Viral Antigens
Product List
H3N2 Wisconsin
H3N2 Influenza Virus-A Wisconsin/67/05 Recombinant
Recombinant Full-Length H3N2 A/Wisconsin/67/05 is glycosylated with N-linked sugars, produced using baculovirus vectors in insect cells and its Mw is 72,000 dalton.
H3N2 Wisconsin/67/05
H3N2 Influenza-A Virus Wisconsin/67/05
H3N2 Wyoming
H3N2 Influenza-A Virus Wyoming/3/2003 Recombinant
Accession number: AY531033.
H5N1 Indonesia
H5N1 Influenza-A Virus Indonesia 05/05 Recombinant
Introduction
Influenza, commonly known as the flu, is an infectious disease caused by the influenza virus. It primarily affects the respiratory system, including the nose, throat, and lungs. Influenza viruses are classified into four types: A, B, C, and D. Among these, Influenza A and B are the most common and are responsible for seasonal flu epidemics. Influenza A viruses are further subtyped based on the hemagglutinin (HA) and neuraminidase (NA) proteins on their surface, such as H1N1 and H3N2.
Key Biological Properties: Influenza viruses are enveloped, single-stranded RNA viruses belonging to the Orthomyxoviridae family. They have a segmented genome, which allows for genetic reassortment and high mutation rates.
Expression Patterns: Influenza viruses express several proteins, including HA, NA, matrix proteins (M1 and M2), nucleoprotein (NP), and non-structural proteins (NS1 and NS2).
Tissue Distribution: Influenza primarily infects epithelial cells in the respiratory tract. The virus binds to sialic acid receptors on the surface of these cells, facilitating entry and replication.
Primary Biological Functions: The primary function of influenza viruses is to replicate within host cells and produce progeny virions. This process involves the hijacking of the host’s cellular machinery to synthesize viral RNA and proteins.
Role in Immune Responses: Influenza viruses trigger both innate and adaptive immune responses. The innate immune response includes the production of interferons and other cytokines, while the adaptive immune response involves the activation of B cells and T cells to produce antibodies and cytotoxic T lymphocytes.
Pathogen Recognition: Influenza viruses are recognized by pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs) and RIG-I-like receptors (RLRs), which detect viral RNA and initiate immune signaling pathways.
Mechanisms with Other Molecules and Cells: Influenza viruses interact with host cell receptors, primarily sialic acid residues, to gain entry. Once inside, the viral RNA is released into the host cell’s cytoplasm, where it is transcribed and replicated.
Binding Partners: The HA protein binds to sialic acid receptors on host cells, while the NA protein helps release newly formed virions by cleaving sialic acid residues.
Downstream Signaling Cascades: Upon recognition by PRRs, signaling cascades such as the NF-κB and IRF pathways are activated, leading to the production of interferons and other cytokines that mediate antiviral responses.
Transcriptional Regulation: The transcription of viral RNA is regulated by the viral RNA polymerase complex, which consists of the PB1, PB2, and PA proteins. This complex recognizes and binds to the viral RNA promoter regions.
Post-Translational Modifications: Influenza viral proteins undergo various post-translational modifications, including glycosylation, phosphorylation, and ubiquitination, which are essential for their function and stability.
Biomedical Research: Influenza viruses are extensively studied in biomedical research to understand viral pathogenesis, host immune responses, and mechanisms of viral evolution.
Diagnostic Tools: Rapid diagnostic tests, polymerase chain reaction (PCR), and viral culture are commonly used to detect influenza infections.
Therapeutic Strategies: Antiviral drugs such as oseltamivir (Tamiflu) and zanamivir (Relenza) are used to treat influenza. Vaccination is the most effective preventive measure, with annual flu vaccines formulated to target the most prevalent strains.
