Introduction

HBV was of moderate endemicity in Iraqi population with a rate of 3% [1]. The highest concentrations of infectious HBV are in blood, serum and serum-derived body fluids, such as semen and saliva [2]. It has been reported earlier in 2002 that the hepatitis B virus can live for several days in dried blood on table surfaces, needles, syringes and razors [3,4]. The World Health Organization (WHO) estimates that hepatitis B result in 563 000 deaths annually from the estimated 350 million carriers [5,6]. The hepatitis B virus is transmitted by contact with infected blood or body fluids of an infected person. Chronic infection after exposure to hepatitis B virus (HBV) has been observed in 30% to 90% of children aged less than five years. On the other hand, exposed adults become chronic carriers of HBV in only 2 to 5% of cases [7]. Based on the prevalence of HBV chronic carriers (individuals positive for hepatitis B surface antigen) amongst adults in the general population, countries are classified as having low endemicity <2%, intermediate endemicity 2%-8% or high endemicity >8% of infection) [8]. Even with three effective doses of the vaccine available, hepatitis B remains a stubborn, unrelenting health problem, especially in Africa and other developing areas. The disease and its complications cause an estimated one million deaths globally each year [9]. Studies in the Middle East showed that the prevalence of HBs Ag ranged from 3% to 11% in Egypt [10]. Hepatitis B vaccination is the most effective measure to prevent HBV infection and its consequences. However, for persons already infected with HBV, antiviral agents are available that may prevent the serious sequel of chronic liver disease, which highlights the importance of identifying infected individuals.

       In a recent study [11], the national estimate of HBs antigen prevalence rate was 1.6%. Anti-HBs IgG (total) had a higher prevalence rate of 16.9% and HBc antibodies 9.8%. The prevalence of HBsAg was lowest in the first decade of life (0.9%), and increase with age to reach a maximum prevalence rate of 2.4% in the fifth decade of life. The risk of testing positive for HBs antigen is almost doubled in the 3rd decade of life compared to 1st decade of life. Being in the fifth decade of life significantly increased the risk of having positive HBs antigen by 2.6 times compared to 1st decade of life. Male gender significantly increases the risk of having positive HBs antigen by 41% compared to females. The prevalence rate of positive HBs antigen was lowest in Maysan, Dhi Qar, Al Qadisiyah and Al Muthanna (<0.5%). The prevalence rate was highest in An Najaf, Dahuk, Salah ad Din and Babil (>3%).  The prevalence of anti-HBs antibodies was lowest in the 3rd decade of life (12.2%), and is slightly, but not significantly higher in older ages. The prevalence rate of positive anti-HBs anti-bodies is highest in the first decade of life 32.2%. Compared to the 3rd decade of life the risk of testing positive is significantly increased by 38% in the 2nd decade of life and by 2.63 times in the first decade of life. Male gender significantly increased the risk of having positive anti-HBs IgG antibodies by 33% compared to females. The anti-HBc IgG antibodies shows a positive age trend as opposed to the negative age trend observed with anti-HBs IgG antibodies. The anti-HBc IgG antibodies prevalence rate was lowest in the first decade of age (3.8%) and highest in the 5th decade of life (14%). Gender showed no important or statistically significant association with anti-HBc antibodies.

           HBV infections are among the most prevalent infectious diseases in humans worldwide. The infections are associated with a broad range of clinical presentations ranging from acute or fulminant hepatitis to chronic infection that may be clinically asymptomatic or may progress to chronic hepatitis and liver cirrhosis [12]. The prevalence of infection with HBV varies from one country to another depending upon a complex mixture of behavioral, environmental and host factor. The prevalence of HBs antigen (HBsAg) positivity in different populations ranges from less than 0.5% to as high as 20%. A study conducted in Aurangabad reported 6.42% carriage in resident doctors [13]. Another study con-ducted in Delhi reported 6.9% transfusion associated hepatitis (TAH) among patients receiving blood transfusion for cardiac surgery; of the total TAH cases 20% were related to HBV [14]. The spread of hepatitis B virus continues to be at an alarming rate worldwide and this created an impact on many countries. Although the rate of expo-sure to HBV in Pakistan is not fully confirmed, Awan et al [15] reported ~38% prevalence of different hepatitis B markers, with a 4% HBs Ag carrier rate and 32% with anti-HBV surface antibodies (Anti HBs Ab) by natural conversion [15]. High prevalence of HBV was observed in geographical areas of low economic status, which underscores the importance in controlling this disease [16,17]. The present study gives a highlight on HBV activity in Iraq. It demonstrated that the prevalence rate of HBs Ag in apparently healthy individuals was 1.6%. It was more frequent in age group above 40 years and in males more than females. The results of Attalla et al [11] survey comply with the results of other published articles in neighbor populations. Schreiber et al. [18] reported an intermediate prevalence of 2-8% for HBV infection in Egypt. Another study reported the prevalence of HBsAg among Kuwaiti national and non-Kuwaiti Arab at 1.1 and 3.5%, respectively [19]. High prevalence results of HBV in males compared to females have been observed in earlier studies in Pakistan [8,20]. Similar results have also been obtained in Bangladesh where the researchers reported higher prevalence in males (67.86%) than females (32.14%) [21].The aforementioned gender disproportion may be explained by the increased frequency of high risk jobs and behavior in men, like multiple sexual partners, drug use and unhygienic barber shaving practices. The prevalence of HBV infection rises gradually with age. Higher risk of infection was found in the older subjects as compared to the younger ones. The higher prevalence among older age groups may be attributed to the more frequent and continuous exposure to risk factors of hepatitis B (HBV infection).

