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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A cold-adapted (ca) influenza B reassortant that derived two genes encoding the hemagglutinin and neuraminidase from influenza B/Ann Arbor/1/86 wild-type virus and six internal RNA segments from ca influenza B/Ann Arbor/1/66 virus was evaluated in 66 adult volunteers having a serum hemagglutination inhibition antibody titer less than or equal to 1:8. The ca reassortant was attenuated and elicited the production of systemic and local antibodies; the 50% human infectious dose was 10(6.4) TCID50. Six weeks after vaccination, 12 unvaccinated volunteers and 13 recipients of ca virus (10(7.5) TCID50) were challenged experimentally with homologous wild-type influenza B virus. The ca vaccine completely protected against illness, and the magnitude of shedding was 50-fold less in vaccinees than in unimmunized controls, five of whom became ill. These findings indicate that the six internal RNA segments of the ca influenza B/Ann Arbor/66 donor virus confer desirable properties of a live virus vaccine to a reassortant derived from a virulent virus. Such reassortants may be suitable vaccines for healthy adults.
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PMID:Evaluation of the infectivity, immunogenicity, and efficacy of live cold-adapted influenza B/Ann Arbor/1/86 reassortant virus vaccine in adult volunteers. 232 38

The cold-adapted reassortant of influenza A, which is a candidate live virus vaccine, interfered with the replication of parental wild-type virus in mixed infections of either MDCK cells or embryonated eggs. The interference occurred at either the permissive or nonpermissive temperature for the cold-adapted virus. In doubly infected cells, the yield of the wild-type virus was reduced by as much as 3000-fold and the protein synthesis phenotype expressed was that of the cold-adapted virus. The interference was detected even when infection with wild-type virus was carried out at a 9-fold excess or 2 hr before infection with the cold-adapted virus. As well as interfering with its wild-type parental virus, the cold-adapted virus also inhibited the replication of a heterologous influenza A subtype. In addition to its immunogenic potential, the ability to interfere with the replication of wild-type viruses is a desirable trait for any live, attenuated virus vaccine.
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PMID:Cold-adapted vaccine strains of influenza A virus act as dominant negative mutants in mixed infections with wild-type influenza A virus. 232 71

In 1985, we enrolled 189 school-age children by family in a double-blind study to determine protection against influenza by a single dose of cold-recombinant bivalent A vaccine or commercial trivalent inactivated vaccine compared with placebo. All children in school or day care, 3 to 18 years of age, in an enrolled family received the same preparation. Following vaccination, 60% and 21% of cold-recombinant bivalent A vaccine recipients and 73% and 83% of trivalent inactivated vaccine recipients demonstrated fourfold or greater response in hemagglutination-inhibition antibody titer to A/H1N1 and A/H3N2, respectively. Sixty-seven percent of all trivalent inactivated vaccine recipients demonstrated a fourfold or greater serologic response to H1N1, H3N2, and influenza B following a single dose of vaccine. During the 1985-1986 influenza B/Ann Arbor epidemic, heterotypic protection afforded by the influenza B/USSR component of trivalent inactivated vaccine was 62% compared with placebo. A single dose of trivalent inactivated vaccine protected school-age children, 6 to 19 years of age, from influenza B infection; the rate of protection was 64% against infection and 73% against febrile illness.
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PMID:Live attenuated and inactivated influenza vaccine in school-age children. 233 Sep 29

The biological function of a cold-adapted (ca) mutation residing on the PB2 gene of an influenza A/Ann Arbor/6/60 (A/AA/6/60) ca variant virus in the viral replication cycle at 25 degrees C was studied. The viral polypeptide synthesis of A/AA/6/60 ca variant at 25 degrees C was evident approximately 6 hours earlier than the wild type (wt) virus and yielded twice as many products. The quantitative analysis of viral complementary RNA (cRNA), synthesized in the presence of cycloheximide, revealed that A/AA/6/60 ca variant and a single gene reassortant that contains only the PB2 gene of the ca variant with remaining genes of the wt virus produced equal amount of cRNA at 25 degrees and 33 degrees C, which was an amount approximately four fold greater than the wt virus' cRNA synthesized at 25 degrees C. These results strongly suggest that the ca mutation residing on the PB2 gene of A/AA/6/60 ca variant affects the messenger RNA synthesis at 25 degrees C in the primary transcription.
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PMID:Biological characteristics of a cold-adapted influenza A virus mutation residing on a polymerase gene. 242 Mar 13

Influenza H1 subtype-specific CTL can be induced by secondary stimulation of a hybrid protein of the first 81 amino acids of the viral NS1 non-structural protein and the HA2 subunit of A/Puerto Rico/8/34(H1N1) hemagglutinin. In addition, a derivative of this protein with 65 amino acids deleted from the N-terminal end of HA2 can also generate H1 subtype-specific CTL in bulk cultures. CTL clones established by stimulation with the derivative protein demonstrated cross-reactive lysis of target cells infected with virus strains of the H1 and H2 subtypes. Cold target competition experiments with CTL clones as effectors demonstrated that the Ag specificity between these two hybrid proteins is identical. Adoptive transfer of the CTL clone significantly reduced virus titers in the lungs of mice infected with the virus strains of the H1 or H2 subtype but not those infected with the H3 subtype virus in vivo, which reflects the in vitro CTL clone activity. These experiments demonstrate that an epitope on the hemagglutinin that is conserved on virus strains of the H1 and H2 subtypes induces a protective CTL response. These results suggest an alternative approach for developing influenza vaccines by using conserved antigenic sites on the hemagglutinin HA2 subunit to avoid the problem of frequent antigenic mutations of the HA1 subunit antibody binding sites.
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PMID:HA2 subunit of influenza A H1 and H2 subtype viruses induces a protective cross-reactive cytotoxic T lymphocyte response. 244 98

