Early Neural Markers of Implicit Attitudes: N170 Modulated by Intergroup and Evaluative Contexts in IAT

The Implicit Association Test (IAT) is the most popular measure to evaluate implicit attitudes. Nevertheless, its neural correlates are not yet fully understood. We examined event related potentials (ERPs) in response to face- and word processing while indigenous and non-indigenous participants performed an IAT displaying faces (ingroup and outgroup members) and words (positive and negative valence) as targets of category judgments. The N170 component was modulated by valence of words and by ingroup/outgroup face categorization. Contextual effects (face–words implicitly associated in the task) had an influence on the N170 amplitude modulation. On the one hand, in face categorization, right N170 showed differences according to the association between social categories of faces and affective valence of words. On the other, in word categorization, left N170 presented a similar modulation when the task implied a negative-valence associated with ingroup faces. Only indigenous participants showed a significant IAT effect and N170 differences. Our results demonstrate an early ERP blending of stimuli processing with both intergroup and evaluative contexts, suggesting an integration of contextual information related to intergroup attitudes during the early stages of word and face processing. To our knowledge, this is the first report of early ERPs during an ethnicity IAT, opening a new branch of exchange between social neuroscience and social psychology of attitudes

Application of a monoclonal antibody recognizing protein p30 to detect African swine fever virus-infected cells in peripheral blood

Monoclonal antibody (MAb) 174F11.8 recognizes an epitope of the African swine fever (ASF) virus-induced protein, p30, a protein expressed on the plasma membrane of infected cells. This MAb has been used to analyze infected cell populations in peripheral blood of experimentally inoculated pigs with a virulent or attenuated ASF virus. Flow cytometric analysis of peripheral blood at different days postinfection using this MAb, showed expression of p30 mainly in the monocyte/macrophage cell lineage. Additionally, a small percentage of granulocytes also expressed p30 during infection. This methodology allowed the quantification of fluctuations in the pool of infected monocyte/macrophage cells in the inoculated pigs, maximum percentages ranging between 6 and 31%. Significant differences in the percentages of cell populations expressing p30 were not found between virulent or attenuated virus infection. However, a 2- to 4-day delay in the maximum percentage of cells expressing p30 was observed during infection with the attenuated virus when compared to virulent virus infection. Percentages of infected cells detected by the expression of p30 and viral titres obtained in peripheral blood showed positive correlation. Consequently, MAb 174F11.8 constitutes a marker to follow evolution of ASF virus infection, allowing quantification of percentages of infected cells in peripheral blood. © 1995

Modulation of immune cell populations and activation markers in the pathogenesis of African swine fever virus infection

African swine fever (ASF) virus induces immune cell alterations that may be detected by changes in peripheral blood cells phenotypic antigens and activation markers which were examined by flow cytometry, analyzing both cell proportion and/or expression intensity of superficial antigens. These studies were conducted in pigs with experimental acute or chronic ASF infection to determine whether changes among important surface activation markers and phenotypic antigens, and their correlative lymph node status, reflected similar or disparate aspects of immune pathology. In acute infection produced by virulent viruses, macrophage and B lymphocyte populations decreased in peripheral blood after a short activation period at the beginning of the infection. A significative decrease of interleukin 2 receptor (IL 2R) expression was also observed in those pigs. These variations correlated with lymph node cell depletion due to an intense lymphoid cell death by apoptosis, affecting mainly the B lymphocyte subpopulation as determined by immunohistochemistry. Nevertheless, pigs infected with an attenuated isolate undergoing chronic persistent infection, presented a distinct pattern of modification, according with a different clinicopathological evolution. Changes consisted in systemic immune activation coincident with the highest viremra titer, with an augmentation in CD8+ T lymphocyte, macrophage, and B cell populations, and MHC (major histocompatibility complex) antigens. Percentage elevation of circulating immune subpopulations was accompanied by cell accumulation with lymphoid hyperplasia but a conserved distribution of B lymphocytes in lymphoid organs of chronically infected pigs

Macrophage tropism of rabbit hemorrhagic disease virus is associated with vascular pathology

To delineate the interactions between rabbit hemorrhagic disease virus (RHDV) and host cells, organ and cellular targets of infection were identified in vivo. Viral specific antigens were detected by immunohistochemistry in liver, lung, spleen and lymph nodes cells. Also, intravascular infected cells were detected in most organs including kidneys, myocardium, thymus and central nervous system. To further characterize infected target cells, viral proteins and cell-specific surface antigens were identified simultaneously in double labeling experiments. Numerous lymphoid organ macrophages, from the splenic red pulp, circulating monocytes, alveolar macrophages and Kupffer cells were double labeled, demonstrating that cells of the mononuclear phagocyte lineage are major hosts for RHDV. Double labeling for other specific cell markers were negative. The distribution of viral antigens in these tissues coincided with those areas where cells presented morphology of apoptosis. Association of intravascular monocyte infection and apoptosis, could represent a possible mechanism to develop disseminated intravascular coagulation. Copyright (C) 1999 Elsevier Science B.V

Apoptosis A mechanism of cell killing and lymphoid organ impairment during acute African swine fever virus infection

Induction of programmed cell has been described during infection with many differentviruses. We have investigated the influence of African swine fever virus (ASFV) on apoptosis of different cell populations during in vitro and in vivo infection. We observed apoptosis in ASFV-infected monocyte/macrophage and peripheral blood mononuclear cell cultures. Apoptosis was demonstrated in these cells by DNA fragmentation, DNA staining and DNA-associated histone fraction detection assays. Flow cytometry analysis of infected cultures also showed morphological and functional alterations, including changes in the cell cycle and percentage of cell fractions stained with propidium iodide. After in vivo infection with three different virulent strains of ASFV, apoptosis of infected cells from the mononuclear phagocytic system and closely related elements from different tissues was observed. Additionally, infected pigs showed an intense degree of apoptosis of lymphocytes, which are not infected by the virus. In lymph nodes and other lymphoid organs, broad bands of apoptotic cells presented typical nuclear changes under light microscopy. The occurrence of DNA fragmentation was confirmed in these tissues using terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling. These findings, together with the pathological observations in infected pigs of a depletion in cell populations in lymphoid organs, suggest that virus interference with programmed cell death plays a central role in pathogenesis of this disease, being responsible for lymphoid organ impairment in acute ASFV infection

Neutralizing antibodies to different proteins of African swine fever virus inhibit both virus attachment and internalization.

African swine fever virus induces in convalescent pigs antibodies that neutralized the virus before and after binding to susceptible cells, inhibiting both virus attachment and internalization. A further analysis of the neutralization mechanisms mediated by the different viral proteins showed that antibodies to proteins p72 and p54 are involved in the inhibition of a first step of the replication cycle related to virus attachment, while antibodies to protein p30 are implicated in the inhibition of virus internalization