[Risk for the transmission of Newcastle disease by contaminated poultry products]. / Risques de transmission de la maladie de Newcastle par des produits avicoles contaminés.

Poultry products contaminated with pathogenic strains of Newcastle disease virus are a source of virus transmission to susceptible poultry flocks. The probability of contamination varies according to the type of product. Research conducted by various laboratories in Europe has shown that pathogenic virus can be isolated from the carcasses of chickens, whether vaccinated or not, during a brief period after experimental infection. Eggs laid by hens infected with Newcastle disease virus present a very low risk. Furthermore, feathers, bones, blood and offal present potential risks if they are incorporated in poultry feed. Finally, poultry droppings used as a fertiliser can present a major risk of infection in certain circumstances.

Repair of the in vitro HIV-1-induced immunosuppression and blockade of the generation of functional suppressive CD8 cells by anti-alpha interferon and anti-Tat antibodies.

The acute human immunodeficiency virus type 1 (HIV-1) infection of activated peripheral blood mononuclear cells (PBMCs) from normal donors results in inhibition of cell proliferation and generation of functional suppressive T cells. Cultured HIV-1 infected PBMCs but not uninfected PBMCs, following irradiation, can inhibit the proliferation of antigen-activated autologous T cells in a dose-dependent way. CD8+ cell subpopulation is responsible for this inhibition. The presence of anti-alpha interferon (IFN alpha) and anti-Tat antibodies in the culture medium counteracts the HIV-1-induced immunosuppression and prevents the generation of suppressive T cells by these PBMCs. The reported data should have major implications for strategies of AIDS treatment which, in association with antiviral drugs, aim at targetting immune disorders.

Evidence for an antiviral effect and interferon neutralizing capacity in human sera; variability and implications for HIV infection.

The antiviral effect (AVE) and interferon neutralizing capacity (INC) of sera originating from either seronegative or HIV-infected individuals were determined. As a rule, sera from seropositive subjects exhibited higher AVE titers than sera from seronegative individuals. Similarly, the INC of sera from HIV-infected patients, was most often stronger than that of sera from seronegative individuals. Furthermore, sera from HIV-infected patients actively immunized with i-IFN alpha invariably expressed INC in response to treatment, which was not the case for sera from control unimmunized patients. All sera from HIV-infected patients were found by ELISA to contain antibodies specifically directed to IFN alpha.

Biological effect of active anti-IFN alpha immunization in HIV-infected patients.

Circulating interferon (IFN) was investigated in HIV-1 seropositive patients by measuring the IFN alpha antiviral effect in the serum. While serum of healthy seronegative individuals exhibits an antiviral effect, not due to IFNs, considered as background, serum of seropositive patients showed an additional antiviral effect due to the abnormal presence of IFN alpha. Increased titers of IFN alpha were found in the course of the HIV infection and seemed to correlate with the evolution of AIDS disease. Furthermore, patients immunized against IFN alpha had both stabilized CD4 cell count and decreased IFN alpha in their serum. HIV-1-infected patients also exhibited higher titers of natural anti-IFN antibodies than seronegative controls and the level of specific antibodies (Abs) markedly increased in immunized patients. Finally, serum from immunized patients, when compared to seronegative controls, exhibits an interferon neutralizing capacity.

Effect of purified IgGs from HIV-1-infected and non infected individuals on immune activation.

The purification and analysis of IgGs from sera of HIV-1-infected and non infected individuals are reported. The effect of antibodies purified from sera of infected individuals on antigen-induced T cell proliferation was investigated in relation to their possible involvement in an autoimmune reaction in AIDS, in view of the previously unravelled striking peptide similarities between HIV-1 gp120 and the immunoregulatory CD4 and Fas molecules. However, our data do not allow definite conclusions to be drawn. The necessity of purifying antibodies against specific peptides to show their direct effect on T-cell activation is further stressed.

Pathogenic disorders involved in immunosuppression and T cell depletion characterizing AIDS.

Four cardinal immune disorders interacting with each other may promote the progressive T cell depletion and immunosuppression characterizing AIDS. Immune activation of HIV-1 infected T4 cells leads to virus release and premature cell death. Both virus release with its resulting viral load and dead cells are the source of gp120 stimulus. Anergy of non-infected CD4 cells, resulting in cytokine dysregulation may be promoted by impairing the CD4-MHC interaction during CD4 cell activation either directly through the SLWDQ pentapeptide identity with the CD4 molecule and the CD4 binding region or through a gp120-induced autoimmune reaction to CD4. Overproduction of IFN alpha, the known antiproliferative and cytolytic cytokine may promote in a paracrine manner to neighbouring cells the immunosuppression generated by the lack of IL2 secretion following CD4 cell anergy. Apoptosis of activated non infected T cells could be induced by effector components of the autoimmune reaction (CTL, Lymphotoxins or Abs?) directed towards the 2 consensus gp120 sequence identity/similarity (INCTR and FYCNST) shared with the APO/Fas molecule. These two sequences are known as immunodominant sites of the gp120. Furthermore, IFN alpha overproduction may also render circulating memory T cells competent to apoptosis by upregulating the cascade of metabolic events leading to programmed cell death.

Safety of infectious bursal disease vaccines: assessment of an acceptability threshold.

This study was undertaken to check the safety of commercially available infectious bursal disease (IBD) vaccines in terms of bursal damage, and their immunodepressive effects as evaluated by testing the birds after vaccination for their response to Newcastle disease vaccination. Further requirements are proposed to establish a suitable safety standard.

[Statistical analysis of the evolution of histopathological lesions during the course of experimental infection of chicken by the Marek's disease virus]. / Etude statistique de l'evolution des lesions histologiques au cours de l'infection experimentale du poulet par le virus de la maladie de Marek.

The evolution of histopathological lesions of sciatic and brachial nerves, bursa, thymus and spleen was studied during a long observation period following the challenge of chicken by the Marek's disease virus (MDV). Factorial analysis of correspondences allowed a synthetic study completed by classical statistical tests. In the nerves the sequence of type A, B and C lesions as demonstrated.At the same time a lymphoid depletion of bursa, thymus and spleen was observed This became less severe after a period and recovery in these organs was total. This study suggests the interest of multifactorial analysis for histopathological interpretation of lesions.