Flu: Immunology & Genetics

Immune responses to viral infections involve a complex orchestration between innate signals and adaptive responses of specific T and B cells. Advances in T-Cell Therapies and several antiviral compounds have been developed against influenza virus to interfere with specific events in the replication cycle. Among them, the inhibitors of viral uncoating (amantadine), nucleoside inhibitors (ribavirin), viral transcription and neuraminidase inhibitors (zanamivir and oseltamivir) are reported as examples of traditional virus-based antiviral strategies. Thus, the discovery of novel anti-influenza drugs that target general cell signaling pathways essential for viral replication, irrespective to the specific origin of the virus, would decrease the emergence of drug resistance and increase the effectiveness towards different strains of influenza virus. The genome of an influenza virus particle is encased in a capsid that consists of protein. The influenza A capsid contains the antigenic glycoproteins hemagglutinin (HA) and neuraminidase (NA). For genetic analysis Genome sequencing is used which is the process that determines the order, or sequence, of the nucleotides in each of the genes present in the virus’s genome. There are Next Generation Sequencing and Sanger reaction available methods for genome sequencing. Influenza viruses undergo continual antigenic variation, which requires the annual reformulation of trivalent influenza vaccines, making influenza unique among pathogens for which vaccines have been developed. Reverse genetics techniques are also proving to be important for the development of pandemic influenza vaccines, because the technology provides a means to modify genes to remove virulence determinants found in highly pathogenic avian strains.

Influenza is an RNA virus associated with five different viral proteins and is surrounded by a lipid membrane. Two glycoprotein molecules, known as hemagglutinin (HA) and neuraminidase (NA) on the lipid envelope and plays crucial role in the infection of the epithelial cells of the upper respiratory tract. The pathogenicity and virulence of the influenza virus is determined by several Host and Viral factors. Viruses have evolved this way in order to escape the immune systems of their hosts. The influenza virus can only replicate after invading selected living cells and growing inside them. It makes thousands of new virus particles from the cellular machinery and then goes on to infect other cells. immune mechanisms can lead to both localized as well as systemic effects. Cytokines, rapidly produced after infection by epithelial and immune cells of the respiratory mucosa, are local hormones that activate cells, especially within the immune system.

  • Molecular virology and immunology
  • Viral replication strategies and host genetics of infections
  • Virulence and pathogenicity
  • Virus host cell interaction
  • Innate immunity and infection
  • Influenza antibodies and proteins
  • Cancer patients and risk for complications from influenza
  • Genetics of orthomyxovirus and other respiratory virus
  • Influenza virus genome sequencing and genetic characterization

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