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Ethnic federalism in Ethiopia proved non-viable in practice because it came to be widely seen as a political tool used by the Tigray People's Liberation Front (TPLF)-dominated Ethiopian People's Revolutionary Democratic Front (EPRDF), whose ideological foundation was inspired by Soviet system of 'democratic centralism': a benign façade that veneered an authoritarian vanguard party operating under a token parliament. This article examines the dynamics of statehood and nationhood: antithetical forces of integration and differentiation, which play out around the commonly shared albeit highly contested polity of the nation-state. The need to dialectically resolve these antagonistic though mutualistic stakes lies at the epicentre of political debate in contemporary Ethiopia, ultimately pointing to the constitutional reform dilemmas it now faces. By drawing on literature on political theory, the article argues that the federal constitution proved antagonistic to the inherited politico-cultural orientations that posited the nation-state as the principal supranational identity. By redefining narrow forms of collective identity that were anchored precisely on ethnic sentiments that grew largely in reaction to perceived injustices, the federal constitution appeared neither to embrace, as a system of legitimation, the characteristic and authoritative dimensions of 'Ethiopian' identity as a supra-national universal habitus of loyalty and identification. Nor did it provide integrative cohesion to an otherwise essentially differentiated primordial ethnic and linguistic identity features that now came to be diffused and indeed accentuated at sub-national regions as rigid and hermetic sites of conflict and strife, rather than discursive, reflexive, and interactive domains of cultural and social life. [ABSTRACT FROM AUTHOR]

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SUMMARY Intestinal parasitic infections have been suggested to cause persistent immune activation leading to an unbalanced immune state. Such a state has been proposed to be a major factor in the pathogenesis of AIDS in an African context. The present study investigated the effect of incidental parasitic infection and treatment on the profile of T cell differentiation and activation markers on CD4+ and CD8+ T cells from HIV-1 infected and uninfected adult Ethiopians. Cryopreserved PBMCs from 64 subjects (41 HIV-negative and 23 HIV-positive) with follow-up visits at 6-monthly intervals were used to compare the effect of incidental intestinal parasites and their treatment upon T cell subset profiles and activation status. The samples were stained with antibodies to various T cell differentiation and activation markers allowing naive, memory, effector, memory/effector, activated and resting CD4+ and CD8+ T cell subsets to be quantified by triple-colour FACScan. Incidental intestinal parasitic infections resulted in a significant increase in memory CD4+ T cell numbers both in HIV-negative and HIV-positive subjects (P < 0·05). There was also a significant increase in the percentage of CD8+ HLA-DR+ T cells (P < 0·05) in HIV-positive subjects co-infected with parasites. In HIV-negative subjects, a significant decline in activated cells and a significant increase in resting CD8+ T cells (P < 0·05) was observed after treatment for parasites. These data suggest that intestinal parasitic infections could result in the alteration of T cell subset counts and also in the up-regulation of T cell activation markers in peripheral blood. Treatment of parasitic infections showed a tendency to reduce the activation suggesting that, together with other community based intervention strategies, such treatment could be used to down-regulate immune activation and hence protect the host... [ABSTRACT FROM AUTHOR]

There are speculations that the puberty-related hormone dehydroepiandrosterone sulphate (DHEAS) might influence the intensity of infection and immune responses during Schistosoma infections. We studied the relationships between DHEAS, intensity of Schistosoma mansoni infection and humoral immune responses in 135 residents of Ethiopia. Serum levels of eight antibody isotypes against worm and egg antigens were determined by ELISA. DHEAS was measured with an immunoluminometric assay. There was a significant negative correlation between serum levels of DHEAS and intensity of S. mansoni infection. A significant increase in serum levels of DHEAS in the age group 15–19 years was accompanied by a progressive decline in the intensity of infection. Peak level of DHEAS coincided with the lowest intensity of infection in the age group 20–29 years. Multiple regression analysis showed that DHEAS alone had a significant (p<0.0001) negative effect when the effect of age was removed. Age also had a significant (p<0.0001) negative effect on the intensity of infection, after removing the effect of DHEAS. The two predictive variables accounted for 34.4% of the decline in the intensity of infection. Age accounted for 24.9%, whereas DHEAS accounted for 15.2% when the effect of each of the variables was removed. DHEAS had significant negative effects on AWA-specific IgG (p=0.02) and IgG1 (p=0.018) and SEA-specific IgG1 (p=0.009), after adjusting for the effect of age. [ABSTRACT FROM AUTHOR]