate that a safe and effective RSV drug or vaccine is likely to attain blockbuster status. Today RSV receives an insignificant fraction of the R&D budget compared with AIDS, for example. This article reviews the present status of the anti-RSV regimen, covers drugs in the market and in development, and attempts to link basic research to industrial drug development, animal models of RSV, clinical trials, current clinical management, and present and future market projections. It is hoped that the unmet medical need of the victims of RSV will encourage continued involvement of the pharmaceutical and biotechnology industry in developing safe and effective prevention and treatments for RSV.

Aged↗
PubMed2001

Membrane-associated respiratory syncytial virus F protein expressed from a human rhinovirus type 14 vector is immunogenic.

Human rhinovirus (HRV) replicons have the potential to serve as respiratory vaccine vectors for mucosal immunization in humans. However, since many vaccine immunogens of interest are glycosylated, an important concern is whether HRV replicons are capable of expressing glycosylated proteins. The human respiratory syncytial virus (RSV) fusion (F) protein was chosen as a model glycoprotein and the HRV replicon DeltaP1FVP3 was generated by inserting the F protein-coding sequence in frame and in lieu of the 5' proximal 1489 nucleotides of the capsid-coding segment in the HRV-14 genome. When transfected into H1-HeLa cells, DeltaP1FVP3 replicated and led to the expression of the F protein. Inhibition with guanidine demonstrated that F-protein expression was dependent on DeltaP1FVP3 replication and did not result from translation of input RNA. Although most of the F protein remained as an immature, glycosylated precursor (F0), a readily detectable fraction of the protein was processed into the mature glycosylated subunit F1, an event known to occur within the Golgi apparatus. Packaged DeltaP1FVP3 replicons were generated in transfected HeLa cells by coexpression of homologous HRV capsid proteins using the vaccinia virus/T7 RNA polymerase hybrid system. Packaged replicon RNAs were capable of infecting fresh cells, leading to accumulation of the F protein as in RNA-transfected cells. Mice immunized with HeLa cell lysates containing F protein expressed from DeltaP1FVP3 produced neutralizing antibodies against RSV. These results indicate that an HRV-14 replicon can express a foreign glycosylated protein, providing further support for the potential of HRV replicons as a vaccine delivery system.

Animals↗
PubMed2001

Chimeric subgroup A respiratory syncytial virus with the glycoproteins substituted by those of subgroup B and RSV without the M2-2 gene are attenuated in African green monkeys.

Using the existing reverse genetics system developed for the subgroup A respiratory syncytial virus (RSV), a chimeric virus (designated rA-G(B)F(B)) that expresses subgroup B-specific antigens was constructed by replacing the G and F genes of the A2 strain with those of the 9320 strain of subgroup B RSV. rA-G(B)F(B) grew well in tissue culture, but it was attenuated in the respiratory tracts of cotton rats and African green monkeys. To further attenuate this chimeric RSV, the M2-2 open reading frame was removed from rA-G(B)F(B). rA-G(B)F(B)DeltaM2-2 was highly attenuated in replication in the respiratory tracts of the infected monkeys, but it provided complete protection against wild-type subgroup B RSV challenge following two doses of infection. In this study, rA2DeltaM2-2 (a recombinant A2 RSV that lacks the M2-2 gene) was also evaluated in African green monkeys. The replication of rA2DeltaM2-2 was highly restricted in both the upper and lower respiratory tracts of the infected monkeys and it induced titers of serum anti-RSV neutralizing antibody that were slightly lower than those induced by wild-type rA2. When rA2DeltaM2-2-infected monkeys were challenged with wild-type A2 virus, the replication of the challenge virus was reduced by approximately 100-fold in the upper respiratory tract and 45,000-fold in the lower respiratory tracts. rA2DeltaM2-2 and rA-G(B)F(B)DeltaM2-2 could represent a bivalent RSV vaccine composition for protection against multiple strains from the two RSV subgroups.

Animals↗
PubMed1995

Antigenic analysis of the F protein of the bovine respiratory syncytial virus: identification of two distinct antigenic sites involved in fusion inhibition.

From two independent fusions, fifteen MAbs directed to the F protein of the bovine respiratory syncytial virus (BRSV) were characterized by radio-immunoprecipitation assays. Competition binding assays among these MAbs identified two distinct antigenic sites (A and B) and one overlapping site (AB). All of the MAbs specific to epitopes belonging to site A neutralized the infectivity of the virus in vitro and recognized human and bovine RSV strains. Only two out of the five MAbs directed to epitopes of site B were neutralizing and three reacted with all of the RSV strains tested, suggesting that the epitopes constituting this domain present heterogeneous characteristics. In each of sites A and B, one of the neutralizing MAbs also inhibited cell fusion. The biological relevance of these domains was established by competing representative MAbs and sera from BRSV-infected calves.

