Comparative cross-sectional study of Interferon Gamma inducible protein-10 in mono and co-infected human Immunodeficiency Virus patients in Alexandria, Egypt

Document Type : Original Article

Authors

1 Department of Molecular and Diagnostic Microbiology, Medical Research Institute, Alexandria University, Alexandria, Egypt

2 Department of Molecular and Diagnostic Microbiology, Medical Research Institute, Alexandria University, Alexandria, Egypt.

3 Pharmacy Department, Alexandria Hepatology, Gastroenterology and Infectious Disease Hospital, Alexandria, Egypt

4 Department of Microbiology and Immunology, Faculty of Pharmacy, Pharos University in Alexandria, Egypt

Abstract

Background: Humanimmunodeficiencyvirus (HIV) infection is a global health issue. Upon invasion, the virus induces many inflammatory cytokines; especially interferon-γ induced protein 10 (IP-10). The aim of our study was to detect and compare the serum IP- 10 levels in HIV mono- infected, hepatitis C virus (HCV) mono- infected patients, and HIV co-infected patients with HCV. Methods: The study included 30 HIV patients (15 mono- infected and 15 co-infected with HCV), 15 HCV infected patients and15 healthy controls. HIV RNA, HCV RNA, CD4+T cell counts, IP-10 levels and Fibrous -4 score were estimated. Results: The mean value for HIV PCR was 1.04*104 ± 3.86*104 in HIV co-infected patients and 4.14*107 ± 1.58*108 in HIV mono-infected patients. The highest mean value for FIB-4 scores and CD4+T cell counts were among HIV co-infected patients; 1.56 ± 2.17 and 432.80 ± 294.83 respectively. HCV mono-infected patients revealed the highest IP-10 mean value; 472.0±235.28.  No significant difference was found in HIV co-infected (p < /em>= 0.806, 0.327) nor HIV mono-infected patients (p < /em>=0.244,0.581) regarding the relation between CD4+T counts 5(> 400 or < 400) with the IP-10 levels and FIB-4 scores respectively. Conclusions: High IP-10 levels were associated with low CD4 cell count in HIV mono and co-infected patients. IP-10 secretion may be related to HIV pathogenesis and immune depletion. HIV/HCV co-infection did not influence HIV disease progression.

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