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Recognition of genomic patterns associated with Influenza A virus escape mechanisms from the antiviral activity of oseltamivir

Grant number: 24/18784-2
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Start date: December 01, 2024
End date: November 30, 2025
Field of knowledge:Biological Sciences - Microbiology - Biology and Physiology of Microorganisms
Principal Investigator:Marielton dos Passos Cunha
Grantee:João Pedro Balzano Junqueira Guimarães
Host Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil

Abstract

Influenza is a disease caused by the Influenza virus, member of the Orthomyxoviridae family, which is classified into four different types (A, B, C, and D). The subtypes H1N1, H2N2, and H3N2 (which are variants of the Influenza A virus - IAV) were responsible for causing pandemics throughout the 20th century, in addition to a more recent one at the beginning of the 21st century (in 2009, by the H1N1 subtype), highlighting the transmission potential and prevalence of these viruses in the global human population. In order to prevent outbreaks, epidemics, or even widespread pandemics, it is necessary to understand the genomic patterns and mutations associated with the escape mechanisms of IAV from the antiviral activity of oseltamivir (a widely used medicine in clinical practice and essential for slowing the progression of flu symptoms, as well as reducing virus transmission and circulation). In this context, this project aims to investigate how IAV develops resistance to the antiviral action of oseltamivir. To make this possible, the material to be investigated will come from genomic sequences available in public databases, and then the use of nucleotides and codons will be characterized, and integrated with information related with resistance to antiviral therapy. The methods to be employed involve computational tools for genomic data analysis, integration, and data mining. The expectation is, with the results obtained, it will be possible to better understand the escape molecular mechanisms of IAV from oseltamivir action and the consequent associated resistance.

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