Animals↗
PubMed1996

A model for respiratory syncytial virus (RSV) infection based on experimental aerosol exposure with bovine RSV in calves.

Five conventionally kept calves aged between 17 and 24 days were experimentally infected with bovine respiratory syncytial virus (BRSV) by aerosol in order to mimic the natural infection route. The calves were killed and autopsies performed 7 days after the first virus challenge. The BRSV isolate used induced tracheitis, bronchitis and atelectasis in infected calves. The only virus which could be isolated from the lungs of the calves was BRSV. In addition, Mycoplasma bovirhinis was isolated from the lungs or/and trachea of two calves. The clinical and histopathological findings, as well as the detection of BRSV antigens by immunofluorescence in the epithelial cells of lung and trachea, and the reisolation of the virus from bronchoalveolar lavage fluids of all inoculated calves, provided confirmation of successful infection with BRSV.

Aerosols↗
PubMed2004

Safety and efficacy of immune-stimulating complex-based antigen delivery systems for neonatal immunisation against respiratory syncytial virus infection.

To protect against human respiratory syncytial virus (hRSV)-induced bronchiolitis in early infancy, vaccines need to be designed which are effective in the neonatal period. To test the safety and efficacy of adjuvants in neonatal mice, we injected hRSV surface proteins combined with immune-stimulating complexes (ISCOMs) prepared from fractions A, C or A + C of Quillaja saponins. All were well tolerated in adults, but A + C ISCOMS proved lethal in neonates; A or C fractions alone were well tolerated by neonates up to the adult dose. hRSV-ISCOM A induced antibody responses similar to combined fractions, and potent in vitro cytotoxic T cell responses. Adult-like in vitro cytotoxicity against hRSV-infected targets and precursor cytotoxic T cell frequencies were observed within one week of neonatal priming and hRSV-ISCOM A-primed neonates showed virtually complete protection against subsequent viral challenge. hRSV challenge was associated with some pulmonary eosinophilia in both age groups, with higher IL-4 production by lung CD4+ T cells in mice primed as neonates. This was, however, accompanied by only minor (approximately 10%) and transient illness and weight loss. Thus, the identification of hRSV antigen delivery systems with an age-appropriate adjuvanticity/reactogenicity balance may be feasible even in the vulnerable early-life period.

Adjuvants, Immunologic↗
PubMed2004

Recombinant respiratory syncytial virus lacking secreted glycoprotein G is attenuated, non-pathogenic but induces protective immunity.

Respiratory syncytial virus (RSV) causes intense pulmonary inflammatory responses in some infected infants. The surface attachment protein 'G' of RSV has membrane-bound and secreted forms and shows homology to the CX3C chemokine fractalkine. Using recombinant techniques, we generated replication-competent recombinant clonal RSV expressing normal G proteins ('rRSV') or only the membrane-bound form of G ('Gmem rRSV'). Both recombinants grew well in HEp-2 cells, but after primary intranasal infection in mice, pulmonary Gmem rRSV replication was reduced tenfold compared to parental or rRSV; moreover, CCL2 and CCL5 production was greatly reduced and no apparent disease or pulmonary cellular infiltration was observed. However, Gmem rRSV-infected mice developed good antibody responses and were fully protected against subsequent intranasal challenge with parental virus. Even in mice sensitized to G by cutaneous infection with recombinant vaccinia expressing G, intranasal challenge with Gmem rRSV caused insignificant disease. We conclude that secreted G is a key viral product assisting virus replication in vivo, enhancing CCL2 and CCL5 production and promoting illness. Engineered RSV mutants lacking the ability to secrete G are thus promising vaccine candidates.

Animals↗
PubMed2006

Respiratory syncytial virus disease mechanisms implicated by human, animal model, and in vitro data facilitate vaccine strategies and new therapeutics.

Respiratory syncytial virus (RSV) is the leading cause of bronchiolitis, pneumonia, mechanical ventilation, and respiratory failure in infants in the US. No effective post-infection treatments are widely available, and currently there is no vaccine. RSV disease is the result of virus-induced airway damage and complex inflammatory processes. The outcome of infection depends on host and viral genetics. Here, we review disease mechanisms in primary RSV infection that are implicated by clinical studies, in vitro systems, and animal models. Defining RSV disease mechanisms is difficult because there is a wide range of RSV disease phenotypes in humans, and there are disparities in RSV disease phenotypes among the animal models of RSV infection. However, host factors identified by multiple lines of investigation as playing important roles in RSV pathogenesis are providing key insights. A better understanding of RSV molecular biology and RSV pathogenesis is facilitating rational vaccine design strategies and molecular targets for new therapeutics.

