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AbstractThis article argues that through the reinterpretation of the old theory of pouvoir constituantproposed by Sieyès, Carl Schmitt shows the impossibility of political modernity being anything other than authoritarian populism, whether by means of democratic or autocratic procedures. It is not that Schmitt's theory is authoritarian populism, but that modern politics, born out of the French Revolution, cannot be anything else. Schmitt's analyses of the idea of the people in political modernity in Dictatorship(1921), The Crises of Parliamentary Democracy(1923), Volksentscheid und Volksbegehren(1927), Constitutional Theory(1928), and State, Movement, People(1933) provide a fine analysis of the populist character of modernity. Something that those alive in the twenty-first century have been able to experience was theorized by Schmitt in an oracular way. Because of his keen insight he is still worth reading.

Approaches to Nietzsche’s political philosophy abound. In this article, however, we explore the possibility of identifying not only a political philosophy, but also a political-theological reading in Nietzsche’s texts. In fact, such a political-theological reading already has something of a genealogy. In the 1960s, “radical theology” appropriated the Nietzschean topic of the death of God, which engendered a transferred radical political theology consisting in radical democracy. The first part of this article explores twentieth-century political theologies surrounding the death of God. We ask herein if this is the only possible political-theological reading of Nietzsche’s texts. The second part argues that, in fact, we can ascribe to Nietzsche a “theological” intention that is transferable to his political theory in a way that differs from the attempts of radical political theology and other political theologies surrounding the death of God. We conclude that, in any case, Nietzsche’s political theology aims to counterbalance St. Paul’s nihilism more than to constitute a determined political view.

A novel hepatitis-associated virus named TT virus (TTV) has been isolated. However, its hepatotropism has not been proven. We have retrospectively analyzed the presence of TTV-DNA by polymerase chain reaction (PCR) and in situhybridization in liver biopsies from 30 patients with liver disease (15 TTV-DNA-positive and 15 TTV-DNA-negative in serum), and prospectively in serum and liver from eight patients with normal liver histology. TTV-DNA was detected by PCR in the liver from the 15 patients with serum TTV-DNA and in serum and liver of two of the eight patients without liver disease. TTV-DNA titers in liver were 10 times higher than in serum, although no correlation between TTV-DNA titers in serum and liver were observed. In situhybridization shows positive signals in the hepatocytes of the 17 patients infected by TTV but in none of the TTV-DNA-negative patients by PCR. No morphological changes were observed in the hepatocytes showing hybridization signals. The percentage of positive hepatocytes ranged from 2.1% to 30% and correlated with the TTV-DNA titers in liver (r= 0.54; P= 0.037). In conclusion, our results show that TTV is able to infect liver cells although they do not support a role for TTV in causing liver disease.

IgM anti-hepatitis C virus (HCV) and HCV RNA were longitudinally tested for 4.0–8.7 years in 40 patients with chronic HCV infection. Patients in disease remission usually lost IgM antiHCV and HCV RNA, but most patients experiencing disease reactivation had increased levels of the IgM antibody or it reappeared before the biochemical relapse, even when HCV RNA was undetectable. IgM anti-HCV was detectable in most patients with ongoing viral replication and persistent liver disease. Despite long-term disease remission, IgM anti-HCV may persist and be detectable with or without evidence of serum HCV RNA; this indicates a possible disease reactivation, which could occur after several years of sustained transaminase normalization. Detection of IgM anti-HCV in chronic hepatitis C indicates an active immune response to persistent viral infection and should, therefore, be considered as a sensitive marker of active HCV replication and HCV-associated liver disease.