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PubMed1989

Identification of PR8 M1 protein in influenza virus high-yield reassortants by M1-specific monoclonal antibodies.

A panel of monoclonal antibodies to the M1 protein of A/PR8/34 (H1N1) (PR8) influenza A virus was found to distinguish in ELISA high-yielding reassortant viruses derived from reassortment of PR8 and X-31 (H3N2) viruses with recently prevalent field strains of H1N1 or H3N2 subtype. These findings are concordant with results of genotyping that demonstrated the presence of PR8 RNA 7 or M1 protein in high-yield reassortants by RNA or protein PAGE. All high-yield vaccine candidate reassortants Application of the M1 monoclonal antibody panel facilitates the isolation of high-yield vaccine candidate reassortants bearing the PR8 M1 gene, and should aid in epidemiologic strain tracking as well.

Antibodies, Monoclonal↗

PubMed1986

Biochemical and antigenic analysis using monoclonal antibodies of a series of of influenza A (H3N2) and (H1N1) virus reassortants.

Reassortant influenza A viruses with high growth capacity in eggs and suitable as candidate vaccine strains or as standard reagents for influenza HA quantification were prepared using the high yielding A/PR/8/34 (H1N1) as one parent and a number of 'wild' strains of influenza A (H1N1) or (H3N2) viruses as the other parent. The genetic and antigenic composition of the reassortants was determined. The parental derivation of genes in the reassortants was established by electrophoretic analysis of virus RNA and virus induced polypeptides. The haemagglutinin (HA) antigens of the three H1N1 viruses (NIB-6, NIB-7 NIB-12) were found to resemble those of the parental viruses when tested against a panel of monoclonal antibodies and using the HI test. A similar correspondence between the antigenic characteristics of the HA of the influenza A (H3N2) reassortants (NIB-1, NIB-4, NIB-5, NIB-8 and NIB-11) and parental viruses was noted. Therefore laboratory manipulations to produce the reassortants did not result in the selection of significant antigenic variants.

Animals↗

PubMed1991

Immunogenicity and safety of rhesus-human rotavirus reassortant vaccines with serotype 1 or 2 VP7 specificity.

Rhesus-human rotavirus reassortants incorporating the gene expressing the VP7 surface protein of human rotavirus serotypes 1 or 2, and the remaining ten genes from rhesus rotavirus (RRV) were evaluated as candidate oral vaccines in 2-4-month-old infants. A single dose of the serotype 1 reassortant vaccine which had a titre of 10(4) plaque-forming units (p.f.u.) induced a fourfold or greater antibody response in 81% of the recipients by a combination of ELISA and neutralization assays; 51% of the vaccinees developed a neutralizing antibody response to the vaccine strain. A single dose of the serotype 2 vaccine (10(4) p.f.u.) induced a seroresponse in all vaccinees by the combination of assays whereas 67% developed neutralizing antibodies to the vaccine strain. A combination of these two vaccines (0.5 x 10(4) p.f.u. of each) induced an overall seroresponse in 95% of the recipients but only 48% and 24% response in neutralizing antibodies to serotypes 1 and 2, respectively. A trivalent combination which included the two reassortants and RRV (0.33 x 10(4) p.f.u. of each strain) induced an overall response in 82% of the vaccinees, but only 30%, 20% and 65% developed a neutralizing antibody response to serotype 1, serotype 2, and RRV, respectively. Febrile reactions on days 2-5 after vaccination were seen in 23-45% of the infants receiving the various vaccines and combinations and in 5% of the placebo group. It is concluded that rhesus-human reassortant rotaviruses may be combined with each other and with RRV as a polyvalent vaccine, but the VP7-specific neutralizing antibody responses are likely to be lower after combined vaccination than following vaccination with a single reassortant rotavirus.

Animals↗

PubMed2006

Genetic reassortment of infectious bursal disease virus in nature.

