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E C Claas

Publications and source records attributed to E C Claas.

At least 37 records · Page 2Linked to original sources

[The influenza season 1997/'98 and the vaccine composition for 1998/'99].

The 1997/'98 influenza season in the Netherlands was marked by influenza A/H3N2 activity which never reached a true epidemic level. There was no real peak activity either but a prolonged period of increased activity of approximately eight weeks with a maximum in week 13, when sentinel physicians reported 16.6 cases of influenza-like illness per 10,000 inhabitants. It was not until week 18 of 1998 that the influenza activity declined to baseline levels. During the season, almost exclusively influenza A/H3N2 viruses were isolated, of which the majority resembled the new strain influenza A/Sydney/5/97 (H3N2). Further analysis of these variant viruses revealed that, although there was some cross-reactivity with the vaccine strain (A/Nanchang/933/95), no optimal protection could be expected to be induced by the vaccine. Antigenic characterisation of the sporadic influenza A/H1N1 and influenza B viruses showed that these were related to the vaccine strains. As a result of these findings, the World Health Organization (WHO) recommended to change the H3N2 strain in the influenza vaccine for the season 1998/'99 to an influenza A/Sydney/5/97(H3N2)-like strain. Based on epidemiological data from other countries, it was also decided to change the influenza A/H1N1 component to an influenza A/Beijing/262/95 (H1N1)-like strain.

Disease Outbreaks↗

[Influenza A (H5N1) in Hong Kong: Forerunner of a pandemic or just a scientifically interesting phenomenon and a useful exercise in pandemiology?].

In 1997, 18 influenza patients were detected who were infected with influenza A(H5N1) virus. Six patients died. Presumably most of the patients had acquired the infection directly from chickens with the fowl plague prevalent in China in 1997. These are the first reported cases of isolation of influenza viruses belonging to one of the H4-H15 subtypes from human influenza patients. Man-to-man transmission of the virus has not been demonstrated but cannot be excluded in every case. Genetic analyses of seven of these virus isolates showed that no reassortment with a human or porcine influenza virus had occurred. It is unpredictable whether the H5N1-virus in question will start a pandemic in the next few years.

Adolescent↗

[Influenza A(H5N1) in Hong Kong: forerunner of a pandemic or an only scientifically interesting phenomenon and a useful exercise in pandemiology?].

From a three-year old boy in Hong Kong who died in May 1997 with an extensive influenza pneumonia an influenza A virus has been isolated which was, first at the National Influenza Centre of the Netherlands, identified as belonging to subtype H5N1. Presumably the patient had acquired the infection directly from an outbreak of fowl plague among chickens. As far as is known this is the first case of the isolation of an influenza virus belonging to one of the subtypes H4-H15 from a human influenza patient. At the end of 1997 seventeen more cases of human A (H5N1) influenza have been detected in Hong Kong, including five fatal cases. Genetic analyses of seven of these virus isolates did not reveal the occurrence of reassortment with a human or porcine influenza virus, which could have rendered the virus potentially pandemic. Man-to-man transmission of the virus has not been demonstrated but cannot be excluded either. This event has shown that the WHO surveillance of influenza viruses, although perhaps not perfect, has functioned well.

Animals↗

Human influenza A H5N1 virus related to a highly pathogenic avian influenza virus.

BACKGROUND: In May, 1997, a 3-year-old boy in Hong Kong was admitted to the hospital and subsequently died from influenza pneumonia, acute respiratory distress syndrome, Reye's syndrome, multiorgan failure, and disseminated intravascular coagulation. An influenza A H5N1 virus was isolated from a tracheal aspirate of the boy. Preceding this incident, avian influenza outbreaks of high mortality were reported from three chicken farms in Hong Kong, and the virus involved was also found to be of the H5 subtype. METHODS: We carried out an antigenic and molecular comparison of the influenza A H5N1 virus isolated from the boy with one of the viruses isolated from outbreaks of avian influenza by haemagglutination-inhibition and neuraminidase-inhibition assays and nucleotide sequence analysis. FINDINGS: Differences were observed in the antigenic reactivities of the viruses by the haemagglutination-inhibition assay. However, nucleotide sequence analysis of all gene segments revealed that the human virus A/Hong Kong/156/97 was genetically closely related to the avian A/chicken/Hong Kong/258/97. INTERPRETATION: Although direct contact between the sick child and affected chickens has not been established, our results suggest transmission of the virus from infected chickens to the child without another intermediate mammalian host acting as a "mixing vessel". This event illustrates the importance of intensive global influenza surveillance.