           The prevalence of HBV infection and immunity was determined in a representative sample of the US population for the period 1999–2006. National Health and Nutrition Examination Surveys participant’s ≥6 years of age were tested for antibody to hepatitis B core antigen (anti-HBc), hepatitis B surface antigen (HBsAg), and antibody to hepatitis B surface antigen (anti-HBs). The prevalence of anti-HBc increased from 0.6% in children aged 6–19 years to 5.9% among adults 20–49 years of age, and further in-creased to 7.2% among older persons (≥50 years) [22]. In Tarky et al. [11] 2013 study the prevalence of antibody to hepatitis B core antigen (anti-HBc) showed a weak positive age trend. Anti-HBc antibodies is expected to increase with age in a pattern that is similar to HBs Ag marker, since this type of antibodies is only produced by natural infection and not by vaccination.  Prevalence of Anti-HBs IgG was negatively correlated with age, ranging from 53.5% among persons aged 6–11 years to 5.1% among person’s ≥60 years of age [22]. In the current study of Iraqi community the prevalence rate of positive anti-HBs was highest in children and lowest in the 3rd decade of adult life and then rises again. The main reason for this in-crease in prevalence rate of anti- HBs Ab in the first decade of life is the vaccination program, however vaccination give anti-bodies to HBs Ag at a lower titer than that of natural infection, in addition Anti HBs IgG in natural infection is always associated with anti-HBc antibodies. Another fact is that about 60% of vaccinated individuals have no detectable antibody in their blood after 9 to 15 years after vaccination, al-though they were still immune due to avail-ability of memory cells [23]. In Iraq, hepatitis B vaccination was introduced on 1993 for the first time as a part of Expanded  Program of Immunization (EPI) and was applied on children below 5 years of age [24], accordingly those Iraqi whom were above 30 years of age at the time of conducting the study were not vaccinated.

1. Materials and Methods

1.1 Settings: Samara General Hospital and primary health care centers in Samara District.

      1.2. Study Design: The study design of two parts, the first one is a retrospective study and the second part is a Descriptive Case Control Study.

      1.3 Study Population: The study conducted in Samara General Hospital and primary health care centers in Samara District. Records of subjects with hepatitis B viral infections during three years (2011, 2012 and 2013) were included in the study. Their age range from 1 to 59 years, with a mean age of 26.7±4.9 years. The total numbers of tested serum samples were 16165, of them 5683 for 2011, 5809 for 2012 and 4673 for 2013. Of the total 9648 (60%) are male and 6517 (40%) are female (Table 1).

2. Results

       2.1 Prevalence of Hepatitis B virus

In all, 16165 serum samples were processed for HBsAg detection over 3 years period in Samara general hospital. The seroprevalence of HBsAg was found to be 3.2% (518/16165) and none of them was positive for

HIV antibody. The highest seroprevalence of  HBsAg was found in the 2013 collected samples which form 4.73% (221/4673), followed by 3.55% (206/5809) for 2012 and 1.6% (91/5683) for 2011. There was a highly significant (X²=90.3, P=0.000) differences in seroprevalence of HBsAg between the 3 years (Table 2). 

      2.2 Gender Influence on Prevalence of Hepatitis B Virus

Gender influences on seroprevalence of HBsAg are shown in (Table 3).

      2.3  Age Distribution of Hepatitis B Virus                                                         

Age distribution of hepatitis surface antigen is shown (Table 4).

      2.4 Age Group Distribution of the Prevalence of Hepatitis B Virus in Relation to Gender

 The age distributions of the Seroprevalence of HBsAg are shown in (Table 5).

Discussion

Hepatitis B is a major public health problem worldwide [WHO 2002]. This infection with global burden due to its link with the development of liver cirrhosis and hepatocellular carcinoma (HCC), which forms around 2% of all death and is, expected to increase over the next decades [25] were attributed to HBV infections [26].

In any country, the epidemiologic data about HBV provide significant information for health provider and health control programs managers to plan their strategy of prevention and controls [27]. There are few properly published reports on HBV infections because most of them deals with risk groups and only two large retrospective and 2 prospective studies were reported for Iraq [28-30].  The present study deals with prevalence of HBV infections in a mixed population of healthy control individuals came for routine investigations such as pre-marital checkup or employment or pre-operative preparation and those with suspected hepatitis cases. The seroprevalence of HBsAg was 3.2% with a significant increase with time (X²=90, P=0.000), which was 1.6%, 3.55% and 4.74% for 2011, 2012, and 2013 respectively. This finding indicated 2.96 times prevalence for 2013 as compared to 2011. This increase in HBV prevalence represents a public health problem which may be a reflection of increase of vertical and horizontal transmission and /or disruption in the Expanded Program of Immunization (EPI).

Iraq is with intermediate prevalence of hepatitis B virus [28,30]. The present study findings indicated that HBV seroprevalence was lower to that reported for Iraq [31-35], however, higher to other studies in Iraqi population [11,28,29]. Skinho and Al-Kassab [35] reported HBsAg seroprevalence of 3.6% in blood donors, while Hussein [36] reported the same seroprevalence in military personnel blood donors. Omer and Thewaini [32] found that HBsAg prevalence was 3.3% in apparently normal population, while other study reported about the same rate (3.4%) [34] In normal population. However, Omer and Al-Dowri [37] reported a higher (4.3%) in normal population, while other research group reported a prevalence of 4.1% in blood donor.

