Hepatitis C virus infection is one of the major diseases of mankind and is a serious global public health problem. The precise effect of HCV co-infection on the recovery of immune cells and liver enzymes in HIV patients before and after HAART remains controversial. However, a number of studies have suggested that the presence of HIV infection accelerates the course of HCV-related liver disease in HCV/HIV co-infected patients [5, 8]. HIV is known to impair T-helper type 1 immune response which in turn alters the response of immune cells to HCV. This permits greater HCV replication and consequently, greater infection and injury to hepatocytes which leads to more rapid progression to HCV-related liver diseases (fibrosis, cirrhosis and hepatocellular carcinoma) .
Given the above interaction of the two viruses and their implications on the proper management of the co-infected cases, the aim of this work was to describe the prevalence of HCV co-infection among HIV patients at Yekatit-12 and Zenbaba General Hospitals and assess the immunological and clinical chemistry results over a four years period. Results show that the prevalence of HCV among the 387 Addis Ababa resident-HIV patients, who visited the two hospitals during one month (September 2006), was 6.5%. This was low in accordance with the previous HIV/HCV co-infection studies in Ethiopia by Workinesh, et al.  and Addisu et al. which was 8.6% and 10.5% respectively. Compared to Spain (33%), U.S.A (30%), France (24.3%) and Morocco (19.8%), the present prevalence was still low [5, 9]. The co-infection prevalence in under HAART (7.8%) was more than Pre-ART patients (5%). This might be due to the higher numbers of under HAART (N = 206) than the pre-ART (N = 181) patients. In this study, from the 25 co-infected patients more males were co-infected than females (60% Vs 40%). This might be due to the higher number of males than females in the sample population, hence, does not justify to saying that it is gender influenced.
The distribution of HCV/HIV co-infection, in Figure 2 shows the direct link of age to HCV prevalence. It starts with 20% in age group 20–29 and grows to nearly 45% in age groups 40–49 years suggesting an association with age. A higher prevalence in older age groups could be a reflection due to the chronic nature of the disease, sexual behavior or it may be related to hormone and immunity. Our finding was in agreement with the work of Sugimoto, et al. that found HIV/HCV co-infection is higher in males over 40 years of age. This is a serious indicator for over 50-80% of co-infected patients develop chronic infection that gives rise to liver cirrhosis (4-20%) and hepatocellular carcinoma in 1-5% .
The observation on immunological parameters over four years showed that an improvement of CD4+ and CD8+ counts in both HCV positive and negative under HAART patients. However, the CD4+ increase in those not co-infected with HCV was much better when compared with those of HCV infected (426 ± 113 Vs 343 ± 119, P < 0.004). This suggests that although HAART does improve the immune system of HCV co-infected patients, its efficiency is relatively compromised by HCV interactions (Figure 3 and Tables 1 and 2). Our finding was in agreement with researchers who concluded that even though HAART suppresses HIV and increase CD4+ count response, however, it is affected by the presence of HCV co-infection . In addition, HAART adversely affect HCV outcomes by increasing HCV viral load, hepatotoxicity and increased HCV related liver disease progression in HIV/HCV co-infected people .
Variety of factors is incriminated in influencing these treatment outcomes. The factors include presence of high HCV RNA load, low treatment responses of genotypes 1 and 4, high rate replication (1012 virions/day) and its exceptionally high mutation rate producing a genetic variety . Our result though does not have data on the influence of viral interaction, has shown that the presence of HCV decreases the efficiency of HAART when compare to those that were negative for HCV, hence goes well with the conclusions of Kedziora, et al. work . The improvement of the immune status with CD4+ and CD8+ counts on its own improves survival of patients the minimum by slowing viral load and elimination of infected cells.
In the present study, the liver enzyme levels were much higher than the above limits of reference in co-infected than HIV mono-infected patients. In supporting the present study; DeSemone and his colleagues  found that increased liver enzyme level often associated with HCV co-infection. The mean GPT level of pre-ART co-infected group 4 patients during 1st year was at least fivefold greater than that of under HAART co-infected group 2 patients. From 2nd year and onwards, both group 2 and group 4 had comparatively increased levels of liver enzymes (Figure 3 and Table 4). In this study, more than 70% of the co-infected patients showed increased levels of GPT above the limits of reference which agreed with the finding of Lawson  in which only 30% of HCV patients have normal GPT levels.
Moreover, Sulkowski and his colleagues  found that HCV has been confirmed to be a risk factor associated with a 3 to 5-fold chance of developing elevated transaminases during HAART, compared to HIV patients without HCV which was compatible with the present study. However, the present work was incompatible with the study done by Gatti, et al. that showed the synergetic mitochondrial damage by HCV and HAART (especially nucleoside analogs) were responsible for elevation of GPT in HAART groups. In addition, the higher enzyme level in the co-infected pre-ART group in this study indicates that the effect of HCV is more pronounced in pre-ART era than in the era of HAART. Furthermore, the HIV mono-infected group 1 and group 3 had normal amount enzyme levels throughout the follow up time. In supporting the normal enzyme levels of HIV mono-infected group 1 and group 3 in this study, Marina and Vincent  found that HAART do not associated with increased liver enzymes.
The present study has several strengths. Although viral load, HCV genotype and alcohol consumption status of patients are crucial in clinical medicine however, CD4+ count is the main test routinely done to follow immune recovery. The present study clearly showed the pattern of CD4+ changes considering different factors during the time of follow up. The information obtained in this study may promote our understanding of the impact of HCV infection on immunological parameters and liver enzyme levels among HIV/HCV co-infected individuals. Viral load, HCV genotype, alcohol consumption status and other clinical information of patients were not done in this study. Thus, with those limitations, we believe that this cohort may provide an accurate reflection of current clinical trends regarding this dual infection.