You have entered the IISP: Interactive Information System on Pathogenomics
If you would like to insert information about your research or research group, please click to the following link to download the form. After filling it out, please send back to firstname.lastname@example.org or email@example.com.
Here you will find information about Research groups in the PathoGenoMics fields from the ERA-NET partner countries (Austria, Finland, France, Hungary, Israel, Latvia, Portugal, Slovenia and Spain).
This information is supposed to support cooperation between researchers from different European countries
and thus enhance the development of a European Research Area for PathoGenoMics .
The following information is available and can be searched for:
- researcher names
- Institution of the respective researcher, city and country of his/her institution
- Contact data of the researcher (address, phone, email)
- Research topics and studied microorganisms of the researcher
- Special techniques applied by the researcher
- Potential cooperation topics suggested by the researcher
If you have any comments/questions or if you would like to add some information, please contact firstname.lastname@example.org
|Name:||ESTAQUIER , JEROME|
|Address:||INSERM U955 CRETEIL HENRI MONDOR 94010 CRETEIL, France|
|Institution:||CRETEIL HENRI MONDOR|
|Country:||France||Phone:||(33) 1 49 81 36 72|
|Our team uses two complementary approaches — fundamental and physiopathological — to study cell death in the context of responses to infectious agents. AIDS raises questions about the nature of the mechanisms by which infectious agents — the human immunodeficiency virus (HIV) in this case — cause the complete collapse of the immune system via disappearance of the CD4+ T-lymphocyte population and the absence of . The development of a vaccine and improvement of HIV treatments will only be possible if we improve our understanding of the physiopathology of this infection. We used Non Human Primate models infected with the simian homologue of HIV, SIV, to decipher the mechanims involved in order to idenfified host factors that determine the susceptibility of infection. We used Non Human Primate models infected with the simian homologue of HIV, SIV, to decipher the mechanims involved in order to idenfified host factors that determine the susceptibility of infection. We and others have reported the magnitude of CD4+ T-cell apoptosis in HIV-infected individuals and in SIV-infected Rhesus macaques is strongly correlated with the stage of disease.We have demonstrated that the intense apoptosis occurring during the acute phase conditions the prognosis of infection by preventing the antiviral immune response. In contrary, the lack of induction of AIDS in monkeys naturally infected including, Sooty managabey and African green monkeys, contrasts with the capacity of these hosts to support SIV replication. We found that apoptosis discriminate pathogenic and non pathogenic primate models. To date our research focus to identfy host factors involved in the developpment of AIDS and discriminate host/pathogen interaction.|
|Special methods / technologies:|
|Apoptosis, Primates, Infectious disease|
|Suggestions for potential research cooperations:|
|We have at this stage a DNA library for large number of primate species.
Moreover, during the last 20 years, a library (Tissues, and lymphocytes) was realized for each infected monkey.
The objective will be to analyze genome of primates to idenfied host factors