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_|SELECTED RESEARCH ARTICLES ABSTRACTS, JULY 14, 2008|_
Research Articles Abstracts.
Contents:
(1.1) Adamantane resistance in influenza A(H1) viruses increased in 2007 in South East Asia but decreased in Australia and some other countries.
(1.2) Treatment of influenza A (H1N1) virus infections in mice and ferrets with cyanovirin-N.
(1.3) Systemic Release of High Mobility Group Box 1 Protein during Severe Murine Influenza.
(1.4) Hyperinduction of Cyclooxygenase-2-Mediated Proinflammatory Cascade: A Mechanism for the Pathogenesis of Avian Influenza H5N1 Infection.
(1.5) Influenza A Virus Matrix Protein 1-Specific Human CD8+ T Cell Response Induced in Trivalent Inactivated Vaccine Recipients.
(1.6) Natural killer cells regulate T cell proliferation during Human Parainfluenza Virus 3 infection.
(1.7) A SINGLE AMINO ACID RESIDUE CHANGE IN THE P PROTEIN OF PARAINFLUENZA VIRUS 5 (PIV5) ELEVATES VIRAL GENE EXPRESSION.
(1.8) Human parainfluenza virus type 1 C proteins are non-essential proteins that inhibit the host interferon and apoptotic responses and are required for efficient replication in non-human primates.
(1.9) A simple and rapid immunochromatographic strip test for monitoring antibodies to H5 subtype Avian Influenza Virus.
(1.10) Safety and efficacy of live attenuated influenza vaccine in children 2-7 years of age.
(1.11) Why young healthy adults should become a target group for the influenza vaccination: A cardiologist's point of view.
(1.12) Safety and immunogenicity of two subunit influenza vaccines in healthy children, adults and the elderly: A randomized controlled trial in China.
(1.13) Seasonal inactivated influenza virus vaccines.
(1.14) Immunogenicity, safety and consistency of new trivalent inactivated influenza vaccine.
(1.15) Effect of sublingual administration of interferon-alpha on the immune response to influenza vaccination in institutionalized elderly individuals.
See original abstracts at the source site. EDITED.]
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(1.1): Antiviral Res. 2008 Jul 5. [Epub ahead of print]
Adamantane resistance in influenza A(H1) viruses increased in 2007 in South East Asia but decreased in Australia and some other countries.
Barr IG, Deng YM, Iannello P, Hurt AC, Komadina N. - WHO Collaborating Centre for Reference and Research on Influenza, 45 Poplar Road, Parkville, Melbourne, Victoria 3052, Australia; Monash University Gippsland, Churchill, Victoria 3842, Australia.
The adamantanes (amantadine and rimantadine) were the initial antivirals licensed for use against influenza A viruses and have been used in some countries to control seasonal influenza and have also been stockpiled for potential pandemic use.
While high rates of resistance have been observed in recent years with A(H3) viruses, the rates of resistance with A(H1) viruses has varied widely.
In this study we analysed 281 human influenza A viruses isolated in 2007 that were referred to the WHO Collaborating Centre for Reference and Research in Melbourne, mainly from Australia and the surrounding regions, for evidence of resistance to adamantanes and a subset of these was examined for resistance to the neuraminidase inhibitors (NIs).
We found that the rates of adamantane resistance in A(H3) viruses continued to increase in most countries in 2007 but a distinct variation was seen with A(H1) resistance levels.
A(H1) viruses from Australia, New Zealand and Europe had low rates of resistance (2-9%) whereas viruses from a number of South East (SE) Asian countries had high rates of resistance (33-100%).
This difference can be attributed to the spread of A/Brisbane/59/2007-like viruses to many parts of the world with the exception of SE Asia where A/Hong Kong/2652/2006-like viruses continue to predominate.
When these two A(H1) subgroups were compared for their in vitro sensitivity to the other class of influenza antiviral drugs, the neuraminidase inhibitors, no difference was seen between the groups with both showing normal levels of sensitivity to these drugs,
The finding of reducing A(H1) resistance rates in Australia and rising levels in SE Asia in 2007, reverses the trend seen in 2006 when A(H1) resistance levels were rising in Australia and elsewhere but remained low in most of SE Asia.
PMID: 18611414 [PubMed - as supplied by publisher]
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(1.2): Antiviral Res. 2008 Jul 1. [Epub ahead of print]
Treatment of influenza A (H1N1) virus infections in mice and ferrets with cyanovirin-N.
Smee DF, Bailey KW, Wong MH, O'Keefe BR, Gustafson KR, Mishin VP, Gubareva LV. - Institute for Antiviral Research, Utah State University, Logan, UT, USA.
Cyanovirin-N (CV-N), a protein derived from Nostoc ellipsosporum, neutralizes influenza virus infectivity by binding to specific high-mannose oligosaccharides (oligomannose-8 and -9) at glycosylation sites on the viral hemagglutinin HA1 subunit.
Mouse-adapted viruses lose sensitivity to CV-N due to HA1 mutations that eliminate these glycosylation sites.
Recently we created a hybrid (reassortant) influenza A/WSN/33 (H1N1) virus containing the HA gene of A/New Caledonia/20/99 (H1N1) with an Asp225Gly mutation in the HA1, that was lethal to mice yet retained sensitivity to CV-N.
We then utilized this model system to test the efficacy of CV-N against influenza.
CV-N efficacy was dose-responsive from 0.0625 to 1mg/kg/day when administered intranasally (i.n.) twice daily for 4 days starting 4h prior to virus exposure.
In a second study, survival benefit was seen with CV-N treatments (0.5mg/kg/day for 4 days) beginning at -4 or +6h, but was significantly reduced at +12h.
The early treatment resulted in up to 100% survival and 1000-fold reduction in lung virus titer on day 3 of the infection.
In contrast, ribavirin (a positive control-75mg/kg/day) treatment resulted in 30% survival and 30-fold decrease in lung virus titers.
Lung consolidation scores and lung weights were significantly reduced by CV-N and ribavirin treatment on day 6 of the infection.
Ferrets infected with a non-animal adapted influenza A/Charlottesville/31/95 (H1N1) virus were treated intranasally with CV-N (50mug twice daily for 5 days starting 24h before virus challenge).
They exhibited 100-fold lower viral titers in nasal washes than placebos 1 day after treatment, but virus titers were equivalent on days 2-7.
CV-N has the potential for prophylaxis and early initiation of treatment of influenza virus infections.
PMID: 18601954 [PubMed - as supplied by publisher]
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(1.3): J Immunol. 2008 Jul 15;181(2):1454-9.
