50 years in the fight against infectious diseases 1967 – 2017

Mechanisms behind chronic infections (TB, HBV, HIV…) 2016

May 2 - 4, 2016 - Les pensieres, Veyrier du Lac (France)

Background

When a pathogenic microorganism infects the human body, a dramatic activation of the innate and adaptive immune response occurs. In most cases, the interaction between the immune system and the pathogen result in clearance of the infection. However, some pathogens are capable of maintaining their presence, despite the severe attacks of the immune system, giving rise to persistent infection.

To remain and survive for a long period of time in its host, sometimes lifelong, the pathogens have evolved a range of elaborate immune-evasion strategies which may involve (1) hiding from the immune system, (2) interfering with the function of the immune system and/or (3) exploiting the immune system for their own benefit.

Many herpes viruses hide from the immune system by entering into a state known as latency in which the virus does not replicate. No viral proteins or peptides are presented on the surface of the infected cells and the cells cannot be eliminated. Other viruses, like VZV, invade neurons, which carry very little MHC I class molecules making it hard for the CD8 T cells to recognize infected cells.

Certain pathogens interfere with the cells of the immune system to block or dampen its actions. There are similarities in the immuno-modulatory mechanisms used by viruses and bacteria that have to overcome the same host immune system. Indeed, both classes of pathogens can inhibit complement, inhibit cytokines, interfere with TLRs, and block acquired immunity allowing long-term survival.

Pathogens can also exploit immune cells for their own benefit. This mechanism is demonstrated by HIV that replicates in CD4 T cells, EBV in B cells, and Dengue virus that infects Langerhans cells. Another example is M. tuberculosis which is taken up by macrophages but prevents the fusion of the phagosome with the lysosome, protecting itself from the bactericidal actions of the lysosomal contents./p>

This workshop will focus on immune-evasion strategies employed by three pathogens that are responsible for a very high medical burden, namely, tuberculosis, HIV and Hepatitis B infection. We will discuss the current understanding how these pathogens employ evasion mechanisms, and how to translate this knowledge to the development and rational design of new medicines and therapeutic vaccines.

Programme

Monday 2 May

Tuesday 3 May

Wednesday 4 May

Session 1 Biology of infections with HBV, HIV, and TB

Jacques LOUIS

  • 17:30 - 17:50

    Biology of HBV infection

    Maura DANDRI

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  • 18:05 - 18:25

    The basics of HIV infection, reservoir establishment and the dynamics of immune responses

    Asier SAEZ-CIRION

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Session 1 Continued

Session 2 Early host/pathogen interplay: impact on the outcome of infection

Inca KUSTERS

  • 09:05 - 09:25

    SERINCs: novel restriction factors counteracted by HIV Nef

    Heinrich GOTTLINGER

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  • 09:40 - 09:55

    The regulatory HBx protein contributes to evasion from intrinsic antiviral response

    Christine NEUVEUT

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Session 3 Determinant of persistence in chronic infections

David DURANTEL

Session 4 Molecular mechanism of innate immune evasion

Nicolas MANEL

  • 14:30 - 14:50

    Subcellular mechanisms of innate immunity evasion in HBV infection

    David DURANTEL

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Session 5 Molecular mechanism of adaptive immune evasion

Tom OTTENHOFF

Session 6 Immune cell exhaustion in chronic infections and strategies to revert it

Olivier NEYROLLES

Session 7 Immunopathogenesis: mechanisms and therapeutic options

Tom OTTENHOFF

  • 10:45 - 11:05

    HBV Immunopathogenesis

    Robert THIMME

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  • 11:55 - 12:15

    NN cell and viral dynamics within lymph nodes during pathogenic and non pathogenic SIV infection

    Michaela MULLER-TRUTWIN

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  • 14:00 - 14:20

    Sensing of HIV-1 entry triggers a type I interferon response in primary macrophages

    Philippe BENAROCH

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  • 14:35 - 14:50

    Understanding and Intervening in HIV Associated Tuberculosis

    Robert WILKINSON

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Contact

Cindy GRASSO - Conference Coordinator

Send an e-mail

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