The distribution pattern of HDV, investigated by seroprevalence studies of anti-HD in HBsAg-positive patients, is worldwide but not uniform (Gaeta GB et all., 2007;Cross TJ, 2008; Calle Serrano B et all.,2012 ). Regardless of the fact that HDV needs HBV for its life cycle, the distribution pattern of each virus is different. For example, 90% of HBV carriers are infected with both viruses in the Pacific Islands, whereas the rates decline to 8% in Italy and 5% in Japan ( Gaeta GB et all., 2007;Cross TJ et all., 2008). Current estimates suggest that 15–20 million people are infected with HDV. However, one should consider that these estimates are inaccurate and difficult to perform as systematic screening is not performed in HBV-infected individuals, especially if they present with normal liver enzymes (Cross TJ et all, 2008). In addition, anti-HD may be lacking in immunodeficient patients and seroreversion may occur after resolution of the disease, rendering the diagnosis of past infections impossible. Phylogenetic analysis has revealed 8 HDV genotypes ) with evidence of distinct global geographic distributions and pathogenicity (Le Gal et all., 2006., Taylor JM,2012). The implications of genotypes HDV infection in Tajikistan have been unclear.
HDV infection is always associated with HBV infection. Two major patterns of infection can occur: co-infection and superinfection. Co-infection is a simultaneous infection with both viruses that leads to acute hepatitis B and D. From a clinical point of view, this is indistinguishable from acute hepatitis B (Noureddin M, Gish R.,2014), although it may be more severe and two peaks of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) may be observed. Because HBV is essential for HDV, the rate of progression to chronicity is the same as that of acute hepatitis B (5%). Superinfection is the HDV infection of an individual chronically infected with HBV. This way of infection causes severe acute hepatitis, which progresses to chronicity in almost all patients (up to 80%) (Negro F.,2014). Further, different HDV and HBV genotypes may contribute to various disease outcomes. CDH may be frequently associated with hepatocellular carcinoma development although recent studies provided conflicting results.
Once chronic HDV infection is established, it usually exacerbates the pre-existing liver disease due to HBV (Negro F.,2014). HBV replication is, however, usually suppressed to low levels during the acute phase of HDV infection. This suppression becomes persistent in case of a chronic hepatitis D establishment (Alvarado-Mora MV et.all.,2013). Hepatocytes may thus be infected with HDV alone. Infection with HDV is parenterally transmitted. In industrialized countries, high-risk populations include illicit drug users and people exposed to blood or blood products. HDV does not seem to be a typically sexually transmitted disease, as the frequency of infection in sexually promiscuous heterosexual or homosexual groups is lesser than that of HBV or HIV (Abbas Z et all.,2010). In socially and economically disadvantaged populations, many infections occur by inapparent intrafamilial routes of transmission, facilitated by poor hygiene.
It is estimated that 6 to 10% of HIV-infected patients in Western countries have HBV co -infection ( Thio C. L., et al. 2002). Co-infection with HBV has been shown to increase the risk of acute hepatitis, hepatic decompensation, liver-related mortality, and virological failure in HIV-infected patients receiving antiretroviral therapy ( Sheng W. H., et al. 2007). For patients with HIV infection, clinical studies of the impact of HDV infection on patients with HBV and HIV coinfection were limited and yielded inconsistent results before the introduction of antiretroviral therapy (Chang S-Y, Yang C-L, Ko W-S, et al. 2011). Some investigators suggested that HIV coinfection might worsen chronic liver damage by HDV and that patients with chronic HDV infection were more likely to develop cirrhosis than patients with HBV monoinfection (Noureddin M, Gish R.,2014), while others showed that the course of chronic HDV infection was not influenced by concomitant HIV infection (Calle Serrano B et all.,2012; Onali S et all.,2014). With the preexisting high HBV seroprevalence in Tajikistan, we postulated that a high HDV seroprevalence would be observed with the HIV-infected IDU and HDV infection may will occurred among IDU with chronic HBV infection who became HIV infected in this outbreak. In this study, we aim to investigate the molecular epidemiology HDV infection among persons at risk for HIV transmission in Tajikistan.
The results of work, which will determine particularities of etiological structure, clinical course, its character and immunological changes of delta infection will allow us to considerably improve early diagnostics of viral hepatitis D, timely state the adequate treatment tactics and further dispenser observation. The work will evaluate the role of different risk factors and genotypes diversity of delta infection among different population groups.
Expected results and their application.
We shall evaluate the role of various risk factors for HDV infection in different population groups and also determine association of any virological factors.
The results of the work will delineate epidemiological, clinical, virological and immunological characteristics of HDV infection among patients with HIV infection and PWID. These data will help in early and reliable diagnostics of hepatitis D, formulation of prevention and control measures and timely referral of infected patients to care and treatment.