Systemic Release of High Mobility Group Box 1 Protein during Severe Murine Influenza.
Alleva LM, Budd AC, Clark IA. - School of Biochemistry and Molecular Biology, Australian National University, Canberra, Australian Capital Territory, Australia.
Hypercytokinemia is gaining recognition as the mechanism of fatality from influenza.
No work to date has addressed the role of high mobility group box 1 protein (HMGB1) in influenza, the parallel being that in other severe proinflammatory cytokine syndromes (e.g., sepsis and malaria) levels of circulating HMGB1 are elevated and may correlate with death.
Using a commercially available ELISA for HMGB1, we found that HMGB1 was not increased in the plasma of influenza virus-infected mice (A/Japan/305/57) on day 7 post infection, about the time of peak mortality, and peak levels of HMGB1 in the plasma did not occur until relatively late in infection, on day 9 post infection.
In keeping with the late peak of HMGB1 being unassociated with mortality, administration of ethyl pyruvate, which inhibits active secretion but not passive release of HMGB1, to influenza virus-infected mice, did not affect their survival.
Further work is required to determine whether influenza virus infection induces passive release of HMGB1, and whether HMGB1 neutralization with a specific Ab would improve survival.
PMID: 18606700 [PubMed - in process]
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(1.4): J Infect Dis. 2008 Jul 9. [Epub ahead of print]
Hyperinduction of Cyclooxygenase-2-Mediated Proinflammatory Cascade: A Mechanism for the Pathogenesis of Avian Influenza H5N1 Infection.
Lee SM, Cheung CY, Nicholls JM, Hui KP, Leung CY, Uiprasertkul M, Tipoe GL, Lau YL, Poon LL, Ip NY, Guan Y, Peiris JS. - Departments of 1Microbiology, 2Pathology, 3Anatomy, and 4Pediatric and Adolescent Medicine, University of Hong Kong, 5Department of Biochemistry, Biotechnology Research Institute and Molecular Neuroscience Center, Hong Kong University of Science and Technology, and 6Hong Kong University-Pasteur Research Centre, Hong Kong Special Administrative Region, China; 7Department of Pathology, Siriraj Hospital, Bangkok, Thailand.
The mechanism for the pathogenesis of H5N1 infection in humans remains unclear.
This study reveals that cyclooxygenase-2 (COX-2) was strongly induced in H5N1-infected macrophages in vitro and in epithelial cells of lung tissue samples obtained during autopsy of patients who died of H5N1 disease.
Novel findings demonstrated that COX-2, along with tumor necrosis factor alpha and other proinflammatory cytokines were hyperinduced in epithelial cells by secretory factors from H5N1-infected macrophages in vitro.
This amplification of the proinflammatory response is rapid, and the effects elicited by the H5N1-triggered proinflammatory cascade are broader than those arising from direct viral infection.
Furthermore, selective COX-2 inhibitors suppress the hyperinduction of cytokines in the proinflammatory cascade, indicating a regulatory role for COX-2 in the H5N1-hyperinduced host proinflammatory cascade.
These data provide a basis for the possible development of novel therapeutic interventions for the treatment of H5N1 disease, as adjuncts to antiviral drugs.
PMID: 18613795 [PubMed - as supplied by publisher]
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(1.5): J Virol. 2008 Jul 9. [Epub ahead of print]
Influenza A Virus Matrix Protein 1-Specific Human CD8+ T Cell Response Induced in Trivalent Inactivated Vaccine Recipients.
Terajima M, Cruz J, Leporati AM, Orphin L, Babon JA, Co MD, Pazoles P, Jameson J, Ennis FA. - Center for Infectious Disease and Vaccine Research, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, Massachusetts, 01655, U.S.A.
Among seventeen HLA-A2-positive healthy adults CD8(+) T cell responses against an HLA-A2-restricted matrix protein 1 (M1) epitope increased after immunization with trivalent inactivated influenza vaccine (TIV) in two individuals.
The presence of M1 in TIV was confirmed by Western blotting.
T cell cytotoxicity assays showed that TIV is processed and the epitope is presented by antigen presenting cells to an M1 epitope-specific CD8(+) T cell line for specific lysis.
These data show that TIV, which is formulated to contain surface glycoproteins to induce serotype-specific antibody responses, also contains M1 capable of inducing subtype cross-reactive CD8(+) T cell responses in some vaccinees.
PMID: 18614638 [PubMed - as supplied by publisher
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(1.6): J Virol. 2008 Jul 9. [Epub ahead of print]
Natural killer cells regulate T cell proliferation during Human Parainfluenza Virus 3 infection.
Noone CM, Paget E, Lewis EA, Loetscher MR, Newman RW, Johnson PA. - Viral Immunology laboratory, School of Biotechnology, Dublin City University, Glasnevin, Dublin 9; ZLB Behring, Wankdorfstrasse 10, 3000 Bern 22, Switzerland; National Institute of Biological Standards and Controls, Blanch lane, South Mimms, Potters Bar, Herts EN6 3QG, UK.
Parainfluenza Virus Type 3 is a major respiratory pathogen in humans.
Failure to induce immunological memory associated with Human Parainfluenza Virus 3 infection has been attributed to inhibition of lymphocyte proliferation.
We demonstrate that the inability of mixed lymphocytes to respond to virally infected Antigen Presenting Cells is due to an IL-2 dependent, non-apoptotic mechanism involving Natural Killer cells and their influence is exerted in a contact dependent manner.
These results suggest a novel regulatory mechanism for NK cells during HPIV3 infection, offering an explanation for viral persistence and poor memory responses.
PMID: 18614637 [PubMed - as supplied by publisher]
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(1.7): J Virol. 2008 Jul 9. [Epub ahead of print]
A SINGLE AMINO ACID RESIDUE CHANGE IN THE P PROTEIN OF PARAINFLUENZA VIRUS 5 (PIV5) ELEVATES VIRAL GENE EXPRESSION.
Timani KA, Sun D, Sun M, Keim C, Lin Y, Schmitt PT, Schmitt AP, He B. - Department of Veterinary and Biomedical Sciences, Intercollege Graduate Program in Cell and Developmental Biology, Graduate Program in Pathobiology, Center of Molecular Immunology and Infectious Disease, Pennsylvania State University, University Park, PA 16802.
Parainfluenza virus 5 (PIV5) is a prototypical paramyxovirus.
The V/P gene of PIV5 encodes two mRNA species through a process of pseudo-templated insertion of two G residues at a specific site during transcription, resulting in two viral proteins, V and P, whose N-termini of 164 amino acid residues are identical.
