Title: Role of Previous Adenovirus Infection and Its Association with IFN-α in Occurrence of Celiac Disease in Iraqi Patients

Authors: Hashim Raheem Tarish, Wasan Sami Hameed, Raad Jasim Abdul-Mehdi, Hashim Ali Abdulameer Alsherees

 DOI:  http://dx.doi.org/10.18535/jmscr/v4i4.58

Abstract

Celiac disease (CD) is a chronic small intestinal immune-mediated enteropathy precipitated by exposure to dietary gluten in genetically predisposed individuals, many environmental triggering factors are suggested to participate in its pathogenesis, Several studies were  struggled to establish the association between some microbial infections  and CD development, some of these studies were suggested an association between adenovirus infections and CD development, but this association still un confirmed yet, so that, this study aims to evaluate the role of previous adenovirus infections and its association with  IFN-α in occurrence of celiac disease. Sample of 80 Iraqi celiac patients  has been chosen from all suspected patients who attending to Al-Suder- Medical center during the period of  April  2015 to  November 2015, also 80 healthy individuals (control)  were  included in this study, all patients were undergo blood investigations for anti- adenovirus IgG ,AGA-IgA, AGA-IgG, tTG-IgA, tTG-IgG  and IFN-α tests. Results showed no significant difference in levels of anti-adenovirus IgG in celiac patients compared to healthy group, p >0.05 and there is no significant correlation between IFN-α and anti-adenovirus IgG in celiac patients, P > 0.05. Alsono significant correlation between anti-adenovirus IgG and AGA-IgA,P > 0.05 and no significant correlation between anti-adenovirus IgG and AGA-IgG, P > 0.05, andno significant correlation between anti-adenovirus IgG and tTg-IgG, P > 0.05. In other hand, there is significant correlation between anti-adenovirusIgG and tTg-IgA, P < 0.01.

Key words: Celiac disease, adenovirus, IFN-α, AGA, tTG-IgA.

References

    

   1.      Trier, J.S. (1997). Celiac Sprue and Refractory Sprue. In Sleosenger and Fordrans Gastrointestinal and Liver Disease / 6th Edition. Vol-2.

2.      Rostami-Nejad  M,  Ishaq S, Al Dulaimi D, Zali MR,  and Rostami K.( 2015).The Role of Infectious Mediators and Gut Microbiome in the Pathogenesis of Celiac Disease. Arch Iran Med ;18(4): 244 – 249.

3.      Van Heel DA, Franke L, Hunt KA, Gwilliam R, Zhernakova A, Inouye M, Wapenaar MC, Barnardo MC, Bethel G, Holmes GK, Feighery C, Jewell D, Kelleher D, Kumar P, Travis S, Walters JR, Sanders DS, Howdle P, Swift J, Playford RJ, McLaren WM, Mearin ML, Mulder CJ, McManus R, McGinnis R, Cardon LR, Deloukas P, Wijmenga C.( 2007). A genome-wide association study for celiac disease identifies risk variants in the region harboring IL2 and IL21. Nature Genetics; 39( 7): 827–829.

4.      SollidL M, Markussen G, Ek  J, Gjerde  H, Vartdal  F, Thorsby E. (1989). Evidence for a primary association of celiac disease to a particular HLA-DQ alpha/beta heterodimer. The Journal of experimental medicine; 169: 345-350.

5.      Bethune M T, Khosla C.(2008). Parallels between pathogens and gluten peptides in celiac sprue. PLoS Pathogens, vol. 4, no. 2, article e34.

6.      KagnoffMF, Paterson YJ, Kumar PJ, Kasarda DD, Carbone FR, Unsworth DJ and Austin RK. (1987). Evidence for the role of a human intestinal adenovirus in the pathogenesis of coeliac disease. Gut;28 (8): 995–1001.

7.      Pozo-Rubio M, Marta O,  Esther N,  Giada D P,  Jorge  R,  Maria D F,  Ascensi M. and Yolanda S.(2012).Immune Develop-ment and Intestinal Microbiota in Celiac Disease. Clinical and Developmental Immunology; Vol. 2012,Review  Article ID 654143, 12 pages.doi:10.1155/2012/654143.

8.      Mahon  J, Blair G E, Wood G M, Scott B B, Losowsky M  S, and Howdle P  D.(1991). Is persistent adenovirus 12 infection involved in coeliac disease? A search for viral DNA using the polymerase chain reaction. Gut; 32(10):1114–1116.

9.      LahdeahoM L, Lehtinen M, Rissa H R, Hyoty H, Reunala T, and Maki M.(1993). Antipeptide antibodies to adenovirus E1b protein indicate enhanced risk of celiac disease and dermatitis herpetiformis. International Archives of Allergy and Immunology; 101( 3): 272–275.

10.  HowdleP D, Zajdel M E B, Smart C  J, Trejdosiewicz L K, Blair G  E, and Losowsky  M  S. (1989). Lack of a serologic response to an E1B protein of adenovirus 12 in coeliac disease. Scandinavian Journal of Gastroenterology; 24(3):282-286.

11.  Gabriel S, Alexandru P, Nicolae  M, Mariana A, Victor C, and Doru D.(2011).ADENOVIRUSURI ÎN BOALA CELIACĂ LA COPIL.Romanian Journal of Infectious Diseases ; 14 (1): 5-9.

12.  VesyCJ, Greenson JK, Papp AC, Snyder PJ, Qualman SJ, and Prior TW.(1993).Evaluation of celiac disease biopsies for adenovirus 12 DNA using a multiplex polymerase chain reaction.Mod Pathol;6(1):61-64.

13.  StepniakD, Koning F. (2006).General introduction: Celiac disease - sandwiched between innate and adaptive immunity.Hum Immunol ;67(6):460-8.

Corresponding Author

Hashim Ali Abdulameer Alsherees

Assist. Lecture, Department of Microbiology

College of Medicine/University of Kufa