Influenza virus peptides
Influenza viruses are part of the Orthomyxoviridae virus family. They are highly virulent and represent an important threat to global public health. According to WHO, influenza viruses cause each year about 3 to 5 million cases of severe illness, and about 290 000 to 650 000 respiratory deaths worldwide.1 Although there are ways to combat influenza viruses, they have evolved to mutate frequently in order to evade the host’s immune system, making it difficult for scientists to predict what the new seasonal strains will be. This may result in vaccines offering less protection against newly emerging strains due to inaccurate predictions and the virus to become resistant to widely used anti-influenza drugs.
Therefore, more research to understand the influenza viral mechanisms, to develop flu vaccines with broad cross-protection against newly emerging strains2 or to develop new antiviral drugs with different mechanism of action, is urgently needed to protect the populations. In addition, in recent years, the COVID-19 pandemic and the current rise in respiratory syncytial virus (RSV) infections during the winter flu season has created additional challenges due their overlap in symptoms and possible simultaneous co-infection. This also highlights the need for single diagnostic tests that would establish the presence or absence of diseases in order to support better treatment decisions.
Leveraging our longstanding expertise in custom peptide synthesis and in order to advance research in this area, AltaBioscience is pleased to supply a wide range of high-quality and innovative influenza peptides derived from the influenza virus proteins: matrix protein M1, Nucleoprotein (NP) and the RNA polymerase proteins PA and PB1. Our peptides are purified and validated with HPLC and mass spectroscopy data. Each peptide is supplied in 1 mg aliquots, but should you require larger amounts or custom peptides to different epitopes, please contact us.
To view the full range and pricing, please click here.
Influenza virus types [3,4]
There are four types of influenza virus: A, B, C and D. Influenza A is a highly infectious respiratory pathogen, mainly responsible for seasonal flu epidemics or sporadic global pandemics with higher mortality rates. Influenza A is known to affect both humans and animal species unlike influenza B which only infects human. Wild birds are the primary source of influenza A, but it is also widespread in human and pigs. Influenza C usually causes mild illness and type D is not known to infect or cause illness in people but is commonly found infecting cattle. Influenza A viruses are categorised by subtypes based on the proteins hemagglutinin (H) and neuraminidases (N) on the surface of the virions. In order to evade the immune system of the hosts, influenza viruses have the propensity to evolve rapidly either by point mutations in the genes that encode the surface proteins hemagglutinin and neuraminidase (antigenic drift) or by the re-assortment of viral genomes derived from various strains (antigenic shift).
Structure of the influenza virus.
The influenza virus is an enveloped virus of 80 to 120 nm. It is usually spherical in shape although it can also occur filamentous depending on the strain. Its membrane, a lipid bilayer derived from the plasma membrane of a host cell, is decorated by the glycoproteins hemagglutinin (H), neuraminidase (N) and in smaller proportion the ion channel, M2. On the inner side of the envelop is a protein matrix made of protein M1 that encapsidates a segmented genome comprised of negative sense and single-stranded RNAs (eight for Influenza A and B and seven for Influenza C) which are packed into ribonucleoprotein (vRNP) complexes. In particular, the RNA pieces are packaged with nucleoprotein (NP) into a helical ribonucleoprotein and with a trimeric RNA-dependent RNA polymerase (RdRp) complex comprised of the polymerase basic proteins PB1 and PB2, and the polymerase acidic protein PA. Each RNA gene fragments encode transcripts for viral proteins.
Roles of the influenza virus proteins in viral replication
In order to replicate, viruses must deliver their genome into the host cells. The hemagglutinin spikes on the lipid bilayer membrane allow the virus particles to attach to specific receptors containing sialic acid on the host’s epithelial cells. This result in the virus particles to be internalised via receptor-mediated endocytosis.5
Inside the cell, the endocytic vesicle containing the virion fuses with a lysosome. The resulting acidic environment leads to the fusion of the viral and endosomal membrane. Protons also flow via the M2 ion channel resulting in the release of vRNPs into the cytoplasm, which are then transported into the nucleus where they will be responsible for the transcription and replication of the virus RNA segments. The viral RNA fragments are non-coding and need to be copied into a complementary positive strand by the viral RNA polymerases before being used for translation. This is achieved by the RNA-dependent RNA polymerase complex in a mechanism called cap-snatching where the first 10-20 residues of a host cell RNA are cut off and used as primer to initiate the transcription of viral mRNAs.
Mature viral mRNAs are then exported to the cytoplasm where new viral proteins are synthesised using the host protein synthesis machinery. Newly synthesised hemagglutinin and neuraminidase proteins are secreted through the Golgi apparatus and expressed onto the host cell membrane whereas other viral proteins such as nucleoproteins are transported back into the nucleus where they will bind to new vRNA fragments to form new viral genetic material.
After several rounds of amplification, vRNPs and viral proteins exit the nucleus and are transported to the membrane for packaging and budding. The mature virions bud off the membrane acquiring at the same time hemagglutinin and neuramidase on the cell surface. In a final step, neuraminidase proteins facilitate the release of the newly formed virions from the host cell contributing to the spread of the virus. When taken early, antiviral drugs such as oseltamivir, inhibit neuramidase hence preventing the release of the newly formed virions.
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