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To identify predictors of influenza vaccine acceptance among VHA healthcare workers (HCWs), with emphasis on modifiable factors related to promotion campaigns.
National single-payer healthcare system with 140 hospitals and 321,000 HCWs.
National voluntary sample of HCWs in the Veterans Health Administration (VHA) system.
We invited a random sample of 5% of all VHA HCWs to participate. An 18-item intranet-based survey inquired about occupation, vaccination status, employer policy, and local campaign efforts.
The response rate was 17.4%. Of 2,502 initial respondents, 2,406 (96.2%) provided usable data. This sample includes respondents from all 140 VA hospitals. Self-reported influenza vaccination rates were highest among physicians (95.6%) and licensed independent providers (88.3%). Nonclinical staff (80.7%) reported vaccine uptake similar to other certified but nonlicensed providers (81.2%). The strongest predictor of vaccine acceptance among VHA HCWs was individual awareness of organizational policy. Vaccine acceptance was also higher among HCWs who reported more options for access to vaccination and among those in facilities with more education activities.
Influenza vaccine acceptance varied significantly by employee awareness of employer policy and on-site access to vaccine. Employer-sponsored activities to increase access continue to show positive returns across occupations. Local influenza campaign efforts to educate HCWs may have reached saturation in this target group. These results suggest that focused communications to increase HCW awareness and understanding of employer policy can drive further increase in influenza vaccination acceptance.
Jianming (James) Tang, Division of Geographic Medicine, Department of Medicine, School of Medicine,
Richard A. Kaslow, Department of Epidemiology and International Health, School of Public Health, University of Alabama at Birmingham
Human immunogenetic studies beginning in 1996 have produced clear evidence that initial acquisition of HIV-1 infection can be effectively blocked by homozygosity for a 32-bp deletion (Δ32) in the open reading frame of the beta (C-C motif) chemokine receptor 5 (CCR5) and further inhibited by the Δ32 heterozygous genotype or by Δ32 in combination with another mutation that also introduces a premature stop codon in CCR5. Conversely, homozygosity for the CCR2-CCR5 HHE haplotype defined by several single-nucleotide polymorphisms (SNPs) appears to enhance HIV-1 acquisition. The two closely related CCR2-CCR5 haplotypes HHE and HHG*2 (=CCR5-Δ32) and probably others [e.g., HHF*2 (=CCR2-64I)] are also associated with varying rates of HIV-1 disease progression against certain ethnic backgrounds. Additional but less consistent associations with both HIV-1 infection and disease progression have been documented for SDF-1, RANTES (SCYA5), CX3CR1, and MIP-1α polymorphisms within the chemokine receptor and ligand system. Both chance association and population heterogeneity probably account for some of the inconsistencies. More recent recognition of CCR2-CCR5 haplotype-mediated effects on HIV-1 RNA concentration implies that CCR polymorphisms are important early determinants of the virus–host equilibrium. Evolving usage of chemokine receptors by HIV-1 may cloud the interpretation of newly acquired data and impede translation of this research into improvements in clinical care. The functional complexity of the chemokine system and its interactions with other host and viral factors calls for a comprehensive analytic approach to the elucidation of immunogenetic influences on HIV/AIDS and vigilance for effects of viral adaptation.
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