In this study, type I interferon (IFN-α ve IFN-β) levels, viral load levels, the relationship between viral load and interferons, and the relationship between interferon levels and disease severity and mortality in patients with Crimean-Congo Haemorrhagic Fever (CCHF) were investigated. 100 patients diagnosed with CCHF between April-2010 and September-2011 and 74 healthy individuals were selected as control group. IFN-α ve in patient sera was analysed by IFN-β seviyeleri ELISA method and viral load levels were analysed by Real-Time PCR method. Individuals in the patient group were classified as severe (group1) and mild (group2) patients according to the criteria defined by Swanepoel et al. During the follow-up, 25 of the patients in the severe group died. Patients in the severe group who died were classified as group1a and patients who survived were classified as group1b. INF-α ve β düzeyleri CCHF patients in the control group, group1 patients in group2 and control group was found to be significantly higher than the group (p<0.05). When the viral load levels detected in patients in group1 and group2 were compared, the statistical difference was found to be insignificant (p>0.05). Viral load levels in group1a were statistically significant compared to group1b and group2 (p<0.05). In the ROC analysis performed in terms of IFN-α düzeyleri detected in the first blood samples of the patients, the cut off value for predicting mortality was 25042 pg/ml. In this analysis, the area under the curve (AUC) of IFN-α için was 0.713 and statistically significant (p<0.05). IFN-β için values were statistically insignificant (p>0.05). The cut off value for viral load was 8445500 copies/ml, AUC was 0.870 and statistically significant (p<0.05). There was a significant and positive correlation between IFN-α ile and IFN-β arasında in group1a (r=0.551, p<0.05). In conclusion, we found high levels of interferon and viral load in CCHF patients in this study, suggesting that high levels of interferon are released in CCHF patients, but the secreted interferon cannot prevent viral replication adequately. It is likely that the CCHF virus has various evasion mechanisms to avoid the effect of interferon. Further studies are needed to clarify/confirm this situation.
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