Previously, it has been reported that mutating six amino acid residues within this identical region results in a recombinant PIV5 (rPIV5-CPI-) that exhibits elevated viral protein expression and induces production of cytokines such as interferon beta (IFN-beta) and interleukin 6 (IL-6).
Because the six mutations correspond to the shared region of the V protein and the P protein, it is not clear whether the phenotypes associated with rPIV5-CPI- are due to mutations in the P protein and/or mutations in the V protein.
To address this question, we have used a mini-genome system as well as recombinant viruses to study the effects of mutations on the functions of the P and V proteins.
We found that the P protein with six amino acid residue changes (Pcpi-) was more efficient than wild type P in facilitating replication of viral RNA while the V protein with six amino acid residue changes (Vcpi-) still inhibits mini-genome replication like the wt V protein.
These results indicate that elevated viral gene expression in rPIV5-CPI- virus-infected cells can be attributed to a P protein with increased ability to facilitate viral RNA synthesis.
Furthermore, we found that a single amino acid residue change at position 157 of P protein from ser (the residue in wt P protein) to phe (the residue in Pcpi-) is sufficient for elevated viral gene expression.
Using mass spectrometry and (33)P-labeling, we found that residue S157 of P protein is phosphorylated.
Based on these results, we propose that phosphorylation of the P protein at residue 157 plays an important role in regulating viral RNA replication.
PMID: 18614634 [PubMed - as supplied by publisher]
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(1.8): J Virol. 2008 Jul 9. [Epub ahead of print]
Human parainfluenza virus type 1 C proteins are non-essential proteins that inhibit the host interferon and apoptotic responses and are required for efficient replication in non-human primates.
Bartlett EJ, Cruz AM, Esker J, Casta?o A, Schomacker H, Surman SR, Hennessey M, Boonyaratanakornkit J, Pickles RJ, Collins PL, Murphy BR, Schmidt AC. - Laboratory of Infectious Diseases, Respiratory Viruses Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Department of Health and Human Services. Bethesda, MD, 20892-2007, USA; Cystic Fibrosis/Pulmonary Research and Treatment Center, University of North Carolina at Chapel Hill. Chapel Hill, NC, 27599-7248, USA; Department of Microbiology and Immunology, University of North Carolina at Chapel Hill. Chapel Hill, NC, 27599-7248, USA.
Recombinant HPIV1 (rHPIV1) was modified to create rHPIV1-P(C-), a virus in which expression of the C proteins (C', C, Y1 and Y2) was silenced without affecting the amino acid sequence of the P protein.
Infectious rHPIV1-P(C-) was readily recovered from cDNA, indicating that the four C proteins were not essential for virus replication.
Early during infection in vitro, rHPIV1-P(C-) replicated as efficiently as HPIV1 wt, but its titer subsequently decreased coincident with the onset of an extensive cytopathic effect (cpe) not observed with rHPIV1 wt.
rHPIV1-P(C-) infection, but not rHPIV1 wt infection, induced caspase 3 activation and nuclear fragmentation in LLC-MK2 cells, identifying the HPIV1 C proteins as inhibitors of apoptosis.
In contrast to rHPIV1 wt, rHPIV1-P(C-) and rHPIV1-C(F170S), a mutant encoding a F170S substitution in C, induced IFN and did not inhibit IFN signaling in vitro. However, only rHPIV1-P(C-) induced apoptosis.
Thus, the anti-IFN and anti-apoptosis activities of HPIV1 were separable: both activities are disabled in rHPIV1-P(C-) whereas only the anti-IFN activity is disabled in rHPIV1-C(F170S).
In African green monkeys (AGMs), rHPIV1-P(C-) was considerably more attenuated than rHPIV1-C(F170S), suggesting that disabling the anti-IFN and anti-apoptotic activities of HPIV1 had additive effects on attenuation in vivo.
Although rHPIV1-P(C-) protected against challenge with HPIV1 wt, its highly restricted replication in AGMs and in primary human airway epithelial cultures suggests that it might be over-attenuated for use as a vaccine.
Thus, the C proteins of HPIV1 are non-essential but have anti-IFN and anti-apoptosis activities required for virulence in primates.
PMID: 18614629 [PubMed - as supplied by publisher]
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(1.9): J Virol Methods. 2008 Jul 4. [Epub ahead of print]
A simple and rapid immunochromatographic strip test for monitoring antibodies to H5 subtype Avian Influenza Virus.
Cui S, Chen C, Tong G. - National Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin 150001, China.
A colloid gold strip (CGS) test for detecting antibodies to H5 subtype Avian Influenza Virus (AIV) was developed.
The test is based on membrane chromatography and uses colloidal gold conjugated with inactivated AIV-H5N1 as the tracer.
On the test strip, a baculovirus expressed haemagglutinin (HA) protein was used as the capture complex at the "test line", and anti-HA monoclonal antibody was used as the capture antibody at the "control line".
The assembled test strip was housed in a plastic case.
Compared with the hemagglutination inhibition test, the sensitivity and specificity of the CGS test were 88.8% and 97.6%, respectively, in detecting H5N1 antibodies in 830 serum samples from vaccinated chickens.
Because it is rapid and does not require specialized equipment or technicians, the CGS test should be useful for detecting H5N1 antibodies in the field.
PMID: 18606190 [PubMed - as supplied by publisher]
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(1.10): Vaccine. 2008 Jul 5. [Epub ahead of print]
Safety and efficacy of live attenuated influenza vaccine in children 2-7 years of age.
Belshe R, Ambrose C, Yi T. - Saint Louis University Health Sciences Center, St. Louis, MO, United States.
Three pivotal trials supported the licensure of live attenuated influenza vaccine (LAIV) for children >/=2 years of age: 2 placebo-controlled studies each conducted over 2 seasons, and a 1-year trial comparing LAIV with trivalent inactivated influenza vaccine (TIV).
Analyses were conducted to evaluate the safety and efficacy of LAIV in the subgroup of children >/=2 years of age from these trials.
Efficacy was demonstrated compared with placebo in children aged 2-7 years in seasons with matched strains (69.2% [95% CI: 52.7, 80.4] and 94.6% [95% CI: 88.6, 97.5]), seasons with primarily mismatched strains (87% [95% CI: 77.0, 92.6]), and during late season epidemics (73.8% [95% CI: 40.4, 89.4]).
Compared with TIV recipients, LAIV recipients aged 2-5 years had 52.5% (95% CI: 26.7, 68.7) and 54.4% (95% CI: 41.8, 64.5) fewer cases of influenza illness against matched and mismatched strains, respectively.