Infectious bursal disease virus (IBDV), a double-stranded RNA virus, is a member of the Birnaviridae family. Four pathotypes of IBDV, attenuated, virulent, antigenic variant, and very virulent (vvIBDV), have been identified. We isolated and characterized the genomic reassortant IBDV strain ZJ2000 from severe field outbreaks in commercial flocks. Full-length genomic sequence analysis showed that ZJ2000 is a natural genetic reassortant virus with segments A and B derived from attenuated and very virulent strains of IBDV, respectively. ZJ2000 exhibited delayed replication kinetics as compared to attenuated strains. However, ZJ2000 was pathogenic to specific pathogen free (SPF) chickens and chicken embryos. Similar to a standard virulent IBDV strain, ZJ2000 caused 26.7% mortality, 100% morbidity, and severe bursal lesions at both gross and histopathological levels. Taken together, our data provide direct evidence for genetic reassortment of IBDV in nature, which may play an important role in the evolution, virulence, and host range of IBDV. Our data also suggest that VP2 is not the sole determinant of IBDV virulence, and that the RNA-dependent RNA polymerase protein, VP1, may play an important role in IBDV virulence. The discovery of reassortant viruses in nature suggests an additional risk of using live IBDV vaccines, which could act as genetic donors for genome reassortment.

Amino Acid Substitution↗

PubMed1989

Phenotypes of rotavirus reassortants depend upon the recipient genetic background.

We have previously characterized the biological and immunological properties of a simian rotavirus SA11 variant (4F) with an altered genome segment 4. The SA11-4F variant formed large plaques in the presence of protease, formed small clear plaques in the absence of protease, and grew to high titer in the presence of protease when compared to our standard wild type (SA11 clone 3). To determine the genome segment of the rotavirus SA11 variant 4F that encoded the unique protease-associated phenotypes of the variant, reassortants were generated that segregated the outer capsid genes of 4F onto a genetic background derived from either the bovine rotavirus B223 or our standard SA11 wild type (clone 3), both of which have contrasting protease-associated phenotypes. The parental and reassortant viruses were examined to determine which genes from the 4F variant encoded the ability (i) to form large plaques in the presence of protease, (ii) to form small clear plaques in the absence of exogenous protease, and (iii) to grow to significantly higher titer in the presence of protease. These phenotypes could be transferred to a clone 3 genetic background by a single genome segment from the 4F variant segment 4. However, in the 4F/B223 reassortants a different and unexpected situation was found. On a B223 genetic background the same phenotypes segregated with a combination of a minimum of two 4F genome segments, segments 4 and 9. These results indicate that the recipient genetic background onto which the genes of a donor rotavirus are reassorted can affect the phenotypes conferred by the presence of the donor segments. Thus, the results of segregation mapping experiments using reassortant viruses should be interpreted with caution.

Cell Line↗

PubMed1988

Comparison of live, attenuated H1N1 and H3N2 cold-adapted and avian-human influenza A reassortant viruses and inactivated virus vaccine in adults.

The infectivity, immunogenicity, and efficacy of live, attenuated influenza A/Texas/1/85 (H1N1) and A/Bethesda/1/85 (H3N2) avian-human (ah) and cold-adapted (ca) reassortant vaccines were compared in 252 seronegative adult volunteers. The immunogenicity and efficacy of the H1N1 reassortant vaccine were also compared with those of the trivalent inactivated virus vaccine. Each reassortant vaccine was satisfactorily attenuated. The 50% human infectious dose was 10(4.9) for ca H1N1, 10(5.4) for ah H1N1, 10(6.4) for ca H3N2, and 10(6.5) TCID50 for ah H3N2 reassortant virus. Within a subtype, the immunogenicities of ah and ca vaccines were comparable. Five to seven weeks after vaccination, volunteers were challenged with homologous wild-type influenza A virus. The magnitude of shedding of virus after challenge was greater than 100-fold less in H1N1 vaccinees and greater than 10-fold less in H3N2 vaccinees compared with unimmunized controls. The vaccines were equally efficacious, as indicated by an 86%-100% reduction in illness. Thus, the ah A/Mallard/New York/6750/78 and the ca A/Ann Arbor/6/60 reassortant viruses are comparable.