The above mentioned studied with the exception of five studies [11,28,29,31] were performed in seventies, eighties and nineties. Ataallah et al [28] found HBsAg seroprevalence of 0.66% in blood donors in Baghdad, while Al-Hammieary reported a 1.02% seroprevalence of HBsAg in normal population in Al-Rusafa sector of Baghdad and 0.96% in health care workers. However, other study performed in 2007 in Baghdad reported a seroprevalence rate of 7.33% [31]. Omer and Al-Salmani [38] HBsAg was 1.2% among normal population.  In addition, the mean of the HBsAg seroprevalence before 2000 was 3.6% in normal population and 3.76% in blood donors, while after 2002, it was 0.97% in blood donor and 4.17% in apparently healthy population [29,31,39]. Furthermore, HBsAg seroprevalence was 0.8% in healthy individuals of Babylon [40]. One national large scale community based study performed in Iraq indicated that HBsAg seroprevalence was 1.6% [11].

The seroprevalence of HBsAg in risk group reported for Iraq with a wide range of 5 to 73.1%. In health care workers, HBsAg seroprevalence was with range of 0.96% to 5.4% [29,34,41]. In inherited blood disorders, HBsAg seroprevalence was with range of 0.09% to 32.5% [42], while in those receiving blood transfusion was 40% [43]. Furthermore, the HBsAg seroprevalence was 73.1% in individuals using glass syringe for injection [44] and with a range of 14.28% to 34% in parenteral drug administration [45,46]. In the national community based study, higher prevalence rate was reported for Al Najaf, Salahuldean and Babylon (>3%), while the lowest prevalence was for Maysan, Al-Qadisiyah, DhiQar, and Al Muthana (<0.05%). However, Al Ramadi, Karbala, and Waset were with prevalence of HBsAg of 2.0% - 2.99%, while in Baghdad, Basrah, Diyala, and Al Tameem are with prevalence rate of 1.00% to 1.99%. Ninewa, Arbil and Sulaimania were with prevalence rate of 0.5% to 0.99% [11].

The above data collectively indicated that HBsAg seroprevalence varies considerably with study target population, however, it may be contributed that HBV infections decline in Iraq. The prevalence reduced from that before 2000 to that after, but our data indicated an increase in the prevalence of the disease during study period (2011-2013). Our study seroprevalence was higher to that reported for Baghdad in two recent studies as they report 1.02% and 1.2% [29,38] and the national community based study (1.6%) [11]. This phenomenon was a reflection of many underlying etiology, such as the disruption of health care providing system, improper surveillance of infectious disease, disruption of prevention and control program of notifiable communicable diseases, all of these may lead to unsafe parenteral injection, blood and blood product transfusion. A national effective prevention and control programs application is required and new research community based studies is warranted to clarify the health impact of HBV on community. 

The seroprevalence HBV findings of this study in normal population categorize Iraq in the area of intermediate endemicity, while that of Baghdad categorize it in low endemicity area. This variation could be a reflection of increased HBV transmission in recent years. Considering Iraqi's geographical region, it is similar to United Arab Emirates in having intermediate endemicity while Bahrain, Iran and Kuwait having low endemicity. Jordan, Palestine, Saudi Arabia and Yemen have high endemicity [47-49]. However, within the same country, the origin of the investigated samples may influence the prevalence; for example, HBsAg was with 1.1% prevalence rate in Kuwaiti and 3.5% in non-Kuwaiti nationality [13].  

Recent review [50] of 39 studies of HBV maternal infections in low and intermediate socioeconomic developing countries reported prevalence of 0.34% to 25%. However, a review in 2013 concerning HBV indicated lower range of infection which extends from 1% to 10.8% in Arab Countries [51]. These two reviews illustrated a reduction HBV maternal infection which may be reflected on reduction of vertical transmission of the virus as this method of transmission represent the 1^st contagious pattern of HBV transmission [52].  In China, HBV seroprevalence in child bearing age was from 6.71% to 9.51% [53,54], while it is 1.2% in Spain [55], 1.16% in Greece [56], 0.5% in Nepal [57].

Hepatitis B virus infections occur worldwide [27], with a highest carrier rates in developing countries [58]. The reported global studies indicated a wide variation in HBsAg seroprevalence between countries and in different regions of the same country. HBsAg seroprevalence was 0.2%-8.5% in Brazil [59-61],  0.4% in Canada [62], 0.9% in Ethiopia [63], 1.6%-2.5% in Nepal [57], 0.87%-2% in India [64], 1%-2.28%  in Pakistan [65], 3.58% in Poland [66], 6.71%-9.8% in China [67], 4.8%-18% Asian American [68].

Four recent reviews, 2 for Europe and 2 global, in addition to large American study indicated that implementation of effective vaccination programs has resulted in a significant decrease in the incidence of chronic HBV infection. However, HBV remains an important cause of mortality and morbidity among the chronic HBV infection [58]. Hahne et al [69] reported that HBsAg prevalence in the general population varied widely between European countries, ranged from 0.1% 5.6%. The lower estimated number of chronic HBV infection was found in Ireland, while the higher was found in Turkey. North-western European countries had a low prevalence, whilst those in the south and south-east had an intermediate to high prevalence. Romania with high (5.6%) prevalence of HBV, while Belgium (0.7%), Sweden (0.2%), Germany (0.6%) and the Netherlands (0.1%) have low prevalence. However, Meffre et al. [70] reported that France was with low prevalence of hepatitis B infection in general population. A recent systematic review of chronic hepatitis B virus prevalence in Turkey [71] was reporting west to east gradient rate of prevalence similar to that reported by Hahne et al [69].

