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Introduction Autoimmune and systemic diseases (ADs) were described in HIV infected patients and a classification by immune status was proposed. Methods HIV-infected patients that presented an AD in the infectious diseases department of La Rabta University hospital in Tunis (Tunisia) were retrospectively included. Results Four patients were included. The ADs were spondylo-arthropathy, Behcet disease and psoriasis.Two patients presented Behcet disease. In two patients, the AD preceded HIV infection and in the two others, HIV infection was diagnosed at the same time as the AD. In all cases, ADs occurred in patients with a CD4 T lymphocyte count of more than 200/mm 3 . No co-infection with hepatitis B or C viruses was diagnosed.Three patients received anti-inflammatory drugs and one patient received immunosuppressant treatment with good tolerance. Conclusion AD and autoantibodies are present in HIV infection. AD may develop during acute viral infection (Stage I), with normal to low CD4 counts (Stage II). However, past a threshold where the CD4 count is profoundly low, AD cannot develop (Stage III). Following HAART, immune restoration (normal CD4 count) with possible altered immune regulation may lead to the emergence of AD (Stage IV). More studies are necessary to identify the subgroups of HIV-infected patients that may be prone to develop AD. Co-infection with hepatitis B or C viruses should be screened.

We report the identification of a novel CC chemokine receptor 5 (CCR5) variant that seems associated with resistance to HIV-1 infection. The V130I mutation of the CCR5 receptor is located in the intracellular loop ICL2 known as DRY box and described in the literature as a nonsynonymous mutation present in nonhuman primates group. Extensive molecular modeling and dynamics simulations were performed to elucidate the mechanism by which the V130I mutation may induce conformational change of the CCR5 folding protein and prevent the interaction with the β-arrestin protein. Our study provides new mechanistic insight into how a specific mutation in the regulatory domain of CCR5 might alter the structural folding of the DRY box and the possible ICL2 loop binding with the β-arrestin protein, as described in our previous computational study. The results from our large-scale simulations complement recent experimental results and clinical features and offer useful insights into the mechanism behind CCR5 protein folding and signal transduction. In order for HIV, the entry of the virus to the cells must fuse with the CCR5 receptor that sits on the surface of T-helper immune cells. The described V130I mutation in the gene encoding the CCR5 protein may results in a defective CCR5-Arrestin binding complex that blocks entry of the virus.

Upper urinary tract infections are frequent. Escherichia coli is the main pathogen identified from community acquired infections.We aim to study epidemiologic, clinical and bacterial features of this infection.We identified 261 episodes that occurred in 241 patients. They were 213 females and 48 males aged of 48.75 years. Enterobacteriaceae were the main pathogens isolated in 93.5%: E. coli in 73.3% and Klebsiella pneumoniae in 15.3%. E. coli sensitivity was of 30% for amoxicillin, 98% for cefotaxim, 96% for gentamicin, 90% for ciprofloxacin and 56% for co-trimoxazole. Anterior antibiotic use was associated with low E. coli sensitivity mainly with fluoroquinolones (96 vs 77%) and co-trimoxazole (62 vs 43%). This enhances the role of antibiotic pressure on the resistance emergence.the reasonable use of antibiotics is necessary to limit resistance extent.

The complement system is one of the main effectors of both innate and adaptive immunity. Hereditary complement deficiency, mainly those of the terminal pathway (C5-C9), is at increased risk for septic meningitides particularly meningococcal ones.to assess clinical and biochemical features of 3 Tunisian adults with C5 hereditary complement deficiency (C5D), with a familial study performed for two of them.Functional activity of the classical and the alternative pathway of complement (CH50 and AP50 respectively) were measured according to standards haemolytic procedures. Serum concentration of complement components were determined by nephelemetry and ELISA. C5D was diagnosed when CH50, AP50 and C5 antigenic level were highly decreased.Our patients were 2 men and one woman. All these patients presented clinical symptoms of septic meningitides. Meningococcal orign was confirmed in one case. C5 level varies between 0 and 0.4%. Levels of other complement components: Clq, C3, C4, properdine, C6, C8 and C9 were normal. Antigenic C7 level was 50% in the female patient. Familial study revealed no similar hereditary complement deficiency in relatives.Only 27 cases with C5D were reported in the literature. The description of 3 cases in our series demonstrates that: * C5D is not rare in Tunisia, ** C5D is clinically commonly complicated by meningitides with unconstant severity, *** C5D is biologically caracterised by a variable level of the plasmatic C5 component.

International audience; Prevalence and species distribution of Cryptosporidium spp. were determined among 633 immunocompetent children less than five years of age and 75 patients hospitalized for immunodeficiency who lived in northern Tunisia. Microscopy was used for initial screening to detect positive samples and a nested polymerase chain reaction and restriction fragment length polymorphism analysis was used to determine the species. Cryptosporidium spp. was identified in 2.7% of cases (19 stool samples), and there was a significant difference between samples collected from immunocompromised patients and those collected from healthy children (10.7% versus 1.7%). Prevalence was also significantly higher in diarrheal specimens than in formed specimens (6.3% versus 1.6%). Cyptosporidium hominis and C. parvum were responsible for most Cryptosporidium spp. infections (78.9%). Cryptosporidium hominis was more prevalent in children from urban areas than in those from rural areas, and C parvum was found with similar prevalence rates in the two populations. Cryptosporidium meleagridis was identified in four children on farms.

The chronic granulomatous disease is characterised by the occurence of multiple bacterial and fungal infections since the early childhood. This susceptibility to infections must be prevented by a primary prophlylaxis against the opportunistic germs like pneumocystis and aspergillus. Our case is about a twelve-year-old boy who had a prophylaxis since his fourth month of life. At 10 years he presented a pleuro-pneumonia refractory to a large spectrum antibiotherapy. The aspergillar etiology was established on clinical, radiological and serological arguments. An amphotericine B treatment allowed a good clinical and radiological outcome of this pleuro-pulmonary affection. However, a dorsal spondylodiscitis complicated the course of the disease. A secondary vertebral aspergillosis or a Pott's disease were suspected. The vertebral bipsy was'nt conclusive. The association of antituberculous and antifungal agents with adjuvant molecules (IFN, granulotic transfusions and GM-CSF) permitted a good clinical outcome and the stabilisation of the radiological lesions.