Adult↗

PubMed1989

Attenuation and phenotypic stability of influenza B/Texas/1/84 cold-adapted reassortant virus: studies in hamsters and chimpanzees.

The temperature sensitivity, level of attenuation, and phenotypic stability of an influenza B/Texas/1/84 X B/Ann Arbor/1/66 cold-adapted (ca) reassortant virus that received the RNA segments that encode the hemagglutinin and neuraminidase surface glycoproteins from the B/Texas/84 wild-type virus and the remaining six RNA segments from the B/Ann Arbor/66 ca donor virus were evaluated. In comparison to wild-type virus, the ca reassortant was restricted in replication in the upper and lower respiratory tracts of hamsters and chimpanzees. This clearly demonstrated that the six transferable RNA segments of the B/Ann Arbor/66 ca donor virus specify the attenuation phenotype for animals with a 37 degrees C core body temperature. In addition, the ca virus retained the temperature-sensitive (ts) phenotype after replication in hamsters and chimpanzees. To further evaluate its phenotypic stability, the ca reassortant virus was isolated after 6-15 d of replication in hamsters that were immunosuppressed with cyclophosphamide, and the isolates were tested for their temperature sensitivity in vitro and for their level of replication in immunocompetent hamsters. The isolated viruses retained their ts and attenuation phenotypes even after prolonged replication in vivo. Thus, the B/Ann Arbor/66 ca donor virus can transfer the desired properties of attenuation and phenotype stability to its reassortants. The findings support the continued evaluation of ca reassortant influenza B virus vaccines in humans, including fully susceptible children.

Animals↗

PubMed1993

Influenza A virus haemagglutinin polymorphism: pleiotropic antigenic variants of A/Shanghai/11/87 (H3N2) virus selected as high yield reassortants.

Genetic reassortment of the A/Shanghai/11/87 (H3N2) variant of influenza A virus with A/PR8/34 (H1N1) virus [the standard donor of high yield (hy) genes for influenza vaccine viruses] resulted in the isolation of two reassortants with differing H3 haemagglutinin (HA) phenotypes, X-99 and X-99a. The two HA phenotypes were derived from individual subpopulations of the H3N2 wild-type virus during the reassortment event. The HA mutants and their respectively derived reassortants (identical in RNA genotype) differed in antigenicity, replication characteristics, yield in chick embryos and haemagglutinin gene sequence. Despite antigenic differences in reactions to polyclonal rabbit antisera of 60%, both X-99 and X-99a, the hy reassortants, were equally immunogenic and protective in BALB/c mice to challenge by parental wild-type virus. Differences in HA phenotype were related to a Ser to Ile change at amino acid position 186. These findings emphasize the polymorphism of influenza virus strains as well as the need for caution in selection of vaccine strains from among antigenically distinct viral subpopulations.

Amino Acid Sequence↗

PubMed1998

Multiple genetic reassortment of avian and human influenza A viruses in European pigs, resulting in the emergence of an H1N2 virus of novel genotype.