Chu et al [72] in their review concluded that international migration has an impact on HBV prevalence in six European countries with evident differences between migration and general population in HBV prevalence. Ott et al. [73,74] in a global systematic review from 1999 to 2005 found that the prevalence of chronic HBV infection decreased in most regions. Decrease in chronic hepatitis B infection was evident in Tropical and Central Latin America, Central sub-Saharan Africa, Central Europe and South East Asia. However, the overall number of chronically infected hepatitis B individuals was increasing and the widespread global differences  in hepatitis B virus prevalence call for targeted approaches to tackle hepatitis B virus related mortality and morbidity.

Hwang and Cheung [58] reviewed HBV infection according to the 6 regions defined by the WHO. For America, the United States and Canada was with low prevalence (0.5% - 1%), while Mexico, Central America and South America with significant higher prevalence (0.5% - 8%). In Europe, HBV seroprevalence ranged from 0.1% to 12% [75]. Europe divided into 3 types epidemiological patterns, low carriers (<1%) in Northern Europe, intermediate (0.1%-0.5%) in most Western European countries, the 3^rd pattern in Southern Europe and Eastern  Europe with carrier rate >8% [75,76]. HBV seroprevalence in the Eastern Mediterranean region range from 1% to 10%, making it intermediate to high endemicity [Custer et al 2004]. In Africa, HBV seroprevalence range from 6% to 20%, South- East Asia was with intermediate to high endemicity (1%-10%), while Western Pacific with prevalence range from 0.1% to 30% [58].

From our study findings and that reported for Iraq and Arabian countries, regional and global studies indicated a heterogeneous pattern of HBsAg seroprevalence throughout the world, ranging from <1% to 30%. There is an overall decline in hepatitis virus infection prevalence due to EPI programs, post exposure prophylaxis and antiviral therapy [Hwang and Cheung 2011]. However, hepatitis B virus infection prevalence data are needed at country and sub-national level (Governorate and town level) to estimate disease burden and guide health and vaccine policy [73].        

The overall seroprevalence of HBsAg was 3.12% for male and 3.33% for female, and the difference was not statistically significant (X²=0.553, P>0.05). However, there was a highly significant (X²=29.7, P=0.000) difference in seroprevalence of HBsAg between male (3.67%) and female (7.42%) for 2013. The seroprevalence of HBsAg was twice in female compared with male. In addition, for 2012, HBsAg seroprevalence was significantly (X²=5.43, P=0.02) higher in male (4.08%) compared to female (2.94%). However, there was no significant difference in HBsAg seroprevalence between male and female for 2011. Comparison according to years of data collection indicated a highly significant differences in male (X²=37.9, P=0.000) and female (X²=93.8, P=0.000).

This results show a non consistent pattern of gender influence with time, however, there was significant pattern of increase in HBsAg prevalence in female with time. But HBsAg was lower in 2011 and subsequently increased in 2012, and the decreased in 2013. Thus each gender show different pattern of prevalence with time. The non significant difference in seroepidemiology as this study indicated was not consistent with that reported for Iraq which suggest higher HBsAg in male compared to female [11,29,31,32,34,43, 46]. Two studies reported a non significant difference in prevalence of HBsAg in blood between male and female [28,77].

Some global studies indicated high significant HBsAg in male compared with male [73,78,64], while other studies reported higher prevalence in female [62,79]. However, some studies not reported a significant difference in HBsAg between male and female [63,66,68]. The high prevalence of HBsAg positivity in male explanation might be difficult, however, this may be contributed to that male are exposed more frequently for risk factors than female [80]. Female are more likely to develop anti-HBs [81], and this may influence the decline in HBsAg titre in female, resulting in a shorter duration of the carrier state [82].

Age of hepatitis B virus acquisition is an important determinant of the virus epidemiology. In area with low rate endemicity, the infection occur in adolescents and young adults, and in the area with high endemicity the  infection occur in children with age of 4-8 years [83]. The present study indicated that overall HBsAg seroprevalence was higher in the age group of >45 years of age (8.02%), followed by the age of 1-14 years (4.06%), while the lowest (2.65%) was in the age of 15-45 years. The difference in seroprevalence between the age groups was highly significant for total study population and for years of study and within the age groups, except 5-14 years age group.

Our  study found a prevalence of HBsAg of 4.07% in age of 1-4 years which is higher to that reported before in Iraqi normal population, while the higher seroprevalence in the age >45 years was consistent with its results  [29]. The high seroprevalence in the 1-4 years age group may be due to vertical transmission of the virus or they may not be enrolled in the immunization program. The high prevalence in the older age group may be due to that are not included in the immunization program since it is started in 1993 in Iraq or they are prone to get infection through horizontal way by contamination with blood, blood products or sexual contact [84]. 

The reported studies for Iraq indicated HBsAg prevalence peak of 20-45 [37], 30-39 [44], 30-49 [43, 46] and >40 years [11]. Thus our study not consistent with the national community based study in regard to prevalence in age <10 years, however, it was consistent in regard to old age >40 years.

