Viral hepatitis refers to liver inflammation caused by five distinct viruses (hepatitis A, B, C, D, and E), each characterized by different modes of transmission and disease outcomes [1]. Among them, hepatitis B virus (HBV) infection represents a major global public health concern [2]. It is estimated that approximately 2 billion people worldwide have been infected with HBV at some point in their lives, and about 296 million are living with chronic HBV infection. Each year, 1.5 million new infections occur, and without appropriate treatment, chronically infected individuals remain at high risk of developing severe liver complications such as cirrhosis and hepatocellular carcinoma (HCC) [3][4].

An individual is considered infected with HBV when the virus is demonstrably present in the body, either through the detection of hepatitis B surface antigen (HBsAg) or through the direct identification of HBV DNA in the bloodstream (viral load), regardless of whether the infection is acute, chronic, occult, or mutant. In addition, during the course of infection, biochemical and hematological parameters must also be assessed to ensure optimal patient monitoring.

Sub-Saharan Africa is classified as a region of high endemicity, with an estimated 65 million chronic carriers and approximately 56,000 HBV-related deaths annually [5][6]. The burden is particularly high among young adults, many of whom acquire the infection perinatally or during early childhood, leading to a high likelihood of chronicity [7].

The liver plays a central role in systemic homeostasis through the activity of hepatocytes, which synthesize most plasma proteins, including albumin, hemoglobin-associated globins, immunoglobulins, and clotting factors [8]. It is also one of the main detoxifying organs, protecting bone marrow function by eliminating toxic byproducts [9]. Consequently, hepatic dysfunction due to viral infections may lead to alterations in hematological parameters, including red blood cell indices, leukocyte counts, and platelet levels [10][11].

Despite this potential link, the impact of HBV infection on hematological indices remains insufficiently explored, particularly in African settings where HBV prevalence is high. Previous studies have reported varying degrees of anemia, leukopenia, neutropenia, lymphopenia, and thrombocytopenia in HBV-infected individuals, but findings remain inconsistent across populations [12]-[14].

Liver dysfunction associated with HBV infection can lead to hematological alterations through several well-established mechanisms. Impaired hepatic function reduces the production of key regulatory factors such as thrombopoietin, resulting in decreased platelet synthesis. In addition, progressive liver injury may lead to portal hypertension, which in turn causes splenomegaly and hypersplenism, promoting increased sequestration and destruction of blood cells. These pathophysiological processes provide a strong biological rationale for investigating hematological parameters in HBV-infected patients.

The present study was therefore designed to evaluate hematological parameters in patients with HBV infection compared with HBsAg-negative controls at the Mother and Child University Hospital—Jeanne Ebori Foundation in Libreville, Gabon. Specifically, the study aimed to characterize hematological parameters in HBV-infected and non-infected individuals and to compare variations in key hematological indices between the two groups.

The present study aimed to evaluate hematological parameters in patients with hepatitis B virus (HBV) infection compared with HBsAg-negative controls. A total of 150 patients were included, with a predominance of women (72%). This female predominance was expected, since the study was conducted in a mother-and-child university hospital, whose main mission is maternal and child health care. Interestingly, among HBsAg-positive individuals, women were more frequently represented, which contrasts with previous findings by Ahmad et al. [14], Boungou [18], and Ag Mohamed [2], who reported that men are usually more affected by HBV infection. This difference is most likely due to the demographic profile of our study population, where women were overrepresented.

The mean age of HBV-infected patients was 34 ± 2 years, which is consistent with findings from Diallo et al. [5] in Senegal (mean age 33 years, range 14 - 83 years) and Ag Mohamed [2] (mean age 32.9 years, range 12 - 72 years). In our cohort, the most affected age group was 32 - 43 years, especially among men, which aligns with previous reports indicating that HBV infection primarily affects young adults [1]-[3][5]. This observation is not surprising, as HBV is mainly transmitted through sexual contact, and this age group corresponds to the sexually active population. Similar data were also reported by Kolawole et al. [19], who identified the 30 - 34 years group as the most affected.

Regarding hematological parameters, HBV infection did not appear to significantly alter hemoglobin concentration, mean corpuscular volume (MCV), or mean corpuscular hemoglobin concentration (MCHC). Normochromia was observed in the majority of patients in both groups (92% in HBsAg-positive vs. 84% in HBsAg-negative). These findings are consistent with Francisca et al. [13], who reported no significant changes in red blood cell counts or indices in HBV-infected patients. However, 37% of HBV-infected patients in our study presented with anemia, while 12% had microcytosis and 8% hypochromia. Although we do not have all the parameters to define the viral infection status of our patients (acute or chronic hepatitis), according to the literature, it is known that chronic HBV infection can lead to hepatic complications, such as cirrhosis and hepatocellular carcinoma, which may impair the liver’s role in erythropoiesis and contribute to anemia [20][21]. Indeed, anemia is a well-documented complication of advanced liver disease.