Novel H1N2 influenza A viruses which were first detected in pigs in Great Britain in 1994 were examined antigenically and genetically to determine their origins and establish the potential mechanisms for genetic reassortment. The haemagglutinin (HA) of all swine H 1 N2 viruses examined was most closely related to, but clearly distinguishable both antigenically and genetically from, the HA of human H1N1 viruses which circulated in the human population during the early 1 980s. Phylogenetic analysis of the HA gene revealed that the swine H 1 N2 viruses formed a distinct branch on the human lineage and were probably introduced to pigs shortly after 1980. Following apparent transfer to pigs the HA gene underwent genetic variation resulting in the establishment and cocirculation of genetically and antigenically heterogeneous virus populations. Genetic analyses of the other RNA segments of all swine H1N2 viruses indicated that the neuraminidase gene was most closely related to those of early 'human-like' swine H3N2 viruses, whilst the RNA segments encoding PB2, PB1, PA, NP, M and NS were related most closely to those of avian viruses, which have been circulating recently in pigs in Northern Europe. The potential mechanisms and probable progenitor strains for genetic reassortment are discussed, but we propose that the swine H1N2 viruses examined originated following multiple genetic reassortment, initially involving human H1N1 and 'human-like' swine H3N2 viruses, followed by reassortment with 'avian-like' swine H1N1 virus. These findings suggest multiple reassortment and replication of influenza viruses may occur in pigs many years before their detection as clinical entities.

Animals↗

PubMed1992

Use of single-gene reassortant viruses to study the role of avian influenza A virus genes in attenuation of wild-type human influenza A virus for squirrel monkeys and adult human volunteers.

The transfer of six internal RNA segments from the avian influenza A/Mallard/New York/6750/78 (H2N2) virus reproducibly attenuates human influenza A viruses for squirrel monkeys and adult humans. To identify the avian influenza A virus genes that specify the attenuation and host range restriction of avian-human (ah) influenza A reassortant viruses (referred to as ah reassortants), we isolated six single-gene reassortant viruses (SGRs), each having a single internal RNA segment of the influenza A/Mallard/New York/6750/78 virus and seven RNA segments from the human influenza A/Los Angeles/2/87 (H3N2) wild-type virus. To assess the level of attenuation, we compared each SGR with the A/Los Angeles/2/87 wild-type virus and a 6-2 gene ah reassortant (having six internal RNA segments from the avian influenza A virus parent and two genes encoding the hemagglutinin and neuraminidase glycoproteins from the wild-type human influenza A virus) for the ability to replicate in seronegative squirrel monkeys and adult human volunteers. In monkeys and humans, replication of the 6-2 gene ah reassortant was highly restricted. In humans, the NS, M, PB2, and PB1 SGRs each replicated significantly less efficiently (P less than 0.05) than the wild-type human influenza A virus parent, suggesting that each of these genes contributes to the attenuation phenotype. In monkeys, only the NP, PB2, and possibly the M genes contributed to the attenuation phenotype. These discordant observations, particularly with regard to the NP SGR, indicate that not all genetic determinants of attenuation of influenza A viruses for humans can be identified during studies of SGRs conducted with monkeys. The PB2 and M SGRs that were attenuated in humans each exhibited a new phenotype that was not observed for either parental virus. Thus, it was not possible to determine whether avian influenza virus PB2 or M gene itself or a specific constellation of avian and human influenza A virus specified restriction of virus replication in humans.

Adult↗

PubMed1985

Genetic reassortment of mammalian reoviruses in mice.

Reassortments between type 1 (Lang) and type 3 (Dearing) reoviruses were isolated from suckling mice infected perorally with an inoculum containing both type 1 and type 3 viruses. A total of five distinct reassortants (designated as E1 through E5) were isolated from animals during the course of the experiment. Two reassortants (E1 and E2) represented the majority of the reassortants isolated. The majority of genes of types E1 and E2 were derived from type 1 (Lang). However, E1 had an M2 gene and an S1 gene derived from type 3 (Dearing), while E2 had M2 and S2 genes derived from type 3 (Dearing). Thus, nonrandom reassortment between mammalian reoviruses can be demonstrated in vivo.

Animals↗

PubMed1987

Genome segment reassortment between two serotypes of bluetongue virus in a natural host.