Global studies reported that the peak of HBsAg prevalence was 11-20 years in India [65], 21-40 years in Pakistan [17], 25 -34 years in Bahrain [47], 50-79 years in Canada [63], ≥40 years’ immigrants in USA [69], 20-34 years in China [84], ≥50 years in USA [79], ≥ 30 years in Ethiopia [64], 21-40 years in Nepal [58]. In a recent review [59], reported age prevalence by WHO region and thus the age of peak prevalence was in adults (>20 years), with the exception of Africa (10-20 years) and Mediterranean regions (14-18 years). Most the studies concerning HBsAg age prevalence was illustrated that the infection is more predominant in adult which is mainly a reflection of the effective vaccination programs worldwide.       

The present study indicated that the pattern of HBV seroprevalence  across age in our study population exhibit a rapid increase in the prevalence, peaking first in ages 1-4 years (4.07%) and 5-14 (4.06%) years and later in ages >45 years (8.02%), with a decline in the ages 15-45 years (2.65%). Thus our study shows double peck curve, while Ataalla et al [11] study shows single peak curve. The diversity between the two studies may reflect the difference in sampling. The modes of transmission, age distribution, and prevalence of HBV in any community have important clinical significance as they help to clarify the pattern of infection and successful management. Globally, three patterns of chronic hepatitis B virus infection were described [53]. The 1^st pattern characterized by vertical route of transmission, which followed by high incidence of chronic liver infection (90%) and seen in China and other Asia-Pacific countries [53]. The 2^nd pattern is characterized by horizontal transmission in early childhood, which followed by high incidence of chronic HBV infection (30%) and is seen in South Asia, African in South Asia, Africa and Mediterranean countries. The 3^rd pattern is characterised by horizontal transmission in adults through sexual contact, intravenous drug abuse, or transfusion of infected blood products, which followed by low (2%) of chronic HBV infection and seen in Western countries [53].

In our community, the proposed pattern of chronic hepatitis B infection is a combination of the 1^st and 3^rd patterns, where the infection transmission occurs vertically and horizontally. This pattern illustrates the difficulty of performing control and prevention programs because it must cover a wide range of community. However, implementation of effective antenatal screening, infant vaccination program and safe injection will contribute to reduction in HBV infections and chronicity.

World Health Organization recommends serologic surveys to demonstrate reduction in the prevalence of hepatitis B chronic infection among children born after vaccine introduction [27]. Expanded Program on Immunization technical advisory group in the Eastern Mediterranean Region recommended that Member States [Including Iraq] adopt a goal of reducing the prevalence of chronic HBV infection among cohorts of children born after vaccine introduction to <1%. The present study indicated HBsAg prevalence of 3.20%, which it is too much higher than goal prevalence. Post- vaccination survey in the Eastern Mediterranean Regions that were performed in Oman, Egypt and Saudi Arabia, demonstrate a reduction in the prevalence of chronic hepatitis B infection to <1% [85-87].

The high HBV prevalence at ages of >45 years in both genders suggest that development of comprehensive blood –borne pathogen standard precautions with attendant regulations in Iraq is urgently needed to reduce transmission of hepatitis B and C infection in health care settings. The implementation of such standard needs governance and support at high levels, including legislation and/or regulations to ensure that health care workers are protected and that health care facility are complaint with standards precautions. In addition to legislation, intersectoral collaboration with ministries of labour or social welfare as well as nongovernmental institutions can be helpful in organize these efforts [27]. Occupational safety and health; injection safety and infection control; implementation of infection control; safe blood transfusion and blood product use; and harm reduction strategy are the keys for development of blood-borne HBV standard precautions [81,27]. As an example, in Tikrit city, two general surgeons are carriers of hepatitis B virus and still provide health care to the community in governmental and their private clinics. 

Table 3: Gender Prevalence of Hepatitis B Virus. 

Table 4: Age group Distribution of the Prevalence of Hepatitis B Virus.

Table 5: Age Group Distribution of the Prevalence of Hepatitis B Virus in Relation to Gender.