Amino Acid Sequence↗

Comparison of RNA hybridization, hemagglutination assay, titration of infectious virus and immunofluorescence as methods for monitoring influenza virus replication in vitro.

Rapid and sensitive methods for the monitoring of influenza virus replication in vitro are needed to address several research questions. Four methods based on different principles were compared: the hemagglutination (HA) assay, the measurement of virus infectivity titers in culture supernatants, the enumeration of infected cells by immunofluorescence and RNA hybridization techniques using digoxigenin (DIG) labeled RNA probes. To this end, MDCK cells were infected at different multiplicities of infection (moi) with a recent influenza A virus (A/Netherlands/18/94 H3N2) and the kinetics of virus replication were monitored with these four assays. At high moi, virus released into the culture supernatant of infected cells was detected by the HA assay 12 h post infection, whereas at lower moi (< or = 0.01) the first HA activity was not detected before 24 h post infection. The measurement of infectious viruses in the culture supernatant proved to be more sensitive, since 4-12 h post infection newly produced virus was detected depending on the moi used. This finding was in agreement with results obtained by the immunofluorescence assay using an antibody preparation specific for the nucleoprotein: single infected cells could be detected as early as 4 h post infection. At this time point, positive signals were also obtained when mRNA/cRNA specific hybridization was carried out for the NP gene segment, but not for viral NP RNA or RNA specific for the hemagglutinin, which were only detected at later time points after infection. Thus, besides direct measurement of infectious virus and immunofluorescence, RNA hybridization proved to be a sensitive assay for monitoring influenza virus replication in vitro.

Animals↗

Use of recombinant nucleoproteins in enzyme-linked immunosorbent assays for detection of virus-specific immunoglobulin A (IgA) and IgG antibodies in influenza virus A- or B-infected patients.

The nucleoprotein genes of influenza virus A/Netherlands/018/94 (H3N2) and influenza virus B/Harbin/7/94 were cloned into the bacterial expression vector pMalC to yield highly purified recombinant influenza virus A and B nucleoproteins. With these recombinant influenza nucleoproteins, enzyme-linked immunosorbent assays (ELISAs) were developed for the detection of influenza virus A- and B-specific immunoglobulin A (IgA) and IgG serum antibodies. Serum samples were collected at consecutive time points after the onset of clinical symptoms from patients with confirmed influenza virus A or B infections. Nucleoprotein-specific IgA antibodies were detected in 41.2% of influenza virus A-infected patients and in 66. 7% of influenza virus B-infected patients on day 6 after the onset of clinical symptoms. In serum samples taken on day 21 (influenza virus A-infected patients) or day 28 (influenza virus B-infected patients), nucleoprotein-specific IgA antibodies could be detected in 58.8 and 58.3% of influenza virus A- and B-infected patients, respectively. At the same time, IgG antibody rises were detected in 88.2% of influenza virus A-infected patients and in 95.8% of influenza virus B-infected patients. On comparison, hemagglutination inhibition assays detected antibody titer rises in 81.3 and 72.7% of patients infected with influenza viruses A and B, respectively. In contrast to the detection of nucleoprotein-specific IgG antibodies or hemagglutination-inhibiting antibodies, the detection of nucleoprotein-specific IgA antibodies does not require paired serum samples and therefore can be considered an attractive alternative for the rapid serological diagnosis of influenza.

Animals↗

[Influenza in the 1996/'97 season; vaccine composition for the 1997/'98 season].

The first indication of flu activity in the Netherlands in the 1996/'97 season was the isolation of an A/H3N2 influenza virus in week 48 of 1996. In subsequent weeks influenza viruses were isolated sporadically. The clinical influenza activity increased from week I of 1997 and reached its peak in week 4 of 1997. Simultaneously with the increase of clinical influenza activity, an increasing number of influenza viruses were isolated. The epidemic had a relatively small extent. Initially, A/H3N2 influenza viruses were predominant, but in the second half of the epidemic an increasing number of influenza B viruses were isolated as well. The A/H3N2 viruses were antigenically fairly strongly distinct from the variants prevalent in the preceding years. This season influenza A/HINI viruses did not play a significant role and only one virus of this subtype was isolated. All influenza A/H3N2, A/HINI and B viruses isolated were antigenically similar to the vaccine strains.

