Abstract
Objectives:This study was aimed at exploring the effects of hepatitis B envelope antigen (HBeAg) status on the cellular immune function of patients with hepatitis B virus/treponema pallidum (HBV/TP) co-infection.Methods:The clinical data of 79 patients with HBV/TP co-infection admitted to our hospital from January 2019 to January 2020 were retrospectively analyzed. These patients were divided into two groups according to the different HBeAg statuses before the treatment: 41 HBeAg+ patients were included in the HBeAg+ group, while 38 HBeAg- patients were included in the HBeAg- group. The levels of HBV-DNA, T lymphocyte subsets represented by NK cells and cytokines associated with T cells in the peripheral blood (PB) of the patients were compared between both groups.Results:The HBV-DNA levels in the HBeAg+ group were significantly higher than those in the HBeAg- group (P < 0.05). The levels of CD3+, CD4+, CD4+/CD8+ and natural killer (NK) cells in the HBeAg+ group were higher than those in the HBeAg- group (P < 0.05), while the levels of CD8+ cells were lower than those in the HBeAg- group (P < 0.05). Moreover, the levels of interferon-γ (IFN-γ), tumor necrosis factor (TNF-α), interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-17 (IL-17), transforming growth factor-β (TGF-β) in the HBeAg+ group were all significantly higher than those in the HBeAg- group (P < 0.05), but there was no significant difference in the levels of interleukin-4 (IL-4) and interleukin-10 (IL-10) between the HBeAg+ group and the HBeAg- group (P > 0.05).Conclusion:HBeAg+ can increase the HBV-DNA levels in the PB of patients with HBV/TP co-infection, in turn triggering the body to initiate cellular immunity, increasing the levels of T lymphocyte subsets, and promote the secretion of cytokines.
Highlights
Chronic hepatitis B (CHB) is a transmissible disease that arise out of hepatitis B virus (HBV) infection.[1]
Studies have shown that HBV can produce inhibitory monocytes, initiate the regulation of natural killer (NK) cell differentiation, and induce NK cells to produce IL-10.4 Hepatitis B envelope antigen (HBeAg) is a viral protein released from liver cells into the blood during HBV replication by the pre-core regions and core regions of the virus genes
These patients were divided into two groups according to their HBeAg statuses before the treatment: 41 HBeAg+ patients were included in the HBeAg+ group, while 38 HBeAgpatients were included in the HBeAg- group
Summary
Chronic hepatitis B (CHB) is a transmissible disease that arise out of hepatitis B virus (HBV) infection.[1]. Pak J Med Sci November - December 2021 Vol 37 No 7 www.pjms.org.pk 1871 the body, injuring and damaging liver cells In this process, cellular immunity mediated by T lymphocyte subsets and relevant cytokines plays a key role.[3] Studies have shown that HBV can produce inhibitory monocytes, initiate the regulation of NK cell differentiation, and induce NK cells to produce IL-10.4 Hepatitis B envelope antigen (HBeAg) is a viral protein released from liver cells into the blood during HBV replication by the pre-core regions and core regions of the virus genes. HBeAg+ indicates active replication of HBV.[5] Relevant studies have shown that, pretreatment HBeAg status can affect the long-term antiviral effect of patients with HIV/HBV coinfection.[6] whether HBeAg status can affect the cellular immune function of patients with HBV/TP co-infection still needs further exploration. The clinical data of 79 patients with HBV/TP co-infection were reviewed, after which the effects of different HBeAg statuses on the cellular immune function of patients with HBV/TP co-infection were explored and reported
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