No unusual or unexpected adverse reactions were noted.
The adverse reactions most commonly associated with LAIV were runny nose/nasal congestion and low-grade fever.
Hospitalizations and medically significant wheezing were increased in children 6-11 and 6-23 months of age who received LAIV, respectively, but were not increased in children 2-5 years of age.
PMID: 18611422 [PubMed - as supplied by publisher
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(1.11): Vaccine. 2008 Jul 3. [Epub ahead of print]
Why young healthy adults should become a target group for the influenza vaccination: A cardiologist's point of view.
Ciszewski A. - Insitute of Cardiology, Alpejka 42, Warsaw, Poland.
PMID: 18602956 [PubMed - as supplied by publisher]
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(1.12): Vaccine. 2008 Jun 17. [Epub ahead of print]
Safety and immunogenicity of two subunit influenza vaccines in healthy children, adults and the elderly: A randomized controlled trial in China.
Zhu FC, Zhou W, Pan H, Lu L, Gerez L, Nauta J, Giezeman K, de Bruijn I. - Jiangsu Provincial Center for Disease Control and Prevention, Nanjing, Jiangsu Province, People's Republic of China.
The burden of influenza is well known in the elderly and at-risk patients, but also in children.
Especially in those under 5 years old, influenza may cause severe morbidity and mortality.
Influenza infections and complications can be reduced by vaccination.
In a randomized, endpoint-blinded, parallel group trial the immunogenicity and safety was studied of two trivalent inactivated surface antigen (subunit) influenza vaccines Influvac((R)) and Agrippal((R)) in healthy children as well as in adults and the elderly.
An open safety part in 30 children aged 3-12 years and 30 adults aged 18-60 years vaccinated with Influvac((R)) was followed by an endpoint-blind, parallel group part in 300 healthy children aged 3-12 years, 300 healthy adults aged 18-59 years, and 240 healthy elderly persons aged 60 years or over, in which subjects were randomized 2:1 to vaccination with either Influvac((R)) or Agrippal((R)).
The primary immunogenicity endpoint was the geometric mean titer (GMT) 4 weeks after vaccination.
Both Influvac((R)) and Agrippal((R)) induced high anti-hemagglutinin antibody titers in the children and in the adult and elderly subjects.
Seroprotection rates were >85% and seroconversion rates >70% for both vaccines in all three age groups for all three-virus strains.
The GMT ratios after vaccination indicated that the immunogenicity of Influvac((R)) was at least comparable with that of Agrippal((R)) in all three age groups.
Both vaccines were well tolerated and safe.
In this trial, Influvac((R)) and Agrippal((R)) were immunogenic, safe and well tolerated in healthy children as well as in adults and elderly people.
PMID: 18602729 [PubMed - as supplied by publisher]
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(1.13): Vaccine. 2008 Jun 17. [Epub ahead of print]
Seasonal inactivated influenza virus vaccines.
Couch RB. - Department of Molecular Virology & Microbiology, Baylor College of Medicine, One Baylor Plaza, MS: BCM280, Houston, TX 77030, United States.
Inactivated influenza virus vaccines are the primary modality used for prevention of influenza.
A system of annual identification of new strains causing illnesses, selections for vaccines, chick embryo growth, inactivation, processing, packaging, distribution and usage has been in place for decades.
Current vaccines contain 15mug of the HA of an A/H1N1, A/H3N2 and B strain and are given parenterally to induce serum anti-HA antibody for prevention of subsequent infection and illness from natural influenza.
Reactogenicity is low and protection among healthy older children and adults is good; protection levels are generally lower in young children and the elderly.
Needs include ensuring antigenic matches of vaccine and epidemic viruses each season, enhancing immunization rates, and providing new and improved vaccines and immunization approaches for the varied populations and circumstances globally.
PMID: 18602728 [PubMed - as supplied by publisher
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(1.14): Vaccine. 2008 Jun 2. [Epub ahead of print]
Immunogenicity, safety and consistency of new trivalent inactivated influenza vaccine.
Talbot HK, Keitel W, Cate TR, Treanor J, Campbell J, Brady RC, Graham I, Dekker CL, Ho D, Winokur P, Walter E, Bennet J, Formica N, Hartel G, Skeljo M, Edwards KM. - Vanderbilt University School of Medicine and Pediatrics, Vanderbilt University Medical Center, CCC 5311 MCN, 1161 21st Avenue South, Nashville, TN 37232, United States.
To augment the available influenza vaccine supply, a phase III study was conducted to evaluate the immunogenicity, safety, and consistency of a new trivalent inactivated influenza vaccine manufactured by CSL Limited.
Healthy adults (ages 18-64) were randomized to receive either a single dose of TIV from multi-dose vials with thimerosal, TIV from pre-filled syringes without thimerosal, or placebo.
Of the TIV recipients, 97.8% achieved a post-vaccination titer >/=40 against H1N1, 99.9% against H3N2 component, and 94.2% against influenza B.
Few local or systemic adverse events were noted after vaccination with either TIV presentation.
TIV was well tolerated and immunogenic.
PMID: 18602726 [PubMed - as supplied by publisher
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(1.15): Vaccine. 2008 Jun 4. [Epub ahead of print]
Effect of sublingual administration of interferon-alpha on the immune response to influenza vaccination in institutionalized elderly individuals.
Launay O, Grabar S, Bloch F, Desaint C, Jegou D, Lallemand C, Erickson R, Lebon P, Tovey MG. - Universit? Paris Descartes, Facult? de M?decine, Paris, France; Assistance Publique-H?pitaux de Paris, Groupe Hospitalier Cochin-Saint Vincent de Paul, P?le de M?decine, CIC de Vaccinologie Cochin-Pasteur (CIC BT505), Paris, France; INSERM, CIC de Vaccinologie Cochin-Pasteur, Paris, France.
A randomized double-blind placebo-controlled study was conducted to determine the effect of sublingual administration of IFNalpha on the immune response to influenza vaccination in elderly institutionalized individuals.
Sublingual administration of 10 million IU of IFNalpha immediately prior to vaccination, reduced the geometric mean haemagglutination inhibitory (HAI) and IgG2 circulating antibody titers, and the secretory IgA (sIgA) response in saliva, to the New York strain of influenza A virus, 21 days post-vaccination, without detectable drug-related local or systemic toxicity.
IFN treatment did not inhibit the immune response to the other components of the vaccine; the New Caledonia strain of influenza A virus, or the Jiangsu strain of influenza B virus.
At the dose tested sublingual administration of IFNalpha reduces the immune response to influenza vaccination in elderly institutionalized individuals.
