-Small ruminant lentiviruses (SRLV = maedi-visna in sheep and caprine arthritis encephalitis in goats) are distributed throughout most countries of the world, particularly Europe. Laboratories from 16 European countries established collaborations within the framework of a COST (CO-operation in the field of Scientific and Technical Research) action sponsored by the European Union in order to (i) better organize their research programmes on SRLVs and (ii) to coordinate efforts to combat these two diseases. After five years, a consensus conference -the first one in the veterinary medicine field -concluded the work of this network of laboratories by reviewing the present position and discussing three important questions in the field of SRLVs: routes of transmission, consequences of infection and potential role of eradication programmes at either a European or local level, according to the situation in each country or region. This paper brings together existing information regarding these questions and identifies areas for future research.Maedi-visna / caprine arthritis-encephalitis virus / lentivirus / small ruminants / European consensus conference

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The observation that couples tended to share genetically indistinguishable clones was highly suggestive of transmission between partners. This phenomenon may, in part, explain the pathogenesis of oropharyngeal candidiasis and the increased frequency of fluconazole resistance both in vitro and in vivo.

Two cases of rhinoscleroma in patients infected with the human immunodeficiency virus (HIV) who had stayed in an area of endemic Klebsiella rhinoscleromatis are reported. One of the patients presented with oropharyngeal lesions, an unusual clinical picture. Both patients suffered from a major cellular immune deficiency. The importance of Klebsiella rhinoscleromatis infection in AIDS-related oropharyngeal pathology and the possible treatment of such infection in HIV-positive patients are not yet clearly established.

SUMMARYWe studied immune reconstitution against the parasite T. gondii in HIV-infected patients treated for 1 years with highly active antiretroviral therapy (HAART). We used SCID mice, humanized with peripheral blood mononuclear cells (PBMC) from patients, which were then infected with T. gondii cysts. Mice humanized with PBMC from patients before the start of HAART were highly susceptible to infection. In contrast, mice humanized with PBMC from patients who had received HAART for 6 months displayed higher survival rates, correlating with lower intracerebral parasite loads. However, this resistance was lost during follow up because mice humanized with PBMC from patients treated with HAART for 12 months survived for no longer than mice that had not been humanized. Specific lymphocyte proliferation assays showed that the increase in proliferative response depended on treatment duration and that HAART induced changes in IFN-g secretion in the presence of Toxoplasma antigens. Thus, our results indicate partial immune reconstitution against T. gondii in HIV-infected patients following HAART, possibly due to changes in the patterns of specific IFN-g production and redistribution of functional memory CD4 + cells.

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We reconstituted cytomegalovirus (CMV)-specific T-cell responses in human immunodeficiency virus-1-positive, CMV-positive patients receiving highly active antiretroviral treatment (HAART). We used several combinations of functionality parameters to determine the degree of T-lymphocyte reconstitution obtained during 1 year of treatment. Untreated patients displayed CMV-specific cytotoxic T-lymphocyte (CTL) activity despite the absence of CMV-specific lymphoproliferative responses (LPRs) and despite the fact that interferon-g (IFN-g) and interleukin-2 (IL-2) were not secreted. The absence of LPRs, IFN-g and IL-2 before antiretroviral treatment suggests that CMV-specific immunity was deregulated despite the high CD4 þ T-cell counts presented by our cohort, which are critical to the reactivation of CMV disease. After 6 months of HAART, CTL activity had increased compared with the baseline, as had the levels of secreted IFN-g and LPR. However, the levels of specific IL-2 produced did not change during therapy, and no specific IL-2 was detected during the follow-up period. Taken together, our findings suggest that 1 year of HAART led to the recovery of some, but not all, CMV-specific responses in our cohort of patients.