« Förderinformationen
Priority Programme "Innate Sensing and Restriction of Retroviruses" (SPP 1923)
Termin:
04.03.2019
Fördergeber:
Deutsche Forschungsgemeinschaft (DFG)
In March 2015, the Senate of the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) established the Priority Programme "Innate Sensing and Restriction of Retroviruses" (SPP 1923). The programme was launched in 2016 and is intended to run for six years. This call invites proposals for the second three-year funding period.
Retroviruses comprise a diverse group of exogenous and endogenous viruses defined by their unique replication strategy to reverse-transcribe their RNA genome into a complementary DNA. Millions of years of coevolution with their mammalian hosts gave rise to highly pathogenic as well as apathogenic members of this family of viruses and to species-specific differences in their pathologic potential. Evidence is emerging that cell-type specific cell-autonomous components of the innate immune system, including specialised pattern recognition receptors and broadly active antiviral restriction factors, represent key determinants of the fundamentally different outcomes of retroviral infections. However, the specific host cell machineries involved in recognising retroviral infection, viral evasion strategies thereof, and their relative contribution to retroviral pathogenesis in specific target cells and organs remain to be defined. This Priority Programme thus aims at the identification of the full molecular sensing and restriction machinery involved in cell-autonomous immunity against retroviruses, its regulation, virus-encoded countermeasures, and pathophysiological consequences. An important aspect of the programme will also be to visualise innate immune recognition events, assess their dynamics and define the stoichiometry of key components involved.
SPP 1923 will integrate retrovirologists, immunologists, and experts in key technologies to accomplish these goals.
o Proposals submitted to this call should address several of the following aspects:
o Identity and regulation of host cell machinery mediating innate immune recognition of retroviruses
o Retroviral components recognised by the host cell innate immune system
o Specificity and potency of innate anti- or pro-retroviral immune responses
o Retroviral countermeasures and evasion strategies of innate immune recognition
o Evolution of retroviral innate immune recognition and antagonism thereof
o Development and application of customised enabling technology for visualisation and quantification of innate immune recognition, including quantification of key host and virus components involved
Retroviruses to be studied include pathogenic exogenous orthoretroviruses (HIV, SIV, HTLV, MLV), spumaretroviruses (foamy viruses) as well as endogenous retroviruses and retroviral elements. Pathogenic and apathogenic retroviruses will be investigated in cell systems ranging from monotypic cell cultures to complex ex vivo and animal models. Interdisciplinarity of projects, e.g. in the context of joint applications of two principle investigators is encouraged, in particular for projects aimed at the development and application of customised enabling technology.
Further information:
http://www.dfg.de/foerderung/info_wissenschaft/info_wissenschaft_18_87/index.html
Retroviruses comprise a diverse group of exogenous and endogenous viruses defined by their unique replication strategy to reverse-transcribe their RNA genome into a complementary DNA. Millions of years of coevolution with their mammalian hosts gave rise to highly pathogenic as well as apathogenic members of this family of viruses and to species-specific differences in their pathologic potential. Evidence is emerging that cell-type specific cell-autonomous components of the innate immune system, including specialised pattern recognition receptors and broadly active antiviral restriction factors, represent key determinants of the fundamentally different outcomes of retroviral infections. However, the specific host cell machineries involved in recognising retroviral infection, viral evasion strategies thereof, and their relative contribution to retroviral pathogenesis in specific target cells and organs remain to be defined. This Priority Programme thus aims at the identification of the full molecular sensing and restriction machinery involved in cell-autonomous immunity against retroviruses, its regulation, virus-encoded countermeasures, and pathophysiological consequences. An important aspect of the programme will also be to visualise innate immune recognition events, assess their dynamics and define the stoichiometry of key components involved.
SPP 1923 will integrate retrovirologists, immunologists, and experts in key technologies to accomplish these goals.
o Proposals submitted to this call should address several of the following aspects:
o Identity and regulation of host cell machinery mediating innate immune recognition of retroviruses
o Retroviral components recognised by the host cell innate immune system
o Specificity and potency of innate anti- or pro-retroviral immune responses
o Retroviral countermeasures and evasion strategies of innate immune recognition
o Evolution of retroviral innate immune recognition and antagonism thereof
o Development and application of customised enabling technology for visualisation and quantification of innate immune recognition, including quantification of key host and virus components involved
Retroviruses to be studied include pathogenic exogenous orthoretroviruses (HIV, SIV, HTLV, MLV), spumaretroviruses (foamy viruses) as well as endogenous retroviruses and retroviral elements. Pathogenic and apathogenic retroviruses will be investigated in cell systems ranging from monotypic cell cultures to complex ex vivo and animal models. Interdisciplinarity of projects, e.g. in the context of joint applications of two principle investigators is encouraged, in particular for projects aimed at the development and application of customised enabling technology.
Further information:
http://www.dfg.de/foerderung/info_wissenschaft/info_wissenschaft_18_87/index.html