PMID: 18602725 [PubMed - as supplied by publisher]
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Contents:
(1.1) Adamantane resistance in influenza A(H1) viruses increased in 2007 in South East Asia but decreased in Australia and some other countries.
(1.2) Treatment of influenza A (H1N1) virus infections in mice and ferrets with cyanovirin-N.
(1.3) Systemic Release of High Mobility Group Box 1 Protein during Severe Murine Influenza.
(1.4) Hyperinduction of Cyclooxygenase-2-Mediated Proinflammatory Cascade: A Mechanism for the Pathogenesis of Avian Influenza H5N1 Infection.
(1.5) Influenza A Virus Matrix Protein 1-Specific Human CD8+ T Cell Response Induced in Trivalent Inactivated Vaccine Recipients.
(1.6) Natural killer cells regulate T cell proliferation during Human Parainfluenza Virus 3 infection.
(1.7) A SINGLE AMINO ACID RESIDUE CHANGE IN THE P PROTEIN OF PARAINFLUENZA VIRUS 5 (PIV5) ELEVATES VIRAL GENE EXPRESSION.
(1.8) Human parainfluenza virus type 1 C proteins are non-essential proteins that inhibit the host interferon and apoptotic responses and are required for efficient replication in non-human primates.
(1.9) A simple and rapid immunochromatographic strip test for monitoring antibodies to H5 subtype Avian Influenza Virus.
(1.10) Safety and efficacy of live attenuated influenza vaccine in children 2-7 years of age.
(1.11) Why young healthy adults should become a target group for the influenza vaccination: A cardiologist's point of view.
(1.12) Safety and immunogenicity of two subunit influenza vaccines in healthy children, adults and the elderly: A randomized controlled trial in China.
(1.13) Seasonal inactivated influenza virus vaccines.
(1.14) Immunogenicity, safety and consistency of new trivalent inactivated influenza vaccine.
(1.15) Effect of sublingual administration of interferon-alpha on the immune response to influenza vaccination in institutionalized elderly individuals.
See original abstracts at the source site. EDITED.]
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(1.1): Antiviral Res. 2008 Jul 5. [Epub ahead of print]
Adamantane resistance in influenza A(H1) viruses increased in 2007 in South East Asia but decreased in Australia and some other countries.
Barr IG, Deng YM, Iannello P, Hurt AC, Komadina N. - WHO Collaborating Centre for Reference and Research on Influenza, 45 Poplar Road, Parkville, Melbourne, Victoria 3052, Australia; Monash University Gippsland, Churchill, Victoria 3842, Australia.
The adamantanes (amantadine and rimantadine) were the initial antivirals licensed for use against influenza A viruses and have been used in some countries to control seasonal influenza and have also been stockpiled for potential pandemic use.
While high rates of resistance have been observed in recent years with A(H3) viruses, the rates of resistance with A(H1) viruses has varied widely.
In this study we analysed 281 human influenza A viruses isolated in 2007 that were referred to the WHO Collaborating Centre for Reference and Research in Melbourne, mainly from Australia and the surrounding regions, for evidence of resistance to adamantanes and a subset of these was examined for resistance to the neuraminidase inhibitors (NIs).
We found that the rates of adamantane resistance in A(H3) viruses continued to increase in most countries in 2007 but a distinct variation was seen with A(H1) resistance levels.
A(H1) viruses from Australia, New Zealand and Europe had low rates of resistance (2-9%) whereas viruses from a number of South East (SE) Asian countries had high rates of resistance (33-100%).
This difference can be attributed to the spread of A/Brisbane/59/2007-like viruses to many parts of the world with the exception of SE Asia where A/Hong Kong/2652/2006-like viruses continue to predominate.
When these two A(H1) subgroups were compared for their in vitro sensitivity to the other class of influenza antiviral drugs, the neuraminidase inhibitors, no difference was seen between the groups with both showing normal levels of sensitivity to these drugs,
The finding of reducing A(H1) resistance rates in Australia and rising levels in SE Asia in 2007, reverses the trend seen in 2006 when A(H1) resistance levels were rising in Australia and elsewhere but remained low in most of SE Asia.
PMID: 18611414 [PubMed - as supplied by publisher]
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(1.2): Antiviral Res. 2008 Jul 1. [Epub ahead of print]
Treatment of influenza A (H1N1) virus infections in mice and ferrets with cyanovirin-N.
Smee DF, Bailey KW, Wong MH, O'Keefe BR, Gustafson KR, Mishin VP, Gubareva LV. - Institute for Antiviral Research, Utah State University, Logan, UT, USA.
Cyanovirin-N (CV-N), a protein derived from Nostoc ellipsosporum, neutralizes influenza virus infectivity by binding to specific high-mannose oligosaccharides (oligomannose-8 and -9) at glycosylation sites on the viral hemagglutinin HA1 subunit.
Mouse-adapted viruses lose sensitivity to CV-N due to HA1 mutations that eliminate these glycosylation sites.
Recently we created a hybrid (reassortant) influenza A/WSN/33 (H1N1) virus containing the HA gene of A/New Caledonia/20/99 (H1N1) with an Asp225Gly mutation in the HA1, that was lethal to mice yet retained sensitivity to CV-N.
We then utilized this model system to test the efficacy of CV-N against influenza.
CV-N efficacy was dose-responsive from 0.0625 to 1mg/kg/day when administered intranasally (i.n.) twice daily for 4 days starting 4h prior to virus exposure.
In a second study, survival benefit was seen with CV-N treatments (0.5mg/kg/day for 4 days) beginning at -4 or +6h, but was significantly reduced at +12h.
The early treatment resulted in up to 100% survival and 1000-fold reduction in lung virus titer on day 3 of the infection.
In contrast, ribavirin (a positive control-75mg/kg/day) treatment resulted in 30% survival and 30-fold decrease in lung virus titers.
Lung consolidation scores and lung weights were significantly reduced by CV-N and ribavirin treatment on day 6 of the infection.
Ferrets infected with a non-animal adapted influenza A/Charlottesville/31/95 (H1N1) virus were treated intranasally with CV-N (50mug twice daily for 5 days starting 24h before virus challenge).
They exhibited 100-fold lower viral titers in nasal washes than placebos 1 day after treatment, but virus titers were equivalent on days 2-7.
CV-N has the potential for prophylaxis and early initiation of treatment of influenza virus infections.
PMID: 18601954 [PubMed - as supplied by publisher]
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(1.3): J Immunol. 2008 Jul 15;181(2):1454-9.
Systemic Release of High Mobility Group Box 1 Protein during Severe Murine Influenza.