The occurrence of genome segment reassortment between two antigenically related orbiviruses was demonstrated in cattle. Individual virus clones were isolated by cell culture plaque assays directly from the blood of a calf infected with two serotypes of bluetongue virus. The majority (89%) of progeny viruses isolated from the calf represented reassortant viruses. A minimum of six genome segments participated in reassortment, with 16 unique reassortant constellations being identified. Such genome segment reassortment between unique, though antigenically related, orbiviruses has undoubtedly played a major role in generating the extensive phenotypic and genotypic diversity that is characteristic of this serogroup.

Animals↗

PubMed1999

Reassortment and insertion-deletion are strategies for the evolution of influenza B viruses in nature.

The evolution of influenza B viruses is poorly understood. Reassortment of influenza B viruses in nature as a means of genetic variation has not been considered to be a major contributor to their evolution. However, the current practice of assigning evolutionary relationships by antigenic analysis of the hemagglutinin of influenza B viruses would fail to detect reassortants. In this study, influenza B viruses isolated within the past 10 years from sites in the United States and China were studied by nucleotide sequencing of the hemagglutinin and neuraminidase genes and construction of phylogenetic trees to assess evolutionary relationships. A group of viruses represented by B/Houston/1/92 possess a hemagglutinin derived from a B/Yamagata/16/88-like strain and a neuraminidase derived from a B/Victoria/2/87-like strain. A second reassortment event between the hemagglutinin of a B/Yamagata/16/88-like virus closely related to the B/Beijing/184/93 strain and the neuraminidase of a B/Victoria/2/87-like strain is represented by a single virus, B/Memphis/3/93. The neuraminidase of the reassortant viruses is most closely related to that of B/Victoria/2/87-like viruses currently circulating in Nanchang, China. A pattern of insertions and deletions in the hemagglutinin and the neuraminidase of different strains of influenza B viruses is observed. Reassortment plays a role in the evolution of influenza B viruses and may necessitate a change in the methods used to assess and identify new influenza viruses.

Animals↗

PubMed1983

Experimental infection of chipmunks and snowshoe hares with La Crosse and snowshoe hare viruses and four of their reassortants.

The infection of chipmunks (Tamias striatus), the vertebrate host of La Crosse (LAC) arbovirus, or snowshoe hares (Lepus americanus), the host of snowshoe hare (SSH) virus, was analyzed following subcutaneous inoculation with either LAC or SSH or certain LAC-SSH reassortant viruses. After inoculation, no adult hares or chipmunks developed signs of illness. Another reassortant, genotype LAC/LAC/SSH, has exhibited a marked inability to infect chipmunks and was avirulent for mice, probably because of a mutation in its L RNA segment. In chipmunks inoculated with reassortant viruses, neither the durations of viremias nor the maximum titers attained were demonstrably different from those found after inoculation with the parent LAC or SSH viruses. However, viruses with a SSH M RNA induced a higher viremia in snowshoe hares than viruses with a LAC M RNA. Also, the amount of virus needed to produce a detectable infection of chipmunks or hares was lower for viruses in which the M RNA came from the SSH parent than for those viruses having a LAC M RNA. Convalescent phase chipmunk and hare sera from animals infected with SSH virus or reassortant viruses having a SSH M RNA, neutralized parental SSH virus more effectively than did LAC virus. Conversely, the sera of animals infected with LAC virus or reassortants having a LAC M RNA, neutralized LAC virus more efficiently than did SSH virus.

Animals↗

PubMedDate not supplied

[A mechanism for limiting reproduction influenza A virus reassortants with incomplete functional compatibility of hemagglutinin and neuraminidase gene products].

The mechanism of decrease in the level of virus accumulation in reassortants with hemagglutinin (HA) and neuraminidase (NA) genes from different parents is studied. The reassortant viruses and their passage variants do not differ by the rate of virus protein production or their stability in infected cells. Electron microscopy and titration of infectious virus in culture fluid and cell-associated virus showed that the variants selected by serial passages accumulated mainly in the culture fluid, whereas the initial reassortant virions were predominantly cell-associated. These data suggest that incomplete removal of sialic acid residues by viral neuraminidase N1 in some reassortants results in re-attachment of virions to the infected cells and thus impairs the virus dissemination, which may be regarded as a reassortant-limiting factor probably significant for virus evolution.

