Two outbreaks of influenza A (H3N2) in a Japanese nursing home in the winter of 1996-1997, with differing vaccine efficacy.
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Sixty of 128 (46.9%) residents of a nursing home were immunized with two doses of the trivalent split influenza vaccine. They developed 7.4-11.5-fold antibody increases, with a 69-82% protection rate, presenting good immune response rates to the influenza vaccine. Two outbreaks of influenza A (H3N2) occurred. There were no significant antigenic differences among the vaccine strain and the strains isolated from both outbreaks in haemagglutination-inhibition tests, suggesting that the second might have been a reoccurrence. There were no residents who were infected in both outbreaks. The vaccine efficacy against clinical illness in the first outbreak of typical influenza-like-illness (ILI) was 51% (relative risk: 0.49), and the febrile period was reduced significantly by vaccination. In the second outbreak, however, in which all patients had atypical ILI with a high fever but not respiratory symptoms, vaccine efficacy was not apparent for unknown reason. (+info)
Influenza activity was low during October 3-November 6, 1999; influenza virus isolates were reported from 30 states, and four long-term-care facility outbreaks were reported from three states. The predominant viruses isolated were influenza type A(H3N2) viruses. This report summarizes influenza activity in the United States during October 3-November 6, 1999. It also summarizes U.S. influenza surveillance methodology, including the four primary sources of surveillance data, a modification to pneumonia and influenza (P&I) mortality reporting, and discusses detection and control of institutional influenza outbreaks. (+info)
Differential requirement for CD80 and CD80/CD86-dependent costimulation in the lung immune response to an influenza virus infection.
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The CD28 costimulatory pathway is critical to T cell activation. Blockade of the interaction of CD28 with its ligands CD80 and CD86 using CTLA4-Ig has been proposed as a therapy for a number of immune-based disorders. We have used a murine model of influenza virus infection to study the role of CD28-dependent costimulation in the development of antiviral immune responses. In vivo treatment with CTLA4-Ig to block the interaction of CD28 with CD80 and CD86 reduced virus-specific cytotoxicity and IFN-gamma production by bronchoalveolar lavage fluid CD8+ T lymphocytes in vitro. It also resulted in decreased numbers of virus-specific CD8+ T lymphocytes in the bronchoalveolar lavage fluid, lung, and spleen and lowered virus-specific Ab titers. Mice treated with CTLA4-Ig were able to control and clear the virus infection, but this was delayed compared with controls. Treatment with Y100F-Ig, a mutant form of CTLA4-Ig which selectively binds to CD80 and blocks the CD28-CD80 interaction leaving CD28-CD86 binding intact, did not affect Ab production, spleen cytotoxic precursors, or clearance of virus. However, Y100F-Ig treatment had a clear effect on lung effector cell function. Secretion of IFN-gamma by bronchoalveolar lavage fluid CD8+ T lymphocytes in vitro was decreased, and the number of virus-specific CD8+ T lymphocytes in the bronchoalveolar lavage fluid and lungs of infected mice was reduced. These results indicate that CD28-dependent costimulation is important in the antiviral immune response to an influenza virus infection. The individual CD28 ligand, CD80, is important for some lung immune responses and cannot always be compensated for by CD86. (+info)
Risk of influenza A (H5N1) infection among health care workers exposed to patients with influenza A (H5N1), Hong Kong.
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The first outbreak of avian influenza A (H5N1) occurred among humans in Hong Kong in 1997. To estimate the risk of person-to-person transmission, a retrospective cohort study was conducted to compare the prevalence of H5N1 antibody among health care workers (HCWs) exposed to H5N1 case-patients with the prevalence among nonexposed HCWs. Information on H5N1 case-patient and poultry exposures and blood samples for H5N1-specific antibody testing were collected. Eight (3.7%) of 217 exposed and 2 (0.7%) of 309 nonexposed HCWs were H5N1 seropositive (P=.01). The difference remained significant after controlling for poultry exposure (P=.01). This study presents the first epidemiologic evidence that H5N1 viruses were transmitted from patients to HCWs. Human-to-human transmission of avian influenza may increase the chances for the emergence of a novel influenza virus with pandemic potential. (+info)
Impact of sample type on rapid detection of influenza virus A by cytospin-enhanced immunofluorescence and membrane enzyme-linked immunosorbent assay.
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Cytospin-enhanced direct fluorescent-antibody assay (DFA) detected 49 (92.5%) and rapid membrane enzyme-linked immunosorbent assay (ELISA) detected 40 (75.5%) of 53 influenza virus A-positive samples. All 15 positive nasopharyngeal aspirates from children were detected by both tests. In contrast, 34 of 38 (89.5%) positive swabs from adults were detected by DFA, but only 25 (66%) were detected by ELISA. (+info)
Distinct pathogenesis of hong kong-origin H5N1 viruses in mice compared to that of other highly pathogenic H5 avian influenza viruses.