Alleva LM, Budd AC, Clark IA. - School of Biochemistry and Molecular Biology, Australian National University, Canberra, Australian Capital Territory, Australia.
Hypercytokinemia is gaining recognition as the mechanism of fatality from influenza.
No work to date has addressed the role of high mobility group box 1 protein (HMGB1) in influenza, the parallel being that in other severe proinflammatory cytokine syndromes (e.g., sepsis and malaria) levels of circulating HMGB1 are elevated and may correlate with death.
Using a commercially available ELISA for HMGB1, we found that HMGB1 was not increased in the plasma of influenza virus-infected mice (A/Japan/305/57) on day 7 post infection, about the time of peak mortality, and peak levels of HMGB1 in the plasma did not occur until relatively late in infection, on day 9 post infection.
In keeping with the late peak of HMGB1 being unassociated with mortality, administration of ethyl pyruvate, which inhibits active secretion but not passive release of HMGB1, to influenza virus-infected mice, did not affect their survival.
Further work is required to determine whether influenza virus infection induces passive release of HMGB1, and whether HMGB1 neutralization with a specific Ab would improve survival.
PMID: 18606700 [PubMed - in process]
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(1.4): J Infect Dis. 2008 Jul 9. [Epub ahead of print]
Hyperinduction of Cyclooxygenase-2-Mediated Proinflammatory Cascade: A Mechanism for the Pathogenesis of Avian Influenza H5N1 Infection.
Lee SM, Cheung CY, Nicholls JM, Hui KP, Leung CY, Uiprasertkul M, Tipoe GL, Lau YL, Poon LL, Ip NY, Guan Y, Peiris JS. - Departments of 1Microbiology, 2Pathology, 3Anatomy, and 4Pediatric and Adolescent Medicine, University of Hong Kong, 5Department of Biochemistry, Biotechnology Research Institute and Molecular Neuroscience Center, Hong Kong University of Science and Technology, and 6Hong Kong University-Pasteur Research Centre, Hong Kong Special Administrative Region, China; 7Department of Pathology, Siriraj Hospital, Bangkok, Thailand.
The mechanism for the pathogenesis of H5N1 infection in humans remains unclear.
This study reveals that cyclooxygenase-2 (COX-2) was strongly induced in H5N1-infected macrophages in vitro and in epithelial cells of lung tissue samples obtained during autopsy of patients who died of H5N1 disease.
Novel findings demonstrated that COX-2, along with tumor necrosis factor alpha and other proinflammatory cytokines were hyperinduced in epithelial cells by secretory factors from H5N1-infected macrophages in vitro.
This amplification of the proinflammatory response is rapid, and the effects elicited by the H5N1-triggered proinflammatory cascade are broader than those arising from direct viral infection.
Furthermore, selective COX-2 inhibitors suppress the hyperinduction of cytokines in the proinflammatory cascade, indicating a regulatory role for COX-2 in the H5N1-hyperinduced host proinflammatory cascade.
These data provide a basis for the possible development of novel therapeutic interventions for the treatment of H5N1 disease, as adjuncts to antiviral drugs.
PMID: 18613795 [PubMed - as supplied by publisher]
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(1.5): J Virol. 2008 Jul 9. [Epub ahead of print]
Influenza A Virus Matrix Protein 1-Specific Human CD8+ T Cell Response Induced in Trivalent Inactivated Vaccine Recipients.
Terajima M, Cruz J, Leporati AM, Orphin L, Babon JA, Co MD, Pazoles P, Jameson J, Ennis FA. - Center for Infectious Disease and Vaccine Research, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, Massachusetts, 01655, U.S.A.
Among seventeen HLA-A2-positive healthy adults CD8(+) T cell responses against an HLA-A2-restricted matrix protein 1 (M1) epitope increased after immunization with trivalent inactivated influenza vaccine (TIV) in two individuals.
The presence of M1 in TIV was confirmed by Western blotting.
T cell cytotoxicity assays showed that TIV is processed and the epitope is presented by antigen presenting cells to an M1 epitope-specific CD8(+) T cell line for specific lysis.
These data show that TIV, which is formulated to contain surface glycoproteins to induce serotype-specific antibody responses, also contains M1 capable of inducing subtype cross-reactive CD8(+) T cell responses in some vaccinees.
PMID: 18614638 [PubMed - as supplied by publisher
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(1.6): J Virol. 2008 Jul 9. [Epub ahead of print]
Natural killer cells regulate T cell proliferation during Human Parainfluenza Virus 3 infection.
Noone CM, Paget E, Lewis EA, Loetscher MR, Newman RW, Johnson PA. - Viral Immunology laboratory, School of Biotechnology, Dublin City University, Glasnevin, Dublin 9; ZLB Behring, Wankdorfstrasse 10, 3000 Bern 22, Switzerland; National Institute of Biological Standards and Controls, Blanch lane, South Mimms, Potters Bar, Herts EN6 3QG, UK.
Parainfluenza Virus Type 3 is a major respiratory pathogen in humans.
Failure to induce immunological memory associated with Human Parainfluenza Virus 3 infection has been attributed to inhibition of lymphocyte proliferation.
We demonstrate that the inability of mixed lymphocytes to respond to virally infected Antigen Presenting Cells is due to an IL-2 dependent, non-apoptotic mechanism involving Natural Killer cells and their influence is exerted in a contact dependent manner.
These results suggest a novel regulatory mechanism for NK cells during HPIV3 infection, offering an explanation for viral persistence and poor memory responses.
PMID: 18614637 [PubMed - as supplied by publisher]
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(1.7): J Virol. 2008 Jul 9. [Epub ahead of print]
A SINGLE AMINO ACID RESIDUE CHANGE IN THE P PROTEIN OF PARAINFLUENZA VIRUS 5 (PIV5) ELEVATES VIRAL GENE EXPRESSION.
Timani KA, Sun D, Sun M, Keim C, Lin Y, Schmitt PT, Schmitt AP, He B. - Department of Veterinary and Biomedical Sciences, Intercollege Graduate Program in Cell and Developmental Biology, Graduate Program in Pathobiology, Center of Molecular Immunology and Infectious Disease, Pennsylvania State University, University Park, PA 16802.
Parainfluenza virus 5 (PIV5) is a prototypical paramyxovirus.
The V/P gene of PIV5 encodes two mRNA species through a process of pseudo-templated insertion of two G residues at a specific site during transcription, resulting in two viral proteins, V and P, whose N-termini of 164 amino acid residues are identical.
