17
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Anticuerpos anti-C1q e infección por el virus de la hepatitis C Translated title: Anti-C1q antibodies in hepatitis C virus infection

      rapid-communication

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          La hepatitis causada por el virus de la hepatitis C frecuentemente evoluciona hacia una enfermedad crónica con varias manifestaciones extrahepáticas, de autoinmunidad, y la posible formación de autoanticuerpos con diversas especificidades. La deficiencia del componente C1q del sistema complemento afecta la eliminación de células infectadas mediante la apoptosis, el mantenimiento de la tolerancia inmunológica y favorece el desarrollo del lupus eritematoso sistémico, en particular, y de los fenómenos autoinmunes, en general; todo lo cual pudiera agravarse por la presencia de anticuerpos anti-C1q. En este trabajo se determinó la prevalencia de los anticuerpos anti-C1q en 39 pacientes (23 femeninos y 16 masculinos) y 109 controles por un ensayo inmunoenzimático tipo ELISA (Anti-C1q ORGENTEC Diagnostika GmbH). Se observó una frecuencia significativamente mayor (p < 0,05) de estos autoanticuerpos en el grupo de pacientes con respecto al grupo control. Al comparar los pacientes según el sexo, la proporción de casos positivos resultó significativamente mayor (p < 0,05) en el sexo femenino, y cuando se clasificaron los pacientes en un grupo de 14 hematológicos y otro de 25 no hematológicos, se observó que la proporción de casos con autoanticuerpos anti-C1q en el grupo de los hematológicos fue muy inferior. Resulta importante realizar una evaluación longitudinal de los pacientes para detectar tempranamente la aparición de autoanticuerpos, profundizar en el conocimiento de su posible relación con las manifestaciones de autoinmunidad, con la aparición de otros autoanticuerpos, así como la posible influencia en su tratamiento.

          Translated abstract

          Hepatitis C often develops into a chronic disease with several extrahepatic manifestations, autoimmunity, and the possible formation of autoantibodies with different specificities. C1q deficiency affects the elimination of infected cells by apoptosis, the maintenance of immunological tolerance and it also favors the development of systemic lupus erythematosus in particular and of autoimmune phenomena in general, all of which could be exacerbated by the presence of anti-C1q. In this study, the prevalence of anti-C1q antibodies in 39 patients (23 females and 16 males) and 109 controls was determined by an ELISA type immunoassay (Anti-C1q ORGENTEC Diagnostika GmbH). A significantly higher frequency (p < 0.05) of these autoantibodies was observed in the patients group than in the control group. When separating the patients according to sex, the proportion of positive cases were significantly higher (p < 0.05) in females; and when the patients were divided into a group of 14 hematological and 25 nonhematological the proportion of cases with anti -C1q in the hematological group was lower. We concluded that it would be important to perform a longitudinal evaluation of our patients that will allow us to detect the early appearance of autoantibodies, to deepen our knowledge of their possible connection to autoimmune conditions, to the appearance of other autoantibodies, as well the possible influence of treatment.

          Related collections

          Most cited references43

          • Record: found
          • Abstract: found
          • Article: not found

          Hepatitis C virus triggers mitochondrial fission and attenuates apoptosis to promote viral persistence.

          Mitochondrial dynamics is crucial for the regulation of cell homeostasis. Our recent findings suggest that hepatitis C virus (HCV) promotes Parkin-mediated elimination of damaged mitochondria (mitophagy). Here we show that HCV perturbs mitochondrial dynamics by promoting mitochondrial fission followed by mitophagy, which attenuates HCV-induced apoptosis. HCV infection stimulated expression of dynamin-related protein 1 (Drp1) and its mitochondrial receptor, mitochondrial fission factor. HCV further induced the phosphorylation of Drp1 (Ser616) and caused its subsequent translocation to the mitochondria, followed by mitophagy. Interference of HCV-induced mitochondrial fission and mitophagy by Drp1 silencing suppressed HCV secretion, with a concomitant decrease in cellular glycolysis and ATP levels, as well as enhanced innate immune signaling. More importantly, silencing Drp1 or Parkin caused significant increase in apoptotic signaling, evidenced by increased cytochrome C release from mitochondria, caspase 3 activity, and cleavage of poly(ADP-ribose) polymerase. These results suggest that HCV-induced mitochondrial fission and mitophagy serve to attenuate apoptosis and may contribute to persistent HCV infection.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Relationship between hepatitis C virus infection and type 2 diabetes mellitus: meta-analysis.