With regard to white blood cell (WBC) counts, most patients in both groups exhibited normal values (81% in HBsAg-positive vs. 79% in HBsAg-negative). Nevertheless, leukopenia was more frequent in HBV-infected patients (8 cases) compared with controls (2 cases). Given that WBCs play a central role in the immune response by targeting and destroying HBV-infected hepatocytes, their reduction during viral infection is not unexpected. Our results partially diverge from those of Ahmad et al. [14], who found no significant differences in total WBC counts. Moreover, neutropenia and lymphopenia were more frequent among HBV-infected individuals (11 vs. 6 for neutrophils; 15 vs. 6 for lymphocytes). HBV infection may impair leukopoiesis, leading to reduced neutrophil and lymphocyte counts. Neutrophils are the first line of defense against pathogens, mainly through phagocytosis, while lymphocytes recognize and attack HBV-infected hepatocytes. Thus, the observed cytopenias may reflect immune system exhaustion or viral-induced suppression. These findings are in agreement with Ahmad et al. [14], who reported lymphocyte depletion in HBV patients, and Kayhan et al. [9], who observed neutropenia in chronic HBV infection.

Thrombocytopenia was also more common in HBV-infected patients (22 cases) compared with controls (14 cases). Thrombocytopenia is a well-recognized hematological abnormality associated with chronic liver disease and HBV infection [22][23]. The main mechanisms proposed include increased platelet destruction, peripheral sequestration, and hypersplenism secondary to portal hypertension [22].

Taken together, our findings suggest that HBV infection does not substantially impact red blood cell indices (hemoglobin, MCV, and MCHC) but is associated with a higher prevalence of anemia, leukopenia (particularly neutropenia and lymphopenia), and thrombocytopenia. These abnormalities may result from both direct viral effects and secondary complications of chronic liver disease.

In this study, most hematological parameters did not differ significantly between HBsAg-positive patients and HBsAg-negative controls. Hemoglobin levels, MCV, MCHC, and platelet counts showed comparable distributions between the two groups, suggesting that HBV infection alone may not substantially alter these parameters in asymptomatic or early-stage individuals. These findings are consistent with reports indicating that hematological abnormalities in HBV infection often emerge only in advanced disease stages, during hepatic decompensation, or in the presence of associated conditions such as hypersplenism or bone marrow suppression.

However, a significant difference was observed in total white blood cell count (WBC) (p = 0.042). This finding may reflect an inflammatory or immunological imbalance associated with active viral infection. HBV is known to interact with the host immune system, particularly through antiviral T-cell responses, cytokine activation, and liver-mediated immunomodulation, which may influence circulating leukocyte profiles. An altered WBC distribution in HBsAg-positive individuals could indicate early immune activation even in the absence of clinical symptoms.

This observation highlights the potential value of incorporating inflammatory markers—such as the neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR)—into routine evaluation of HBV-infected patients. These ratios have emerged as inexpensive, accessible indicators of systemic inflammation and may complement standard hematological parameters. Further studies integrating NLR, PLR, and biochemical markers (ALT, AST, bilirubin) could provide a more complete picture of disease activity and help identify early alterations associated with hepatic or bone marrow involvement.

A limitation of this study was the lack of detailed clinical information on the patients, such as liver disease stage, treatment history, and comorbidities, which could have influenced hematological outcomes. Further studies including larger cohorts and additional clinical parameters are warranted to clarify the mechanisms underlying hematological alterations in HBV infection. In addition, the absence of key virological and biochemical data, such as HBV DNA levels, HBeAg status, and liver enzyme measurements (ALT/AST), also constitutes a limitation in our study due to the retrospective nature of our study.

HBV infection appears to influence hematological parameters, particularly reducing leukocyte and platelet counts. These findings highlight the importance of monitoring hematological indices in HBV-infected patients, both for clinical management and for understanding virus-host interactions. Expanded studies are needed to investigate hematological ratios (NLR, PLR) and their prognostic relevance in HBV-related disease.

This work was supported by CHU Mère Enfant Fondation Jeanne EBORI.

Prior to enrollment, informed consent was obtained from each participant and written informed consent has been obtained from the patients to publish this paper. Women identified with HBV infection were referred to a hepatologist for appropriate medical management.

The datasets generated and/or analyzed during the current study are available from the corresponding author on reasonable request.

*VTMM and ASAE contributed equally.

^#Corresponding author.