1. Wijdan A, Hussein, Abdul Rhida Al – Abassy (2002) Hepatitis Profile In Baghdad 2002, dissertation for board degree in community medicine.2002.AlmustansiryaUniversity.
2. Bond WW, Petersen NJ, Favero MS (1977) Viral hepatitis B: aspects of environmental control. Health Lab Sci 14: 235-252.
3. Workowski KA and Berman SM (2002) CDC sexually trans-mitted diseases treatment guidelines. Clin Infect Dis 35: 135-137.
4. Workowski KA and Berman SM (2006) Sexually transmitted diseases treatment guidelines, 2006. Centers for Disease Control and Prevention1, MMWR Recomm Rep 55: 1-94.
5. Perz JF, Armstrong GL, Farrington LA, Hutin YJ, Bell BP (2006) The contributions of hepatitis B virus and hepatitis C virus infections to cirrhosis and primary liver cancer worldwide. J Hepatol 45: 529-538.
6. Previsani N, Lavanchy D (2002) Hepatitis B. WHO/CDS/CSR/LYO/2002. World Health Organization.
7. Cavalletto L, Chemello L, Donada C (2007) The pattern of response to interferon alpha (alpha-IFN) predicts sustained response to a 6-month alpha-IFN and ribavirin retreatment for chronic hepatitisC. BMC Infect Dis 7: 64.
8. World Journal of Gastroente WHO. Hepatitis B surface Ag assays; operational characteristics. Phase1.Report, World Health Organization 2004.
9. Seo HS, Park JS, Han KY, Bae KD, Ahn SJ, et al. (2008) Analysis and characterization of hepatitis B vaccine particles synthesized from Hansenulapolymorpha. Vaccine 26: 4138-4144.
10. World Health Organization fact sheets, Hepatitis C, World Health Organization.
11. Ataallah MT, Akram W, AL-Naaimi AS, Omer AR (2013) Epidemiology of viral hepatitis B and C in Ragi national survey 2005-2006. Zanco J Med Sci 17: 1.
12. Dasarathy S, Misra SC, Acharya SK, Irshad M, Joshi YK, et al. (1992) Prospective controlled study of post-transfusion hepatitis after cardiac surgery in a large referral hospital in India. Liver 12: 116-120.
13. Ameen R, Sanad N, Al-Shemmari S, Siddique I, Chowdhury RI, et al. (2005) Prevalence of viral markers among first-time Arab blood donors in Kuwait. Transfusion 45: 1973–1980.
14. Usman HR, Akhtar S, Rahbaqr MH, Hamid S, Moattar T, et al. (2003) Injection in health care set-tings: a risk factor for acute hepatitis B virus infec-tion in Karachi, Pakistan. Epidemol Infect 130: 293-300.
15. Awan Z, Idrees M, Rafique S, Rehman I, Akbar H, et al. (2010) Hepatitis B virus YMDD-motif mutations with emergence of lamivudine-resistant mutants: a threat to recovery. Gastroenterology Hepatology from  Bed to Bench 3: 108-114.
16. Akbar N, Basuki B, Mulyanto M, Garabrant DH, Sulaiman A, et al. (1997) Ethnicity, Socioeconomic status, Transfusions and risk of Hepatitis B and Hepatitis C infection. J Gastroenterol Hepatol 12: 752-757.
17. Alam MM, Zaidi SZ, Malik SA, Naeem A, Shau-kat S, et al. (2007) Serology based disease status of Pakistani population infected with Hepatitis B virus. BMC Infect Dis 7: 64.
18. Schriber GB, Busch MP, Kleinman SH, Korelitz JJ (1996) The risk of transfusion transmited viral infection .N Eng J med 334: 1685-1690.
19. Mahtab MA, Rahman S, Karim MF, Khan M, Foster G, et al. (2008) Epidemiology of hepatitis B virus in Bangladeshi general population. Hepatobiliary Pancreat Dis Int 7: 595-600.
20. Wasley A, Kruszon-Moran D, Kuhnert W, Simard EP, Finelli L, et al. (2010) The Prevalence of Hepatitis B Virus Infection in the United States in the Era of Vaccination. J Infect Dis 202: 192-201.
21. CDC Epidemiology & prevention of Vaccine preventable diseases-10 th edition.
22. National Center for Health Statistics. NHANES 1999-2004.
23. NHANES 1999–2000 addendum to the NHANES III analytic guidelines. Centers for Disease Control and Prevention. National Center for Health Statistics (NCHS).
24. EPI/General directorate of preventive medicine /Iraqi MoH,1993.
25. Mathers CD and Loncar D (2006) Projections of global mortality and burden of disease from 2002 to 2030. PLOS Medicine 3: 512.
26. Perz JF, Armstrong GL, Farrington LA, Hutin YJ, Bell BP (2006) The contributions of Hepatitis B virus and Hepatitis C virus infections to cirrhosis and primary liver cancer worldwide. J Hepatol 45: 529-538.
27. The growing threat of Hepatitis B and C in the Eastern Mediterranean region: a call for action.Regional office for Eastern  Mediterranean . WHO 2009: EM/RC56/3.
28. Ataallah TM, Hanan KA, Maysoun KS, Sadoon AA (2011) Prevalence of Hepatitis B and C among blood donors attending the National Blood Transfusion Center in Baghdad from 2006-2009 .Saudi Med J 32: 1046-1050 .
29. AL-Hammieary TK (2009) Seroepidemiology and molecular study of Hepatitis B virus in AL-Rusafa sector of Baghdad .Ph.D. Thesis. College of Science. University of Baghdad.
30. Alter MJ (2003) Epidemiology and prevention of Hepatitis B. Semin Liver Dis 23: 39-46.
31. Hussein AA (2008) Epidemiological study on prevalence of Hepatitis B virus among Baghdad population in 2007. AL-Faith Journal 37.
32. Omer AR and Thewaini AJ (1976) Hepatitis B surface antigen in the Iraqi population. Trans R Soc Trop Med Hyg 70: 527-528.
