Complement and viral pathogenesis.

Department of Microbiology, University of Colorado School of Medicine, Aurora, CO 80045, USA.
Virology (Impact Factor: 3.35). 02/2011; 411(2):362-73. DOI: 10.1016/j.virol.2010.12.045
Source: PubMed

ABSTRACT The complement system functions as an immune surveillance system that rapidly responds to infection. Activation of the complement system by specific recognition pathways triggers a protease cascade, generating cleavage products that function to eliminate pathogens, regulate inflammatory responses, and shape adaptive immune responses. However, when dysregulated, these powerful functions can become destructive and the complement system has been implicated as a pathogenic effector in numerous diseases, including infectious diseases. This review highlights recent discoveries that have identified critical roles for the complement system in the pathogenesis of viral infection.

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background and study aims To search for an immunological parameter that may correlate with the response to interferon (IFN) treatment is very crucial. The objective of this study was to correlate the levels of C3 and C4 complement components with the response to IFN treatment in patients with chronic hepatitis C virus (HCV) infection. Patients and methods This study was conducted on 100 patients and control subjects classified into three groups. Group (I) consisted of 50 patients with chronic hepatitis C who were receiving IFN treatment and showed various responses; group (II) included 25 patients with chronic hepatitis C naive to IFN treatment; and group (III) included 25 healthy subjects matched for age and sex who served as controls. Measurement of the level of complement C3 and C4 was done by a quantitative turbidimetric test. Measurement of complement levels in group (I) was done at the end of treatment at the 48th week. Results Serum levels of C3 and C4 were found to be significantly reduced in all patients with chronic HCV infection in both groups (I and II) compared to the healthy control group (III) (p < 0.05). Moreover, chronic HCV patients treated with IFN and ribavirin had significantly lower levels of C3 and C4 compared with patients naive to IFN and ribavirin treatment. At the end of treatment, both C3 and C4 had significantly increased in responders to IFN when compared to non-responders (p = 0.025 and 0.05, respectively). There was a significant negative correlation between C3 and C4 levels and the concentration of serum alanine aminotransferase (ALT) measured simultaneously. Conclusion Higher C3 and C4 serum concentrations were found to be positively correlated to the end-of-treatment response in patients with chronic HCV infection treated with IFN and ribavirin.
    Arab Journal of Gastroenterology 01/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by multisystem organ involvement, heterogeneity of clinical features, and variety in degree of severity. The differential diagnosis is a crucial aspect in SLE as many other autoimmune diseases portray clinical similarities and autoantibody positivity. Lupus mimickers refer to a group of conditions that exhibit both clinical features and laboratory characteristics, including autoantibody profiles that resemble those present in patients with SLE, and prompt a diagnostic challenge in every-day clinical practice. Thus, lupus mimickers may present as a lupus-like condition (i.e., 2 or 3 criteria) or as one meeting the classification criteria for SLE. Herein we review and classify the current literature on lupus mimickers based on diverse etiologies which include infections, malign and benign neoplasms, medications, and vaccine-related reactions.
    Autoimmunity reviews 05/2014; · 6.37 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Cancer is a traitorous archenemy that threatens our survival. Its ability to evade detection and adapt to various cancer therapies means that it is a moving target that becomes increasingly difficult to attack. Through technological advancements, we have developed sophisticated weapons to fight off tumor growth and invasion. However, if we are to stand a chance in this war against cancer, advanced tactics will be required to maximize the use of our available resources. Oncolytic viruses (OVs) are multi-functional cancer-fighters that can be engineered to suit many different strategies; in particular, their retooling can facilitate increased capacity for direct tumor killing (oncolytic virotherapy) and elicit adaptive antitumor immune responses (oncolytic immunotherapy). However, administration of these modified OVs alone, rarely induces successful regression of established tumors. This may be attributed to host antiviral immunity that acts to eliminate viral particles, as well as the capacity for tumors to adapt to therapeutic selective pressure. It has been shown that various chemotherapeutic drugs with distinct functional properties can potentiate the antitumor efficacy of OVs. In this review, we summarize the chemotherapeutic combinatorial strategies used to optimize virally induced destruction of tumors. With a particular focus on pharmaceutical immunomodulators, we discuss how specific therapeutic contexts may alter the effects of these synergistic combinations and their implications for future clinical use.
    Frontiers in oncology. 01/2014; 4:145.


Available from