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In 1997, an outbreak of virulent H5N1 avian influenza virus occurred in poultry in Hong Kong (HK) and was linked to a direct transmission to humans. The factors associated with transmission of avian influenza virus to mammals are not fully understood, and the potential risk of other highly virulent avian influenza A viruses infecting and causing disease in mammals is not known. In this study, two avian and one human HK-origin H5N1 virus along with four additional highly pathogenic H5 avian influenza viruses were analyzed for their pathogenicity in 6- to 8-week-old BALB/c mice. Both the avian and human HK H5 influenza virus isolates caused severe disease in mice, characterized by induced hypothermia, clinical signs, rapid weight loss, and 75 to 100% mortality by 6 to 8 days postinfection. Three of the non-HK-origin isolates caused no detectable clinical signs. One isolate, A/tk/England/91 (H5N1), induced measurable disease, and all but one of the animals recovered. Infections resulted in mild to severe lesions in both the upper and lower respiratory tracts. Most consistently, the viruses caused necrosis in respiratory epithelium of the nasal cavity, trachea, bronchi, and bronchioles with accompanying inflammation. The most severe and widespread lesions were observed in the lungs of HK avian influenza virus-infected mice, while no lesions or only mild lesions were evident with A/ck/Scotland/59 (H5N1) and A/ck/Queretaro/95 (H5N2). The A/ck/Italy/97 (H5N2) and the A/tk/England/91 (H5N1) viruses exhibited intermediate pathogenicity, producing mild to moderate respiratory tract lesions. In addition, infection by the different isolates could be further distinguished by the mouse immune response. The non-HK-origin isolates all induced production of increased levels of active transforming growth factor beta following infection, while the HK-origin isolates did not. (+info)
Neuraminidase inhibitors for treatment of influenza A and B infections.
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Influenza epidemics are responsible for an average of approximately 20,000 deaths per year in the United States. The main method for preventing influenza and its severe complications is influenza vaccination. Influenza-specific antiviral drugs are an important adjunct to vaccine but are not a substitute for vaccine. In the United States, four antiviral agents are approved for preventing or treating influenza: amantadine, rimantadine, zanamivir, and oseltamivir. Amantadine was approved for prophylaxis of influenza A(H2N2) infection in the United States in 1966 and was approved for prophylaxis and treatment of influenza A infection in 1976; rimantadine was approved for treatment and prophylaxis of influenza A infection in 1993 [corrected]. This report provides information on two neuraminidase inhibitors, zanamivir and oseltamivir, which were approved in 1999. Neuraminidase inhibitors are a new class of antiviral drugs that inhibit influenza A and B viruses. Zanamivir is approved for treatment of uncomplicated acute illness caused by influenza virus in persons aged > or =12 years who have been symptomatic for no more than 2 days. Oseltamivir is approved for treatment of uncomplicated illness caused by influenza infection in adults aged > or =18 years who have been symptomatic for no more than 2 days. Neither zanamivir nor oseltamivir is approved for influenza prophylaxis. This report and the Advisory Committee on Immunization Practices (ACIP) 1999 recommendations on influenza prevention and control (MMWR 1999;48[No.RR-4]:1-28) can be accessed at the website for the Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, CDC, at or at the MMWR website at . (+info)
Enhanced anti-influenza activity of a surfactant protein D and serum conglutinin fusion protein.
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We previously demonstrated that bovine serum conglutinin has markedly greater ability to inhibit influenza A virus (IAV) infectivity than other collectins. We now show that recombinant conglutinin and a chimeric protein containing the NH(2) terminus and collagen domain of rat pulmonary surfactant protein D (rSP-D) fused to the neck region and carbohydrate recognition domain (CRD) of conglutinin (termed SP-D/Cong(neck+CRD)) have markedly greater ability to inhibit infectivity of IAV than wild-type recombinant rSP-D, confirming that the potent IAV-neutralizing activity of conglutinin resides in its neck region and CRD. Furthermore, by virtue of incorporation of the NH(2) terminus and collagen domain of SP-D, SP-D/Cong(neck+CRD) caused substantially greater aggregation of IAV particles and enhancement of neutrophil binding of, and H(2)O(2) responses to, IAV than recombinant conglutinin or recombinant rSP-D. Hence, SP-D/Cong(neck+CRD) combined favorable antiviral and opsonic properties of conglutinin and SP-D. This study demonstrates an association of specific structural domains of SP-D and conglutinin with specific functional properties and illustrates that antimicrobial activities of wild-type collectins can be enhanced through recombinant strategies. (+info)