33. Al-Azawi A and Kadoori MS (1984) The state of blood donors in Iraq. Proceedings of the Second National Symposium on viral hepatitis 27-29 Oct. 1984. Bag.Iraq 78-29.
34. Al-Mashhadani JI (1998) Seroepidemiological study on HBV and HCV   infections among health care workers. Ph. D. thesis. College of Medicine. Baghdad University.
35. Skinhoj P and Al-Kassab S (1973) Letter: Hepatitis-B antigen in Iraq. Lancet 2: 1269.
36. Hussain SK (1976) A Seroepidemiological study of hepatitis B antigen in Iraqi army personnel. M. Sc. Thesis, 1976 ; College of Medicine. University of Baghdad.
37. Omer AR and Al-Dowri S (1984) Viral hepatitis in Iraq normal population. Proceedings of the 6th International congress of virology, Sendai-Japan pp32-36.
38. Omer AR and Al-Salmani AM (2007) Prevalence of Viral Hepatitis in Iraq. Research between Iraqi MOH (CDC) and WHO, (2006-2007). Not publish yet.
39. Weinbaum CM, Williams I, Mast EE, Wang SA, Finelli L, et al. (2008) Recommendations for identification and public health management of persons with chronic hepatitis B virus infection. MMWR Recomm Rep 57: 1-20.
40. Abbas A, AL-Kiali KK, Hasan AS  (2012) Is there any relationship between hepatitis C virus infection and skin diseases. Diyala J Med, 1: 51-56.
41. Al-Alwan AS, Omer AR, Al-Ani FS (1986) Prevalence of Hepatitis B surface antigen and anti-HBs in health care personal in Baghdad. Arb. J of Med, 5: 4-6.
42. Alawady NB (2014) The prevalence of Hepatitis C virus infections among Iraqi patients registered to Babylon center for inherited blood disorders. International J of Advanced Research,1: 383-388
43. Youssif  TH (1998) Immunological study of patients with chronic active Hepatitis B. Ph.D. Thesis. College of Medicine, University of Baghdad.
44. Al-Salmani AM (1987) Clinical and laboratory assessment of Hepatitis B surface antigen healthy carriers. M. Sc. thesis. College of Medicine, University of Baghdad.
45. Al-Waysi AA (2005) Effectiveness of interferon-alfa and lamivudine drugs in the treatment of chronic viral Hepatitis (B &C) among Iraqi patients. Ph.D. thesis. College of Medicine. Baghdad University.
46. Al-Jaaf AMA (2006) A study of Hepatitis B virus pre-core mutation among Iraqi chronic Hepatitis B patients treated with interferon Alfa. M. Sc. thesis. Council of genetic engineering and Biotechnology. University of Baghdad.
47. Janahi EM (2014) Prevalence and risk factors of hepatitis B virus infection in Bahrain, 2000 through 2010.   PLoS One 9: e87599.
48. Alavian SM, Keyvani H, Rezai M, Ashayeri N, Sadeghi HM (2006) Preliminary report of hepatitis B virus genotype prevalence in Iran.   World J Gastroenterol 12: 5211-5213.
49. André F (2000) Hepatitis B epidemiology in Asia, the Middle East and Africa. Vaccine 18: S20-S22.
50. van der Helm JJ, Prins M, del Amo J, Bucher HC, Chêne G, et al. (2011) The hepatitis C epidemic among HIV-positive MSM: incidence estimates from 1990 to 2007. AIDS, 25: 1083-1091.
51. Gasim GI, Murad IA, Adam I (2013) Hepatitis B and C virus infections among pregnant women in Arab and African countries.   J Infect Dev Ctries 7: 566-578.
52. Keeffe EB1, Dieterich DT, Han SH, Jacobson IM, Martin P, et al. (2004) A treatment algorithm for the management of chronic hepatitis B virus infection in the United States. Clin Gastroenterol Hepatol 2: 87-106.
53. Zhang HW, Yin JH, Li YT, Li CZ, Ren H, et al. (2008) Risk factors for acute hepatitis B and its progression to chronic hepatitis in Shanghai, China. Gut 57: 1713-1720.
54. Zhang Y, Fang W, et al. (2013) Hepatitis B surface antigen prevalence among 12-393 rural women of childbearing age in Hainan Province, China: a cross-sectional study. Virology Journal 10: 25.
55. Salleras L, Domínguez A, Bruguera M, Plans P, Espuñes J, et al. (2009) Seroepidemiology of hepatitis B virus infection in pregnant women in Catalonia (Spain). J Clin Virol 44: 329-332.
56. Elefsiniotis IS, Glynou I, Pantazis KD, Fotos NV, Magaziotou I, et al. (2005) Prevalence of chronic HBV infection among 13,581 women at reproductive age in Greece. A prospective single center study. J Clin Virol 32: 179-180.
57. Shrestha SM and Shrestha S (2012) Chronic hepatitis B in Nepal: an Asian country with low prevalence of HBV infection. Trop Gastroenterol 33: 95-101.
58. Hwang EW (2011) Cheung R. Global epidemiology of Hepatitis B virus (HBV). North American J Med Sci 4: 7-13.
59. Scaraveli NG, Passos AM, Voigt AR, Livramento Ad, Tonial G, et al. (2011) Seroprevalence of hepatitis B and hepatitis C markers in adolescents in Southern Brazil. Cad Saude Publica 27: 753-758.
60. Aquino JA, Pegado KA, Barros LP, Machado LF (2008) [Seroprevalence of hepatitis B virus and hepatitis C virus infections among individuals in the State of Pará]. Rev Soc Bras Med Trop 41: 334-337.
61. Bertolini DA, Pinho JR, Saraceni CP, Moreira RC, Granato CF, et al. (2006) Prevalence of serological markers of hepatitis B virus in pregnant women from Paraná State, Brazil. Braz J Med Biol Res 39: 1083-1090.
