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Receptor specificity of the influenza virus hemagglutinin modulates sensitivity to soluble collectins of the innate immune system and virulence in mice.

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The hemagglutinin (HA) glycoprotein of influenza virus binds to cell surface sialic acid (SA) to initiate infection. In this study, a mutant of influenza A virus strain BJx109 (H3N2) was plaque-purified from the lungs of virus-infected mice that had been depleted of airway macrophages. Sequence

Chimeric influenza virus hemagglutinin proteins containing large domains of the Bacillus anthracis protective antigen: protein characterization, incorporation into infectious influenza viruses, and antigenicity.

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Large polypeptides of the Bacillus anthracis protective antigen (PA) were inserted into an influenza A virus hemagglutinin glycoprotein (HA), and the chimeric proteins were functionally characterized and incorporated into infectious influenza viruses. PA domain 1', the region responsible for binding

Preclinical safety and biodistribution of Sindbis virus measles DNA vaccines administered as a single dose or followed by live attenuated measles vaccine in a heterologous prime-boost regimen.

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Measles still causes considerable morbidity and mortality among infants and young children in developing countries. To develop a new public health tool to reduce this burden, we designed two Sindbis virus replicon vaccines encoding measles virus (MV) hemagglutinin (H) and fusion (F) proteins

Clinical and Pathologic Characterization of an Outbreak of Highly Pathogenic Avian Influenza H7N8 in Commercial Turkeys in Southern Indiana.

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Highly pathogenic avian influenza (HPAI) is a systemic lethal disease of poultry caused by several subtypes of influenza A virus and classified on the basis of serologic reactions to hemagglutinin and neuraminidase surface glycoproteins. In January 2016, a novel subtype of HPAI-H7N8-was diagnosed in

Acute respiratory distress syndrome induced by a swine 2009 H1N1 variant in mice.

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BACKGROUND Acute respiratory distress syndrome (ARDS) induced by pandemic 2009 H1N1 influenza virus has been widely reported and was considered the main cause of death in critically ill patients with 2009 H1N1 infection. However, no animal model has been developed for ARDS caused by infection with

Acellular pertussis vaccines for adolescents.

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BACKGROUND The epidemiology of pertussis is changing, with a clear increase in the number of cases diagnosed in adolescents and adults. This development has spurred studies and anticipated licensure of safer diphtheria, tetanus, acellular pertussis combined (Tdap) vaccines for this older

Persistent histological and immunological abnormalities in congenital syphilitic glomerulonephritis after disappearance of proteinuria.

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A 40-day-old male infant suffered from generalized anasarca, proteinuria and hematuria. Serologic study revealed marked elevation of antibody titer against Treponema pallidum, the same serologic finding was also noted in both his parents. Two weeks of treatment with penicillin was given. The edema

An outbreak of highly pathogenic avian influenza subtype H5N1 in broiler breeders, Korea.

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Highly pathogenic avian influenza (HPAI) was diagnosed in broiler breeders, submitted to the National Veterinary Research and Quarantine Service in South Korea. Grossly, the dead breeders had lesions consistent with HPAI, including pancreatic mottling, splenomegaly, pulmonary edema and congestion,

Experimental influenza B virus toxicity in mice. A possible model for Reye's syndrome.

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Mice intravenously injected with concentrated infectious influenza B/Lee/40 virus (LD50 = 6400 hemagglutinin units) developed lethargy, seizures, coma, and death 1 to 3 days later. The cerebrospinal fluid cell count was normal. Serum glutamic oxaloacetic transaminase levels increased 19-fold and

Integrin-mediated localization of Bordetella pertussis within macrophages: role in pulmonary colonization.

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The adherence of Bordetella pertussis to human respiratory cilia is critical to the pathogenesis of whooping cough but the significance of bacterial attachment to macrophages has not been determined. Adherence to cilia and macrophages is mediated by two large, nonfimbrial bacterial proteins,

Influenza virus-induced encephalopathy: clinicopathologic study of an autopsied case.

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BACKGROUND Rapid progressive encephalopathy with a high fever, consciousness loss and recurrent convulsions has been occasionally reported in children during influenza pandemics in Japan since 1995. We examined a 2-year old girl with hemorrhagic shock and encephalopathy syndrome associated with

Inhibition of lectin-mediated innate host defences in vivo modulates disease severity during influenza virus infection.

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Host-mediated recognition of mannose-rich glycans on the surface of pathogens represents an ancient mechanism of innate immune defence. In this study, we demonstrate that the virus strains that differ in the degree of N-linked glycosylation on the globular head of their hemagglutinin glycoprotein

[Mechanisms of multi-organ failure in severe influenza].

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Severe influenza is characterized by cytokine storm and multi-organ failure with edema. We found that the "influenza virus-cytokine-trypsin/MMP-9 cycle" in the endothelial cells is one of the key mechanisms of vascular hyperpermeability, the major pathogen of multi-organ failure. Upregulated

Host envelope glycoprotein processing proteases are indispensable for entry into human cells by seasonal and highly pathogenic avian influenza viruses.

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Influenza A virus (IAV) is one of the most common infectious pathogens in humans and causes considerable morbidity and mortality. The recent spread of highly-pathogenic avian IAV H5N1 viruses has reinforced the importance of pandemic preparedness. In the pathogenesis of IAV infection, cellular

[The course of acquired C 1 esterase inhibitor deficiency in lymphoproliferative syndrome].

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Acquired deficiency in C1 esterase inhibitor (C1 INH) was first described by Caldwell in 1972. Since that date, about 30 cases have been reported, in most cases during proliferative lymphocyte B syndromes. The acquired C1 INH deficiency can provoke episodes of angioneurotic edema as in hereditary

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