Grant: Project Grant
University of British Columbia
$822,376.00
Mechanisms of endogenous retrovirus-mediated antiviral immunity against genital herpes simplex virus 2 infection and disease.
EF 2021-22
Résumé
Herpes simplex virus 2 (HSV-2) is a sexually transmitted virus that affects over 500 million individuals worldwide. HSV-2 establishes a life-long infection with the host and causes lesions, pain, and discomfort in the female genital tract that persists for life. In addition, HSV-2 infection increases the risk of co-infection by HIV or hepatitis C virus as well as pathogenic bacteria that are responsible for bacterial vaginosis. Although the antiviral drug, acyclovir, is available, acyclovir needs to be taken as a daily five dose regimen for the duration of symptoms and does not prevent recurring symptoms. There are currently no vaccines available to treat HSV-2, in part due to inherent challenges associated with the development of mucosal vaccines. The goal of our project is to identify novel host mechanisms that boost antiviral responses against genital HSV-2 infection that will ameliorate the disease caused by this virus.
My group recently found that viral sequences that are present in the genome of most eukaryotes called endogenous retroviruses (ERVs) are involved in the protection against genital HSV-2 infection in mice. Our project will build on this finding and will investigate the molecular interactions between ERVs and vaginal cells that mediates protection against genital HSV-2 infection and disease. We will achieve this using mouse models and human cells in combination with virology, immunology and bioinformatic techniques. This will allow us to identify new molecules that are involved in the protection against HSV-2 infection and disease that can further be targeted to boost antiviral responses in the female genital tract. Ultimately, our work will aid in the development of new host-directed antiviral therapies.
Programme
Project Grant
Bénéficiaire
Emplacement
British Columbia, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
CIHR Funding Decisions Database
Tel que publié
Id
463342
Name
Tokuyama Maria
Region
British Columbia
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Infection and Immunity
Theme2
Biomedical
Prcname2
Virology & Viral Pathogenesis
Projecttitle
Mechanisms of endogenous retrovirus-mediated antiviral immunity against genital herpes simplex virus 2 infection and disease.
Programtype2
Operating Grants
Orgnameinp2
University of British Columbia
Cihramount2
$822,376
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Antiviral Immunity; Endogenous Retroviruses; Genital Infection; Mucosal Infection; Vaginal Epithelium; Virus-Immune Interactions
Abstract
Herpes simplex virus 2 (HSV-2) is a sexually transmitted virus that affects over 500 million individuals worldwide. HSV-2 establishes a life-long infection with the host and causes lesions, pain, and discomfort in the female genital tract that persists for life. In addition, HSV-2 infection increases the risk of co-infection by HIV or hepatitis C virus as well as pathogenic bacteria that are responsible for bacterial vaginosis. Although the antiviral drug, acyclovir, is available, acyclovir needs to be taken as a daily five dose regimen for the duration of symptoms and does not prevent recurring symptoms. There are currently no vaccines available to treat HSV-2, in part due to inherent challenges associated with the development of mucosal vaccines. The goal of our project is to identify novel host mechanisms that boost antiviral responses against genital HSV-2 infection that will ameliorate the disease caused by this virus.
My group recently found that viral sequences that are present in the genome of most eukaryotes called endogenous retroviruses (ERVs) are involved in the protection against genital HSV-2 infection in mice. Our project will build on this finding and will investigate the molecular interactions between ERVs and vaginal cells that mediates protection against genital HSV-2 infection and disease. We will achieve this using mouse models and human cells in combination with virology, immunology and bioinformatic techniques. This will allow us to identify new molecules that are involved in the protection against HSV-2 infection and disease that can further be targeted to boost antiviral responses in the female genital tract. Ultimately, our work will aid in the development of new host-directed antiviral therapies.
Competitiondate
202203
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Tokuyama, Maria
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $822,376~ $0~