62. Rotermann M, Langlois K, Andonov A, Trubnikov M (2013) Seroprevalence of Hepatitis B and C virus infections: results from the 2007-2009 and to 2011 Canadian health measures survey. Health Reports 24: 3-13.
63. Geberemicheal A, Gelaw A, Moges F, Dagnew M (2013) Seroprevalence of Hepatitis B virus infections among health care workers at the Bulle Hora Woreda Governmental health institutions, Southern Oromia, Ethiopia.J Environ Occup 2: 9-14.
64. Sood S and Malvankar S (2010) Seroprevalence of Hepatitis B surface antige, antibodies to the Hepatitis C virus, and human immunodeficiency virus in a hospital-based population in Jaipur, Rajasthan. Indian J. Community Med 35: 165-169.
65. Jafri W, Jafri N, Yakoob J, Islam M, Tirmizi SF, et al. (2006) Hepatitis B and C: prevalence and risk factors associated with seropositivity among children in Karachi, Pakistan. BMC Infect Dis 6: 101.
66. Hartleb M, Gutkowski K, Zejda JE, Chudek J, WiÄ™cek A (2012) Serological prevalence of Hepatitis B virus and C virus infection in the elderly populating  :Polish nationwide survey-Pol Senior. Eur J Gastroenterol Hepatol 24: 1288-1295.
67. Xia GL, Liu CB, Cao HL, Qi XQ (1995) Prevalence Hepatitis B in the general Chinese population: result from a nationwide cross-sectional seroepidemiologic study of Hepatitis A,B,C,D, and E virus infections in China, 1992. International Hepatology Communications 5: 62-73.
68. Sheikh MY, Mouanoutoua M, Walvick MD, Khang L, Singh J, et al. (2011) Prevalence of hepatitis B virus (HBV) infection among Hmong immigrants in the San Joaquin Valley. J Community Health 36: 42-46.
69. Hahné SJ, Veldhuijzen IK, Wiessing L, Lim TA, Salminen M, et al. (2013) Infection with hepatitis B and C virus in Europe: a systematic review of prevalence and cost-effectiveness of screening.   BMC Infect Dis 13: 181.
70. Meffre C, Le Strat Y, Delarocque-Astagneau E, Dubois F, Antona D, et al. (2010) prevalence of Hepatitis B and Hepatitis C virus infections in France in 2004: social factors are important predictors after adjusting for know risk factors. J Med viral 82: 546-555.
71. Toy M, Önder FO, Wörmann T, Bozdayi AM, Schalm SW, et al. (2011) Age- and region-specific Hepatitis B prevalence in Turkey estimated using generalized linear mixed models a systematic review. BMC infect Dis 11: 337.
72. Chu JJ, Wörmann T, Popp J, Pätzelt G, Akmatov MK, et al. (2013) Changing epidemiology of hepatitis B and migration--a comparison of six Northern and North-Western European countries. Eur J Public Health 23: 642-647.
73. Ott JJ, Stevens GA, Groeger J, Wiersma ST (2012) Global epidemiology of hepatitis B virus infection: new estimates of age-specific HBsAg seroprevalence and endemicity. Vaccine 30: 2212-2219.
74. Custer B, Sullivan SD, Hazlet TK, Iloeje U, Veenstra DL, et al. (2004) Global epidemiology of hepatitis B virus.   J Clin Gastroenterol 38: S158-168.
75. Goudeau A (1990) Epidemiology and eradication strategy for hepatitis B in Europe. The European Regional Study Group.   Vaccine 8: S113-116.
76. Magdzik WW (2000) Hepatitis B epidemiology in Poland, Central and Eastern Europe and the newly independent states.   Vaccine 18: S13-16.
77. Affas BB (1988) Hematopatholgical changes in liver disease. M. Sc. Thesis, College of Medicine, University of Baghdad.
78. Wasley A, Kruszon-Moran D, Kuhnert W, Simard EP, Finelli L, et al. (2010) The prevalence of hepatitis B virus infection in the United States in the era of vaccination.   J Infect Dis 202: 192-201.
79. Shrestha MS (1987) Seroepidemiology of viral Hepatitis in Surkhet,Nepal.J Inst Med 9: 1-10.
80. Abebe A, Nokes DJ, Dejene A, Enquselassie F, Messele T, et al. (2003) Seroepidemiology of hepatitis B virus in Addis Ababa, Ethiopia: transmission patterns and vaccine control. Epidemiol Infect 131: 757-770.
81. WHO. The Hepatitis B virus. 2002 ;WHO/CDS/CSR/LYO/2002.2: Hepatitis B.. html (last accessed 15 July 2010).
82. Deinhardt F, Gust ID (1982) Viral hepatitis.   Bull World Health Organ 60: 661-691.
83. Hou J, Schilling R, Janssen HLA, Luo K, Liu D, et al. (2005) Genetic characteristics of hepatitis B virus and response to interferon-alfa treatment. Int J Med Sci 2: 50-57.
84. Chowdhury A (2004) Epidemiology of Hepatitis B virus infection in India. Hep B Annual 1: 17-24.
85. El-Sawy IH and Mohamed ON (1999) Long-term immunogenicity and efficacy of a recombinant hepatitis B vaccine in Egyptian children. East Mediterr Health J 5: 922-932.
86. El Shahat YI, Varma S, Bari MZ, Shah Nawaz M, Abdulrahman S, et al. (1995) Hepatitis C virus infection among dialysis patients in United arab emirates.   Saudi J Kidney Dis Transpl 6: 157-162.
87.  Al-Faleh FZ, Al-Jeffri M, Ramia S, Al-Rashed R, Arif M, et al. (1999) Seroepidemiology of hepatitis B virus infection in Saudi children 8 years after a mass hepatitis B vaccination programme. J Infect 38: 167-170.