Inflammatory responses in influenza A virus infection
Section snippets
Influenza as a disease
Influenza viruses are classified in three types (influenza A, B and C) of which influenza A is clinically the most important one. Influenza A virus is highly contagious and it infects upper respiratory tract of humans in all age groups. It causes infections ranging from sporadic cases to large epidemics or pandemics. The infection is characterized by fever and chills often accompanied by cough, sore throat, headache and myalgia [reviewed in [1]]. The patients may also suffer from general
Influenza A virus and its replication
Influenza viruses are enveloped, negative-stranded RNA viruses, which belong to the family of Orthomyxoviridae. Influenza A virus RNA is composed of eight segmented genes, which encode for ten different proteins; envelope glycoproteins hemagglutinin (HA) and neuraminidase (NA), matrix protein (M1), nucleoprotein (NP), three polymerases (PB1, PB2 and PA), ion channel protein M2, and nonstructural proteins NS1 and NS2 [3]. Influenza A viruses are classified according to their hemagglutinin
Chemokine production
Chemokines are small secretory molecules that are produced by a variety of cells constitutively or in response to microbial infection. Chemokines bind to their specific cell surface receptors in leukocytes, which is followed by a rapid change in cell shape and behavior enabling them to migrate from the blood stream through the vascular endothelium into the site of inflammation [5]. Chemokine receptors are expressed differently on distinct leukocyte subpopulations and chemokines produced vary
Cytokine interplay in innate and adaptive immunity
IFN-α/β functions as a direct antiviral substance. It upregulates the expression of PKR, oligoadenylate synthetases and Mx, which are known to mediate resistance to viral infections [23]. MxA protein has been shown to directly interfere with influenza A virus replication. MxA gene is induced during influenza A virus infection (Fig. 1) [4], [14]. In humans, host's antiviral mechanisms restrict the replication of influenza A virus at early times of infection, which gives the host more time to
Influenza A virus, cytokines and bacterial infections
Influenza A virus infection in the epithelial surfaces is sometimes associated with enhanced bacterial colonization and infection [reviewed in [27], [28]]. Influenza A virus-associated secondary bacterial pneumonia and otitis media [1] are examples of infections, where both viral and bacterial pathogens may be found. The primary target for influenza A virus is the epithelial cell layer of the whole nasopharyngeal area. Virus-infected cells undergo cytolytic or apoptotic death, which impairs
Acknowledgements
We are grateful to Dr Tapani Hovi for critical comments of the manuscript. The expert technical assistance of Valma Mäkinen, Marika Yliselä, and Katja Moilanen is acknowledged. The original work was supported by the Medical Research Council of the Academy of Finland and the Sigrid Juselius Foundation.
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