            To investigate the association between hepatitis C infection and type 2 diabetes mellitus. Observational studies assessing the relationship between hepatitis C infection and type 2 diabetes mellitus were identified via electronic and hand searches. Studies published between 1988 to March 2011 were screened, according to the inclusion criteria set for the present analysis. Authors performed separate analyses for the comparisons between hepatitis C virus (HCV) infected and not infected, and HCV infected and hepatitis B virus infected. The included studies were further subgrouped according to the study design. Heterogenity was assessed using I(2) statistics. The summary odds ratios with their corresponding 95% CIs were calculated based on a random-effects model. The included studies were subgrouped according to the study design. To assess any factor that could potentially affect the outcome, results were further stratified by age group (proportion of ≥ 40 years), gender (proportion of male gender), body mass index (BMI) (proportion of BMI ≥ 27), and family history of diabetes (i.e., self reported). For stability of results, a sensitivity analysis was conducted including only prospective studies. Combining the electronic database and hand searches, a total of 35 observational studies (in 31 articles) were identified for the final analysis. Based on random-effects model, 17 studies (n = 286,084) compared hepatitis C-infected patients with those who were uninfected [summary odds ratio (OR): 1.68, 95% CI: 1.15-2.45]. Of these 17 studies, 7 were both a cross-sectional design (41.2%) and cohort design (41.2%), while 3 were case-control studies (17.6%). Nineteen studies (n = 51,156) compared hepatitis C-infected participants with hepatitis B-infected (summary OR: 1.92, 95% CI: 1.41-2.62). Of these 19 studies, 4 (21.1%), 6 (31.6%) and 9 (47.4%) were cross-sectional, cohort and case-control studies, respectively. A sensitivity analysis with 3 prospective studies indicated that hepatitis C-infected patients had a higher risk of developing type 2 diabetes compared with uninfected controls (summary odds ratio: 1.41, 95% CI: 1.17-1.7; I(2) = 0%). Among hepatitis C-infected patients, male patients (OR: 1.26, 95% CI: 1.03-1.54) with age over 40 years (summary OR: 7.39, 95% CI: 3.82-9.38) had an increased frequency of type 2 diabetes. Some caution must be taken in the interpretation of these results because there may be unmeasured confounding factors which may introduce bias. The findings support the association between hepatitis C infection and type 2 diabetes mellitus. The direction of association remains to be determined, however. Prospective studies with adequate sample sizes are recommended.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: found
              Is Open Access

              Hepatitis C Virus Evasion Mechanisms from Neutralizing Antibodies

              Hepatitis C virus (HCV) represents a major public health problem, affecting 3% of the world’s population. The majority of infected individuals develop chronic hepatitis, which can progress to cirrhosis and hepatocellular carcinoma. To date, a vaccine is not available and current therapy is limited by resistance, adverse effects and high costs. Although it is very well established that cell-mediated immunity is necessary for viral clearance, the importance of host antibodies in clearing HCV infection is being increasingly recognized. Indeed, recent studies indicate that neutralizing antibodies are induced in the early phase of infection by patients who subsequently clear viral infection. Conversely, patients who do not clear the virus develop high titers of neutralizing antibodies during the chronic stage. Surprisingly, these antibodies are not able to control HCV infection. HCV has therefore developed mechanisms to evade immune elimination, allowing it to persist in the majority of infected individuals. A detailed understanding of the mechanisms by which the virus escapes immune surveillance is therefore necessary if novel preventive and therapeutic treatments have to be designed. This review summarizes the current knowledge of the mechanisms used by HCV to evade host neutralizing antibodies.
                Bookmark

                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                hih
                Revista Cubana de Hematología, Inmunología y Hemoterapia
                Rev Cubana Hematol Inmunol Hemoter
                Editorial Ciencias Médicas (Ciudad de la Habana )
                1561-2996
                September 2015
                : 31
                : 3
                : 0
                Affiliations
                [1 ] Instituto de Hematología e Inmunología Cuba
                Article
                S0864-02892015000300011
                bc8fca9a-9257-4e18-9be0-360cc639521f

                http://creativecommons.org/licenses/by/4.0/

                History
                Product

                SciELO Cuba

                Self URI (journal page): http://scielo.sld.cu/scielo.php?script=sci_serial&pid=0864-0289&lng=en
                Categories
                HEMATOLOGY

                Hematology
                anti C1q,hepatitis C,autoantibodies,autoimmunity,anti -C1q,autoanicuerpos,autoinmunidad
                Hematology
                anti C1q, hepatitis C, autoantibodies, autoimmunity, anti -C1q, autoanicuerpos, autoinmunidad

                Comments

                Comment on this article