Animals↗
PubMed2004

Pulmonary delivery of respiratory syncytial virus DNA vaccines using macroaggregated albumin particles.

At present there is no safe and effective vaccine for respiratory syncytial virus (RSV). DNA vaccines encoding RSV surface glycoproteins are one option being examined. Current methods to deliver DNA vaccines generally require repeated high dose intramuscular or intradermal administration for effectiveness. In this study, we examine the efficacy of pulmonary DNA vaccination using low dose DNA vaccines encoding the RSV F glycoprotein conjugated to macroaggregated albumin (MAA-F). Single vaccination of BALB/c mice with 1 microg MAA-F was ineffective, however mice boosted with an additional 1 microg MAA-F, or vaccinated a single time with 10 microg MAA-F, developed substantially improved immunity associated with reduced viral titers, increased anti-F antibody responses, and enhanced Th1 and Th2 intracellular cytokine responses. This study shows that MAA may be a useful carrier for RSV DNA vaccines.

Administration, Intranasal↗
PubMed2004

Bovine respiratory syncytial virus ISCOMs--protection in the presence of maternal antibodies.

The protection induced by immunostimulating complexes (ISCOMs) against bovine respiratory syncytial virus (BRSV) was evaluated and compared to that of a commercial inactivated vaccine (CV) in calves with BRSV-specific maternal antibodies. Following experimental challenge, controls (n = 4) and animals immunized with CV (n = 5) developed moderate to severe respiratory disease, whereas calves immunized with ISCOMs (n = 5) remained clinically healthy. BRSV was re-isolated from the nasopharynx of all controls and from all calves immunized with CV, but from none of the calves immunized with ISCOMs. BRSV-RNA was detected by real-time PCR from a single animal in this group. Significantly higher BRSV-specific nasal IgG, serum IgG1 and IgG2 titers were detected before and after challenge in animals immunized with ISCOMs versus CV. In conclusion, the ISCOMs overcame the suppressive effect of maternal antibodies in calves and induced strong clinical and virological protection against a BRSV challenge.

Adjuvants, Immunologic↗
PubMed2005

DNA vaccination against respiratory syncytial virus in young calves.

A DNA vaccine encoding the fusion (F) gene (DNA-F) of bovine respiratory syncytial virus (BRSV) induced significant protection against BRSV infection in young calves. However, serum antibody to RSV developed more slowly in animals vaccinated with DNA-F when compared with those previously infected with BRSV. Furthermore, protection against BRSV infection was not as great as that induced by prior BRSV infection. Although there was little difference in the level of protection induced in calves vaccinated with DNA-F by either the intramuscular (i.m.) or intradermal (i.d.) routes, only the i.m. route primed for a rapid BRSV-specific IgA response after BRSV challenge. These results indicate that a DNA vaccination may be effective against RSV infection even in very young infants and calves.

Animals↗
PubMed2005

Kinetics of antiviral CD8 T cell responses during primary and post-vaccination secondary bovine respiratory syncytial virus infection.

We have measured antiviral CD8 T cells responses in bovine respiratory syncytial virus (bRSV) infected calves that had been immunized with either formalin-inactivated (FI) or live-attenuated (L) bRSV, with evidence of immunopathology following challenge of calves vaccinated with FI-bRSV. In all cases, bRSV infection induced potent pulmonary CD8 T cell responses. The kinetics of the post-challenge response in L-bRSV immunized animals was accelerated compared to the FI-bRSV and PBS groups, suggesting that only the L-bRSV vaccine, and not the FI-bRSV vaccine, had primed memory T cells. The differences between primary and post-vaccination secondary infection were very minor, in terms of the proliferation status of pulmonary CD8 T cells. Functional IFN-gamma+ CD8 responses were slightly higher in the FI-bRSV vaccinated animals. Furthermore, the existence of strong IFN-gamma+ CD8 responses in FI-bRSV vaccinated animals after challenge suggests (i) that these IFN-gamma+ responses in FI-bRSV immunized animals do not protect against immunopathology, and (ii) that Th-2 biased responses during bRSV challenge after vaccination with FI-bRSV have a limited impact on the CD8 responses in the bronchoalveolar lavage fluid. Thus, several response patterns (Th-l/Th-2) seem to co-exist during bRSV infection.

Animals↗