We have used H-2Db-restricted CTL clones specific for peptide 365 to 380 of the influenza nucleoprotein to seek evidence for interaction between the TCR and peptide Ag. Preincubation of these CTL with peptide 365 to 380 resulted in inhibition of target cell lysis. In addition, CTL lysed allogeneic targets in the presence of soluble peptide Ag. Investigation of the basis of these two phenomena revealed a requirement for expression of H-2Db molecules by the effector cells. Either preincubation with anti-Db mAb or the use of chimera-derived H-2d CTL specific for Db plus peptide ablated both peptide-dependent inhibition and lysis of allogeneic cells, suggesting these activities are a consequence of self-presentation of peptide Ag by CTL. Lysis of allogeneic cells appears to represent bystander lysis by CTL in response to recognition of peptide on other effector cells. Lysis inhibition is attributable to a highly potent form of cold target inhibition in which CTL serve as their own cold targets.
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PMID:Consequences of self-presentation of peptide antigen by cytolytic T lymphocytes. 247 2

A cross-reactive cytotoxic T lymphocyte clone was produced by stimulation with a hybrid protein that contained a portion of the NS1 and the HA2 subunit of A/PR/8/34 (H1N1) virus. Transfer of this clone clears virus from the lungs of mice challenged with H1 or H2 viruses. In these experiments we define the location of the protective CTL epitope to the transmembrane portion of the influenza A virus hemagglutinin which is well-conserved on H1 and H2 subtype viruses. The H1 and H2 cross-reactive CTL clone recognized a synthetic peptide of 23 amino acids (anchor peptide) corresponding to the transmembrane domain of the A/PR/8 (H1) HA as well as the comparable anchor peptide of the A/JAP (H2) HA. The anchor peptide of the A/PR/8 HA competed against the anchor peptide of A/JAP HA in cold target inhibition tests. These results indicate that the epitope recognized by the cross-reactive CTL is located on the transmembrane region of both A/PR/8 HA and A/JAP HA. We prepared synthetic peptides to define the epitope within the transmembrane region of A/PR/8 HA which is recognized by a cross reactive CTL clone. The results indicate that residues 518-528 in the transmembrane region of A/PR/8 HA contain the cross-reactive CTL epitope.
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PMID:Cytotoxic T lymphocytes recognize a cross-reactive epitope on the transmembrane region of influenza H1 and H2 hemagglutinins. 248 3

Volunteers who develop a cold following virus challenge were significantly slower on choice reaction time tasks than those with no illness. This effect was still observed after the clinical symptoms had gone. In contrast to this, influenza illnesses only impaired performance in tasks in which subjects were uncertain where the target stimulus would appear. These results demonstrate that the CNS effects of respiratory virus infections depend on the type of virus, and that performance impairments may remain even after the symptoms of a cold have gone.
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PMID:Effects and after-effects of the common cold and influenza on human performance. 255 60

Mechanisms of aggregation and release reactions of human platelets induced by non-hemolytic influenza virus were studied. The influenza virus (PR/8 strain) caused aggregation of platelets with ATP release in a dose-dependent manner over the range of 640-10,240 HA titers. The aggregation was always preceded by a lag period and subsequent shape changes. The virus-induced aggregation was enhanced by exposure of the reaction mixtures to cold at 4 degrees C for 30 min and inhibited by apyrase, acetylsalicylic acid and dipyridamole. Ingestion of acetylsalicylic acid also inhibited the aggregation. Gel-filtered platelets were aggregated by influenza virus only after the reaction mixtures had been previously incubated at 4 degrees C for 30 min and then stirred at 37 degrees C. In the absence of divalent cations (Ca2+ less than or equal to 2 x 10(-5) M, Mg2+ less than or equal to 1 x 10(-5) M), gel-filtered platelets were not aggregated by influenza virus. These results suggest that influenza virus was absorbed onto the platelet surface and caused the release of ADP from platelets, which in turn, aggregated platelets.
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PMID:[Mechanisms of human platelet aggregation and release reaction induced by influenza virus]. 258 49

Intranasal live attenuated cold-adapted (ca) influenza A/Kawasaki/9/86 (H1N1) reassortant virus and parenteral inactivated influenza A/Taiwan/1/86 (H1N1) virus were given alone or in combination to 80 ambulatory elderly subjects. An enzyme-linked immunosorbent assay was used to measure hemagglutinin-specific (HA) antibodies in serum and nasal wash specimens collected before vaccination and 1 and 3 months later. Serum immunoglobulin G (IgG) and nasal wash IgA HA responses were elicited in 56 and 20%, respectively, of 25 inactivated-virus vaccinees and in 67 and 48%, respectively, of 27 recipients of both vaccines but in only 36 and 25%, respectively, of 28 vaccinees given live virus alone. Inactivated virus, administered alone or with live virus vaccine, induced higher titers of serum antibody than did the live virus alone. In contrast, nasal IgA HA antibody was elicited more often and in greater quantity by the vaccine combination than by either vaccine alone. Despite these differences, the peak titers of local antibody mounted by each group of vaccinees were similar. By 3 months postvaccination, serum IgG and nasal IgA HA antibody titers remained elevated above prevaccination levels in 50 and 17%, respectively, of the inactivated-virus vaccinees and in 46 and 23%, respectively, of recipients of both vaccines but in only 19 and 7%, respectively, of the live-virus and systemic antibodies, if vaccinees. The finding that live ca influenza A virus induced short-lived local and systemic antibodies, if confirmed, suggests that live virus vaccination may not be a suitable alternative or adjunct to inactivated virus vaccination for the elderly.
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PMID:Systemic and local antibody responses in elderly subjects given live or inactivated influenza A virus vaccines. 259 35


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