LETTER TO EDITOR
|Year : 2012 | Volume
| Issue : 1 | Page : 61-62
Coinfection of hepatitis B and hepatitis C in human immunodeficiency virus infected patients in a tertiary care hospital in North West India
Saroj Hooja1, Anita Singhal1, Nitya Vyas1, Subhash Nepalia2, Rekha Bachhiwal1, Leela Vyas1
1 Department of Microbiology, SMS Medical College, Jaipur, Rajasthan, India
2 Department of Gastroenterology, SMS Medical College, Jaipur, Rajasthan, India
|Date of Web Publication||14-Mar-2012|
A-29, Lal Bahadur Nagar, Opp. Hotel Clarks Amer, Jaipur - 302 017, Rajasthan
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Hooja S, Singhal A, Vyas N, Nepalia S, Bachhiwal R, Vyas L. Coinfection of hepatitis B and hepatitis C in human immunodeficiency virus infected patients in a tertiary care hospital in North West India. Indian J Sex Transm Dis 2012;33:61-2
|How to cite this URL:|
Hooja S, Singhal A, Vyas N, Nepalia S, Bachhiwal R, Vyas L. Coinfection of hepatitis B and hepatitis C in human immunodeficiency virus infected patients in a tertiary care hospital in North West India. Indian J Sex Transm Dis [serial online] 2012 [cited 2017 Jan 22];33:61-2. Available from: http://www.ijstd.org/text.asp?2012/33/1/61/93833
Due to shared routes of transmission, human immunodeficiency virus (HIV) patients have a high probability of getting coinfected with hepatitis B virus (HBV) and hepatitis C virus (HCV). Among the 33.3 million HIV-infected patients worldwide,  2-4 million are estimated to have chronic HBV infection, while 4-5 million are coinfected with HCV. They differ in their prevalence by geographic region and the efficiency by which certain types of exposures transmit them.  Improved survival due to success of highly active antiretroviral therapy (HAART) in HIV patients has enabled infections such as chronic viral hepatitis to become a major source of comorbidity.
A study was carried out in the Department of Microbiology, SMS Medical College, Jaipur, from January 2008 to December 2009, where clinically suspected patients were tested for HIV antibodies after pretest counseling and informed consent as per World Health Organization (WHO) guidelines. A total of 600 treatment naïve HIV-infected patients were included in the study. Clinical staging of the disease was done according to Centers for Disease Control and Prevention (CDC) guidelines.  CD4 cell count estimation was done by flow cytometry. All patients were tested for hepatitis B surface antigen (HBsAg) and anti-HCV antibodies by enzyme-linked immunosorbent assay. Sera of HBsAg positive patients were further screened for presence of anti-HBe antibodies and HBe antigen.
Serum samples from 600 HIV negative healthy blood/organ donors (controls) were screened for HBsAg and anti-HCV antibodies and their prevalence was found to be 1.3 and 0.16%, respectively. The mode of transmission was heterosexual in 552/600 (92%) followed by transfusion of blood products 3/600 (0.5%) and in the rest it was unidentified. Majority of coinfected patients were between 31 and 40 years of age.
Of the 600 HIV seropositive patients, 63 (10.5%) were positive for HBsAg. In this group, 42/63 (66.66%) of patients belonged to group C and 30/42 (71.4%) patients of these were HBeAg positive. CD4 counts were significantly lower in the HIV/HBV coinfected group as compared to HIV alone. HBV has considerable potential to activate HIV replication directly. In addition, chronic and persistent activation of the immune system by an ongoing immune response (e.g., an infection with a hepatotropic virus) increases the expression of HIV and may therefore accelerate immunodeficiency and the course of HIV infection.  HCV was detected in 6/600 (1%) of the HIV-positive patients. It appears that HIV-associated immunosuppression stimulates HCV replication and also impairs spontaneous immune-mediated HCV clearance. Thus, the risk of cirrhosis, end-stage liver disease, and hepatocellular carcinoma is higher in coinfected cases.  Majority of our coinfected patients were in CDC stage C indicating that enhanced immunosuppression is associated with a higher rate of HBV and/or HCV replication and HIV disease progression.
Every HIV-positive patient should be screened for HBV/HCV and advised prevention. The WHO's revision of antiretroviral treatment therapy guidelines 2010 advocate starting antiretroviral therapy in all patients living with HIV who have chronic hepatitis B disease irrespective of CD4 cell count. 
As survival of patients with HIV infection improves, therapeutic toxicity and comorbid conditions such as viral hepatitis will be major issues.
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