Adolescent↗

Respiratory syncytial virus specific serum antibodies in infants under six months of age: limited serological response upon infection.

The decline of maternal respiratory syncytial virus (RSV) specific serum antibodies was studied in 45 children during the first 6 months of life, using a virus neutralization assay and competition ELISAs measuring fusion protein and glycoprotein specific antibodies. In all children RSV neutralizing antibodies were demonstrated at birth, with titers ranging from 33 to 1382. The calculated mean half life of these antibodies was 26 days. Furthermore, in a group of 38 children with suspected RSV infection, all younger than 6 months of age on admission, the diagnostic value of serological assays was evaluated. In 32 children RSV infection was confirmed by virus isolation, direct immune fluorescence and RT-PCR. In 7 patients of this group a significant titer rise in virus neutralization assay was demonstrated. Six additional RSV infected children could be identified by showing the presence of RSV-specific IgM or IgA serum antibodies or by showing an increase in fusion protein or glycoprotein specific antibodies. All serological tests together identified 13 (41%) of the 32 RSV infected patients. It is concluded that in children of this age group, which represent the majority of patients hospitalized with RSV infections, serological assays not only have a limited diagnostic value but are of limited value for sero-epidemiological studies.

Antibodies, Viral↗

Induction of protective immunity against influenza virus in a macaque model: comparison of conventional and iscom vaccines.

Cynomolgus macaque monkeys (Macaca fascicularis) were immunized twice intramuscularly, either with a conventional non-adjuvanted subunit vaccine or with a candidate immune-stimulating complex (iscom) vaccine, each containing 10 micrograms envelope glycoprotein of a recent human influenza A(H3N2) virus (A/Netherlands/18/94). In contrast to the macaques vaccinated with the classical subunit vaccine, those immunized with the iscom vaccine developed high titres of specific IgM, IgA and IgG serum antibodies, as well as high titres of haemagglutination-inhibiting and virus-neutralizing serum antibodies. Also, specific proliferative T cell responses were only found in the iscom-vaccinated monkeys and their levels were similar to those found in monkeys experimentally infected with the homologous virus. Upon intratracheal challenge with the homologous virus, the iscom-vaccinated monkeys were completely protected from detectable virus replication in lungs, pharynx and nose, whereas those vaccinated with the classical subunit vaccines were not, or were only partially protected. The kinetics of specific serum antibody development in the iscom-vaccinated monkeys after challenge were quite similar to those of monkeys after secondary infection with the same virus. In contrast, the post-challenge kinetics of serum antibody development in the monkeys vaccinated with the classical subunit vaccines resembled those of naive monkeys, confirming that these vaccines only provided limited protection in such animals.

Adjuvants, Immunologic↗

[Influenza in the 1995/'96 season; vaccine composition for the 1996/'97 season].

The 1995/'96 season in the Netherlands was marked by an influenza A/H3N2 epidemic that peaked in week 5I. In this week, 39 patients with influenza-like illness per 10,000 inhabitants contacted the sentinel physicians. With two exceptions, influenza A/H3N2 viruses exclusively were isolated during this epidemic period. In the first few months of 1996, a substantial number of influenza A/H1N1 and influenza B viruses were isolated as well. Serological characterization of the circulating viruses revealed that they all resembled the virus strains of the influenza vaccine of 1995/'96, which therefore probably will have provided good protection. Based on the epidemiological data from other countries and the fact that similar H3N2 viruses have been circulating since 1993, the World Health Organization has recommended to exchange the H3N2 component of the 1996/'97 vaccine for a Wuhan/353/95 (H3N2)-like strain.

Humans↗

Genetic reassortment in pandemic and interpandemic influenza viruses. A study of 122 viruses infecting humans.