Previously, it has been reported that mutating six amino acid residues within this identical region results in a recombinant PIV5 (rPIV5-CPI-) that exhibits elevated viral protein expression and induces production of cytokines such as interferon beta (IFN-beta) and interleukin 6 (IL-6).
Because the six mutations correspond to the shared region of the V protein and the P protein, it is not clear whether the phenotypes associated with rPIV5-CPI- are due to mutations in the P protein and/or mutations in the V protein.
To address this question, we have used a mini-genome system as well as recombinant viruses to study the effects of mutations on the functions of the P and V proteins.
We found that the P protein with six amino acid residue changes (Pcpi-) was more efficient than wild type P in facilitating replication of viral RNA while the V protein with six amino acid residue changes (Vcpi-) still inhibits mini-genome replication like the wt V protein.
These results indicate that elevated viral gene expression in rPIV5-CPI- virus-infected cells can be attributed to a P protein with increased ability to facilitate viral RNA synthesis.
Furthermore, we found that a single amino acid residue change at position 157 of P protein from ser (the residue in wt P protein) to phe (the residue in Pcpi-) is sufficient for elevated viral gene expression.
Using mass spectrometry and (33)P-labeling, we found that residue S157 of P protein is phosphorylated.
Based on these results, we propose that phosphorylation of the P protein at residue 157 plays an important role in regulating viral RNA replication.
PMID: 18614634 [PubMed - as supplied by publisher]
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(1.8): J Virol. 2008 Jul 9. [Epub ahead of print]
Human parainfluenza virus type 1 C proteins are non-essential proteins that inhibit the host interferon and apoptotic responses and are required for efficient replication in non-human primates.
Bartlett EJ, Cruz AM, Esker J, Casta?o A, Schomacker H, Surman SR, Hennessey M, Boonyaratanakornkit J, Pickles RJ, Collins PL, Murphy BR, Schmidt AC. - Laboratory of Infectious Diseases, Respiratory Viruses Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Department of Health and Human Services. Bethesda, MD, 20892-2007, USA; Cystic Fibrosis/Pulmonary Research and Treatment Center, University of North Carolina at Chapel Hill. Chapel Hill, NC, 27599-7248, USA; Department of Microbiology and Immunology, University of North Carolina at Chapel Hill. Chapel Hill, NC, 27599-7248, USA.
Recombinant HPIV1 (rHPIV1) was modified to create rHPIV1-P(C-), a virus in which expression of the C proteins (C', C, Y1 and Y2) was silenced without affecting the amino acid sequence of the P protein.
Infectious rHPIV1-P(C-) was readily recovered from cDNA, indicating that the four C proteins were not essential for virus replication.
Early during infection in vitro, rHPIV1-P(C-) replicated as efficiently as HPIV1 wt, but its titer subsequently decreased coincident with the onset of an extensive cytopathic effect (cpe) not observed with rHPIV1 wt.
rHPIV1-P(C-) infection, but not rHPIV1 wt infection, induced caspase 3 activation and nuclear fragmentation in LLC-MK2 cells, identifying the HPIV1 C proteins as inhibitors of apoptosis.
In contrast to rHPIV1 wt, rHPIV1-P(C-) and rHPIV1-C(F170S), a mutant encoding a F170S substitution in C, induced IFN and did not inhibit IFN signaling in vitro. However, only rHPIV1-P(C-) induced apoptosis.
Thus, the anti-IFN and anti-apoptosis activities of HPIV1 were separable: both activities are disabled in rHPIV1-P(C-) whereas only the anti-IFN activity is disabled in rHPIV1-C(F170S).
In African green monkeys (AGMs), rHPIV1-P(C-) was considerably more attenuated than rHPIV1-C(F170S), suggesting that disabling the anti-IFN and anti-apoptotic activities of HPIV1 had additive effects on attenuation in vivo.
Although rHPIV1-P(C-) protected against challenge with HPIV1 wt, its highly restricted replication in AGMs and in primary human airway epithelial cultures suggests that it might be over-attenuated for use as a vaccine.
Thus, the C proteins of HPIV1 are non-essential but have anti-IFN and anti-apoptosis activities required for virulence in primates.
PMID: 18614629 [PubMed - as supplied by publisher]
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(1.9): J Virol Methods. 2008 Jul 4. [Epub ahead of print]
A simple and rapid immunochromatographic strip test for monitoring antibodies to H5 subtype Avian Influenza Virus.
Cui S, Chen C, Tong G. - National Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin 150001, China.
A colloid gold strip (CGS) test for detecting antibodies to H5 subtype Avian Influenza Virus (AIV) was developed.
The test is based on membrane chromatography and uses colloidal gold conjugated with inactivated AIV-H5N1 as the tracer.
On the test strip, a baculovirus expressed haemagglutinin (HA) protein was used as the capture complex at the "test line", and anti-HA monoclonal antibody was used as the capture antibody at the "control line".
The assembled test strip was housed in a plastic case.
Compared with the hemagglutination inhibition test, the sensitivity and specificity of the CGS test were 88.8% and 97.6%, respectively, in detecting H5N1 antibodies in 830 serum samples from vaccinated chickens.
Because it is rapid and does not require specialized equipment or technicians, the CGS test should be useful for detecting H5N1 antibodies in the field.
PMID: 18606190 [PubMed - as supplied by publisher]
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(1.10): Vaccine. 2008 Jul 5. [Epub ahead of print]
Safety and efficacy of live attenuated influenza vaccine in children 2-7 years of age.
Belshe R, Ambrose C, Yi T. - Saint Louis University Health Sciences Center, St. Louis, MO, United States.
Three pivotal trials supported the licensure of live attenuated influenza vaccine (LAIV) for children >/=2 years of age: 2 placebo-controlled studies each conducted over 2 seasons, and a 1-year trial comparing LAIV with trivalent inactivated influenza vaccine (TIV).
Analyses were conducted to evaluate the safety and efficacy of LAIV in the subgroup of children >/=2 years of age from these trials.
Efficacy was demonstrated compared with placebo in children aged 2-7 years in seasons with matched strains (69.2% [95% CI: 52.7, 80.4] and 94.6% [95% CI: 88.6, 97.5]), seasons with primarily mismatched strains (87% [95% CI: 77.0, 92.6]), and during late season epidemics (73.8% [95% CI: 40.4, 89.4]).
Compared with TIV recipients, LAIV recipients aged 2-5 years had 52.5% (95% CI: 26.7, 68.7) and 54.4% (95% CI: 41.8, 64.5) fewer cases of influenza illness against matched and mismatched strains, respectively.
No unusual or unexpected adverse reactions were noted.