Animals↗

PubMed2005

An influenza A(H3) reassortant was epidemic in Australia and New Zealand in 2003.

During 2003, Australia and New Zealand experienced substantial outbreaks of influenza. The strain responsible was an A(H3N2) influenza virus described as A/Fujian/411/2002-like, which had circulated as a minor variant in the previous Northern Hemisphere (NH) winter, mainly in Korea and Japan. Early in the year the isolates were very similar to those that had been previously isolated in the NH, however, a reassortant strain emerged early in the New Zealand winter, followed by the appearance of similar viruses in Australia and other regional areas. While the hemagglutinin HA1 sequence of these viruses demonstrated only minor differences from the A/Fujian/411/2002 reference strain, the neuraminidase gene was clearly different from that of other recently circulating H3 viruses and most closely matched an earlier reference strain A/Chile/6416/2001. Three internal genes (NS, NP, M) in the reassortant viruses were also more closely related to the A/Chile/6416/2001 lineage. This reassortant A(H3) virus predominated in Australia and New Zealand in 2003 was also seen in Brazil and Malaysia during 2003 and was widespread in the United States and Europe during their 2003-04 winter. Interestingly most of the strains of A(H3) that were isolated at the beginning of the 2004 winter in Australia, did not have this earlier A/Chile/6416/2001-like neuraminidase but had a neuraminidase that was similar to that of the reference strain A/Fujian/411/2002. This was suggestive of the re-introduction of influenza A(H3) from other countries, however, there was still low level circulation of the reassortant virus in 2004 with isolates detected in Australia and Singapore.

Antigens, Viral↗

PubMed1993

Genetic reassortment between avian and human influenza A viruses in Italian pigs.

Pandemic strains of influenza A virus arise by genetic reassortment between avian and human viruses. To examine the possibility that pigs serve as "mixing vessels" for such reassortment events (Scholtissek et al., Virology 147, 287-294, 1985), we phylogenetically analyzed the internal protein genes of classic H1N1, avian-like H1N1, and human-like H3N2 viruses circulating among Italian pigs. The results show that human-like H3N2 strains isolated from 1985 to 1989 contained the internal protein genes of avian-like H1N1 viruses, whereas those isolated in 1977 and 1983 did not. Thus, at some time between 1983 and 1985, genetic reassortment took place between avian- and human-like viruses in Italian pigs. This study provides the first evidence supporting genetic reassortment between human and avian viruses in a natural swine environment.

Animals↗

PubMed1995

Naturally occurring Sin Nombre virus genetic reassortants.

Genetic reassortment has been shown to play an important role in the evolution of several segmented RNA viruses and in the epidemiology of associated diseases. Sin Nombre (SN) virus is the cause of hantavirus pulmonary syndrome throughout the western United States. Like other hantaviruses, it possesses a genome consisting of three negative-sense RNA segments, S, M, and L. Recent analysis has demonstrated the presence of at least three different hantaviruses in Nevada and eastern California, including SN, Prospect Hill-like, and El Moro Canyon-like viruses. In addition, two distinct lineages of SN virus can be found in Peromyscus maniculatus rodents (sometimes in close proximity) trapped at study sites in this region. Data obtained by phylogenetic analysis of sequence differences detected among the S, M, and L genome segments of these SN viruses are consistent with reassortment having taken place between SN virus genetic variants. The results suggest that M (and to a lesser extent S or L) genome segment flow occurs within SN virus populations in P. maniculatus in this region. No reassortment was detected between SN virus and other hantavirus types present in the area. This finding suggests that as genetic distance increases, the frequency of formation of viable reassortants decreases, or that hantaviruses which are primarily maintained in different rodent hosts rarely have the opportunity to genetically interact.

Animals↗