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Original / Research
HIV, HBV and HCV Co-Infection Study
Shazia M Ahsan, Preeti R Mehta
The routes of transmission are common for HIV, HBV and HCV. There is a paucity of published data on co-infection by these three viruses. Hence a pilot study was undertaken to screen 200 HIV positive serum samples from patients admitted in medical wards of tertiary care charitable hospital for the presence of HBsAg and antiHCV antibodies. 30 sera from patients attending out patient clinic and 30 sera from the HCWs of the hospital who were HIV negative represented the control group. Of the 200 HIV positive sera tested, 7 were found to be coinfected with HBV and 16 with HCV. None of the sera showed the presence of all the three viral markers. On statistical analysis a significant association was found between raised liver enzymes and HIV-HCV co-infection. The prevalence of HIV, HBV and HCV co-infection needs to be studied on a larger scale for the better understanding of the impact on clinical outcome and treatment response.
INTRODUCTION
HIV, HBV, and HCV share common modes of transmission and risk groups. Concurrent infection with HBV or HCV in HIV infected individuals leads to interaction between the viruses altering the natural history and the treatment response of these diseases. At a molecular level, interactions between HIV and hepatic viruses may potentiate HIV replication but clinical studies have been inconclusive.1 There are very few studies done abroad on the prevalence of HBV and HCV co-infection in HIV infected patients but there are no reports from India. Hence, a pilot study was carried out to determine the prevalence of HBV and HCV co-infection in HIV infected patients in our population.
Material and Methods
The study was carried out at an 1800 bedded tertiary care charitable hospital in Mumbai from July 2001 to June 2002. 200 serum samples from patients admitted in medical ward of our hospital reported as HIV positive were included in the study group. There were 130 males and 70 females with a male to female ratio of 2:1 and between the age group of 1.5-70 years. The patients who tested HIV positive were traced to the wards and a detailed history regarding name, age, sex, marital status, if married - duration of marriage, number of sexual partners, mode of transmission, investigation done - ALT, AST, Ultrasonography of liver was taken and recorded in the proforma.
The control group consisted of 2 sub groups of 30 (20 males and 10 females) HIV negative individuals (OPD) patients without high risk behaviour and 30 (20 males and 10 females) healthy HIV negative health care workers. After obtaining written consent, 5 ml of blood was collected in a plain test tube from each of them using aseptic precautions. The blood was allowed to clot at room temperature for 30 minutes. After clotting the serum was transferred to another tube for centrifugation at 3000 rpm for 10 minutes. The clear serum was withdrawn with the help of Pasteur pipette and transferred to a sterile plastic vial for storage. All the 260 serum samples were stored at 20oC.
All the 260 sera were tested for HBsAg using Hepanostika kit (Organon Teknika), and were also tested for presence of anti-HCV antibodies using LG HCD 3.0 (LG Chemical Ltd.). Manufacturer’s instructions were followed for both the assays.
Data was statistically analyzed on computer using SPSS/PC + (V 6) statistical package. P=0.05 was taken as the significance level. 95% Confidence Interval (CI) was calculated to find the limits of prevalence. Chi Square Test, Fishers Exact Test (one tailed) and student’s t Test were applied to the data wherever appropriate.
Results
In the study group, out of the 200 HIV positive sera tested, 7 (3.5%) were HBsAg positive and 16 (8%) were anti HCV positive. No serum was found to contain all the viral markers. In the control groups none of the sera tested positive for HBsAg or anti-HCV.
In our study, the routes of transmission for the three virus infections were found to be as shown in Table 1.
174 patients (87%) were married and 26 (13%) were unmarried. 18/26 unmarried patients had history of sexual contact with commercial sex workers. In married patients, the average length of sexual relationship was 12 years. Married patients had an average of 2 sexual partners whereas unmarried patients had 3.
19/200 had abnormal SGOT and SGPT, 7/200 showed abnormalities on liver sonography. All 7 HBsAg positive patients were having normal SGOT and SGPT and liver sonography. Of the 16 patients co-infected with HCV, nearly half had abnormal liver biochemistry. However, all showed normal findings on liver sonography.
Discussion
In patients infected with HIV and HBV, chronic HBV carriage is more common and HBV DNA levels are increased although hepatic neuroinflammation is reduced. Infection with HIV and HCV results in higher viral load of HCV and greater liver cell damage.1
There are a couple of published reports from India on HIV and HBV co-infection but none on HCV co-infection. However, studies on HIV, HBV and HCV have been reported from abroad as shown in Table 2.
While comparing the prevalence of HIV, HBV and HCV co-infection though the routes of transmission for all are the same, the prevalence of co-infection varies from place to place. The prevalence of HIV and HBV co-infection in our study was 3.5%, which is similar to that reported by Treitinger et al6 however, it is significantly lower (p value < 0.05) than that reported by other Indian as well as foreign studies.2-5,7 This may be due to the differences in the study group and prevalence of HBsAg in the community in that geographical area. Dimitrakopoulos et al7 have reported a very high prevalence of 67.4% of HIV and HBV co-infection. This could be probably because they tested for HBV infection not only by detecting HBsAg but also other markers of HBV infection. The prevalence of HIV and HCV co-infection of 8% in our study is similar to the study done by Dimitrakopoulos et al7 (p value > 0.05).
However, Saillour F et al4 have reported 42.5% prevalence, which is high. They studied the prevalence in two groups namely blood donors and heterosexuals. The prevalence in heterosexual group is 7.3% which is comparable to our study. J Ockenga et al5 have reported 23% prevalence which may be because along with anti-HCV antibodies they also used HCV RNA detection for HCV infection.
In the present study, the prevalence of HIV-HCV co-infection was more as compared to HIV-HBV co-infection (6.38% vs 3.72%). The possible hypothesis for this could be that studies have indicated in HIV positive individuals co-infection with hepatitis C can suppress hepatitis B and hepatitis C remains the dominant illness. Thus in HCV dominant disease the anti-HCV is detectable while the HBV is not.8
In our study the finding of abnormal liver biochemistry in HIV-HCV coinfected patients correlates with the study done by Quaranta et al.9
To summarize the present study, HIV - HCV co-infection was found in 4/11 blood transfusion recipients and 12/188 heterosexuals whereas HIV-HBV co-infection was found only in heterosexuals (7/188). However, this finding was not significant as the number of blood transfusion was very small (11/200), the majority being heterosexuals (188/200).
On statistical analysis, a significant association was found between raised liver enzymes and HIV - HCV co-infection. However association between HIV - HBV co-infection or HIV - HCV co-infection and duration of marriage, number of sexual partners, and liver sonography was not found to be statistically significant.
To conclude, HIV positive individuals with elevated liver enzymes should be screened for HCV. Though reported to be infrequent, our finding of sexual transmission of HCV in HIV infected individuals warrants testing of partners of HIV-HCV co-infected patients for HCV.
Co-infection with HBV and HCV is more in HIV positive individuals as compared to HIV negative individuals. Therefore, all HIV positive individuals and their sexual partners should be screened for HCV.
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