The adverse reactions most commonly associated with LAIV were runny nose/nasal congestion and low-grade fever.
Hospitalizations and medically significant wheezing were increased in children 6-11 and 6-23 months of age who received LAIV, respectively, but were not increased in children 2-5 years of age.
PMID: 18611422 [PubMed - as supplied by publisher
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(1.11): Vaccine. 2008 Jul 3. [Epub ahead of print]
Why young healthy adults should become a target group for the influenza vaccination: A cardiologist's point of view.
Ciszewski A. - Insitute of Cardiology, Alpejka 42, Warsaw, Poland.
PMID: 18602956 [PubMed - as supplied by publisher]
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(1.12): Vaccine. 2008 Jun 17. [Epub ahead of print]
Safety and immunogenicity of two subunit influenza vaccines in healthy children, adults and the elderly: A randomized controlled trial in China.
Zhu FC, Zhou W, Pan H, Lu L, Gerez L, Nauta J, Giezeman K, de Bruijn I. - Jiangsu Provincial Center for Disease Control and Prevention, Nanjing, Jiangsu Province, People's Republic of China.
The burden of influenza is well known in the elderly and at-risk patients, but also in children.
Especially in those under 5 years old, influenza may cause severe morbidity and mortality.
Influenza infections and complications can be reduced by vaccination.
In a randomized, endpoint-blinded, parallel group trial the immunogenicity and safety was studied of two trivalent inactivated surface antigen (subunit) influenza vaccines Influvac((R)) and Agrippal((R)) in healthy children as well as in adults and the elderly.
An open safety part in 30 children aged 3-12 years and 30 adults aged 18-60 years vaccinated with Influvac((R)) was followed by an endpoint-blind, parallel group part in 300 healthy children aged 3-12 years, 300 healthy adults aged 18-59 years, and 240 healthy elderly persons aged 60 years or over, in which subjects were randomized 2:1 to vaccination with either Influvac((R)) or Agrippal((R)).
The primary immunogenicity endpoint was the geometric mean titer (GMT) 4 weeks after vaccination.
Both Influvac((R)) and Agrippal((R)) induced high anti-hemagglutinin antibody titers in the children and in the adult and elderly subjects.
Seroprotection rates were >85% and seroconversion rates >70% for both vaccines in all three age groups for all three-virus strains.
The GMT ratios after vaccination indicated that the immunogenicity of Influvac((R)) was at least comparable with that of Agrippal((R)) in all three age groups.
Both vaccines were well tolerated and safe.
In this trial, Influvac((R)) and Agrippal((R)) were immunogenic, safe and well tolerated in healthy children as well as in adults and elderly people.
PMID: 18602729 [PubMed - as supplied by publisher]
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(1.13): Vaccine. 2008 Jun 17. [Epub ahead of print]
Seasonal inactivated influenza virus vaccines.
Couch RB. - Department of Molecular Virology & Microbiology, Baylor College of Medicine, One Baylor Plaza, MS: BCM280, Houston, TX 77030, United States.
Inactivated influenza virus vaccines are the primary modality used for prevention of influenza.
A system of annual identification of new strains causing illnesses, selections for vaccines, chick embryo growth, inactivation, processing, packaging, distribution and usage has been in place for decades.
Current vaccines contain 15mug of the HA of an A/H1N1, A/H3N2 and B strain and are given parenterally to induce serum anti-HA antibody for prevention of subsequent infection and illness from natural influenza.
Reactogenicity is low and protection among healthy older children and adults is good; protection levels are generally lower in young children and the elderly.
Needs include ensuring antigenic matches of vaccine and epidemic viruses each season, enhancing immunization rates, and providing new and improved vaccines and immunization approaches for the varied populations and circumstances globally.
PMID: 18602728 [PubMed - as supplied by publisher
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(1.14): Vaccine. 2008 Jun 2. [Epub ahead of print]
Immunogenicity, safety and consistency of new trivalent inactivated influenza vaccine.
Talbot HK, Keitel W, Cate TR, Treanor J, Campbell J, Brady RC, Graham I, Dekker CL, Ho D, Winokur P, Walter E, Bennet J, Formica N, Hartel G, Skeljo M, Edwards KM. - Vanderbilt University School of Medicine and Pediatrics, Vanderbilt University Medical Center, CCC 5311 MCN, 1161 21st Avenue South, Nashville, TN 37232, United States.
To augment the available influenza vaccine supply, a phase III study was conducted to evaluate the immunogenicity, safety, and consistency of a new trivalent inactivated influenza vaccine manufactured by CSL Limited.
Healthy adults (ages 18-64) were randomized to receive either a single dose of TIV from multi-dose vials with thimerosal, TIV from pre-filled syringes without thimerosal, or placebo.
Of the TIV recipients, 97.8% achieved a post-vaccination titer >/=40 against H1N1, 99.9% against H3N2 component, and 94.2% against influenza B.
Few local or systemic adverse events were noted after vaccination with either TIV presentation.
TIV was well tolerated and immunogenic.
PMID: 18602726 [PubMed - as supplied by publisher
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(1.15): Vaccine. 2008 Jun 4. [Epub ahead of print]
Effect of sublingual administration of interferon-alpha on the immune response to influenza vaccination in institutionalized elderly individuals.
Launay O, Grabar S, Bloch F, Desaint C, Jegou D, Lallemand C, Erickson R, Lebon P, Tovey MG. - Universit? Paris Descartes, Facult? de M?decine, Paris, France; Assistance Publique-H?pitaux de Paris, Groupe Hospitalier Cochin-Saint Vincent de Paul, P?le de M?decine, CIC de Vaccinologie Cochin-Pasteur (CIC BT505), Paris, France; INSERM, CIC de Vaccinologie Cochin-Pasteur, Paris, France.
A randomized double-blind placebo-controlled study was conducted to determine the effect of sublingual administration of IFNalpha on the immune response to influenza vaccination in elderly institutionalized individuals.
Sublingual administration of 10 million IU of IFNalpha immediately prior to vaccination, reduced the geometric mean haemagglutination inhibitory (HAI) and IgG2 circulating antibody titers, and the secretory IgA (sIgA) response in saliva, to the New York strain of influenza A virus, 21 days post-vaccination, without detectable drug-related local or systemic toxicity.
IFN treatment did not inhibit the immune response to the other components of the vaccine; the New Caledonia strain of influenza A virus, or the Jiangsu strain of influenza B virus.
At the dose tested sublingual administration of IFNalpha reduces the immune response to influenza vaccination in elderly institutionalized individuals.
PMID: 18602725 [PubMed - as supplied by publisher]
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