The human influenza pandemics of 1957 and 1968 were caused by reassortant viruses that possessed internal gene segments from avian and human strains. Whether genetic reassortment of human and avian influenza viruses occurs during interpandemic periods and how often humans are infected with such reassortants is not known. To provide this information, we used dot-blot hybridization, partial nucleotide sequencing and subsequent phylogenetic analysis to examine the 6 internal genes of 122 viruses isolated in humans between 1933 and 1992 primarily from Asia, Europe, and the Americas. The internal genes of A/New Jersey/11/76 isolated from a human fatality at Fort Dix, New Jersey in 1976 were found to be of porcine origin. Although none of the geographically and temporally diverse collection of 122 viruses was an avian-human or other reassortant, cognizance was made of the fact that there were two isolates from children from amongst 546 influenza A isolates obtained from The Netherlands from 1989-1994 which were influenza A reassortants containing genes of avian origin, viruses which have infected European pigs since 1983-1985. Thus, genetic reassortment between avian and human influenza strains does occur in the emergence of pandemic and interpandemic influenza A viruses. However, in the interpandemic periods the reassortants have no survival advantage, and the circulating interpandemic influenza viruses in humans do not appear to accumulate avian influenza virus genes.

Base Sequence↗

[Influenza in the 1994/95 season; composition of vaccine for the 1995/96 season].

The 1994/'95 season in the Netherlands was marked by a limited influenza activity which only emerged in late February. The influenza activity remained elevated until the end of April, which is unusually late, and epidemic activity was only reported in the south of the country. Both influenza A/H3N2 and B viruses were isolated in this period. In addition, influenza A/HINI viruses were isolated for the first time since March 1993, from two patients. The majority of the influenza A strains that circulated in the Netherlands in 1994/'95 reacted well with ferret antiserum raised against the strains of the 1994/'95 influenza vaccine, which therefore probably offered good protection. The reactivity of the B strains to antiserum raised against the vaccine strain, B/Panama/45/90, was only moderate, which implies that the protection against the Dutch influenza B strains was not optimal. Based on the results of the worldwide influenza surveillance, the World Health Organization (WHO) has recommended an alteration in both the A/H3N2 and the B component for the vaccine of 1995/1996.

Disease Outbreaks↗

Interspecies transmission of influenza viruses.

In this report we examine the hypothesis that aquatic birds are the primordial source of all influenza viruses in other species. Two partly overlapping reservoirs of influenza A viruses exist in migrating water-fowl and shorebirds throughout the world. These species harbor influenza viruses of all the known hemagglutinin and neuraminidase subtypes. In contrast to the rapid, progressive changes in both the nucleotide and amino acid sequences of mammalian virus gene lineages, avian virus genes show far less variation and, in most cases, appear to be in evolutionary stasis. There are periodic exchanges of influenza virus genes or whole viruses between species, giving rise to pandemics of disease in humans, lower animals, and birds. The periodic exchange of influenza viruses between species has been illustrated by the appearance of new pandemic influenza viruses in humans, including the Spanish influenza of 1918, the Asian influenza of 1957, and the Hong Kong influenza of 1968. Transmission of avian influenza viruses to swine in Europe in 1979 has resulted in the appearance of human-avian reassortant influenza viruses in pigs in Italy and in children in the Netherlands. These studies provide evidence supporting the possibility that pigs serve as a mixing vessel for reassortment between influenza viruses in mammalian and avian hosts and raise the question of whether the avian influenza viruses now circulating in European swine are the precursors of the next human pandemic virus.

Animals↗

[Influenza in the 1993/'94 season; composition of the vaccine for the 1994/'95 season].

The influenza season 1993/'94 in the Netherlands and the rest of Northwestern Europe was marked by an influenza A/H3N2 epidemic. The morbidity of this epidemic was moderate, but a high mortality rate was observed. The epidemic viruses, represented by A/Netherlands/241/93 (H3N2), were characterised by haemagglutination inhibition assays and nucleotide sequence analysis. The viruses were related to A/Beijing/32/92 (H3N2), the vaccine strain for 1993/'94, but clear antigenic differences were detected. Therefore, the WHO has recommended a new A/H3N2 component, A/Shangdong/9/93, for the vaccine of 1994/'95. The onset of the epidemic was unusually early in the influenza season. An increase in the influenza activity was already noticed in the second week of November and it reached its peak in week 49. As a result of the early epidemic, the influenza vaccination programme had not been completed yet. Therefore, the point of time for vaccinating people at risk may have to be reconsidered and moved up in order to complete the vaccination programme earlier.

Humans↗