Many Ways to Communicate—Crosstalk between the HBV-Infected Cell and Its Environment

Abstract

Chronic infection with the hepatitis B virus (HBV) affects an estimated 257 million people worldwide and can lead to liver diseases such as cirrhosis and liver cancer. Viral replication is generally considered not to be cytopathic, and although some HBV proteins may have direct carcinogenic effects, the majority of HBV infection-related disease is related to chronic inflammation resulting from disrupted antiviral responses and aberrant innate immune reactions. Like all cells, healthy and HBV-infected cells communicate with each other, as well as with other cell types, such as innate and adaptive immune cells. They do so by both interacting directly and by secreting factors into their environment. Such factors may be small molecules, such as metabolites, single viral proteins or host proteins, but can also be more complex, such as virions, protein complexes, and extracellular vesicles. The latter are small, membrane-enclosed vesicles that are exchanged between cells, and have recently gained a lot of attention for their potential to mediate complex communication and their potential for therapeutic repurposing. Here, we review how HBV infection affects the communication between HBV-infected cells and cells in their environment. We discuss the impact of these interactions on viral persistence in chronic infection, as well as their relation to HBV infection-related pathology.

Serum ApoB/ApoA1 ratio in patients with CHB and the occurrence of HBV related cirrhosis and HBV related hepatocellular carcinoma

“…HBV can modulate ApoA1 function through HBx, leading to ApoA1 dysfunction (e.g., decreased self-association ability, elevated carbonyl levels, as well as impaired lipid binding ability 20 , 21 ). Epigenetic silencing of ApoA1 gene expression by CpG island DNA hypermethylation induced by HBV can also reduce serum ApoA1 level 39 . HBV suppresses ApoB production by inhibiting microsomal triglyceride transfer protein expression 24 , overexpression of HBx leads to negative regulation of microsomal TG transfer proteins, which can increase the expression of β-d-mannoside-1, 4-N-acetylglucosaminyl transferase-III, and cause inhibition of ApoB secretion and intracellular accumulation of TG and TCh 40 .…”

Efficacy and safety of regorafenib as a first-line agent alone or in combination with an immune checkpoint inhibitor for advanced hepatocellular carcinoma: a retrospective cohort study

“…Hepatocellular carcinoma (HCC) is the 5th and 7th most common cancer and the 2nd and 6th leading cause of cancer deaths worldwide in adult men and women, respectively ( 1 , 2 ). Hepatitis B virus (HBV) and hepatitis C virus (HCV) cause 60% and 33% of HCCs, respectively, in developing countries, compared to 23% and 20% in developed countries ( 3 , 4 ).…”

Gut Microbiota Dysbiosis, Immunological Response And The Performance Of Non-Invasive Models For Assessing Liver Fibrosis In Patients With Chronic Hepatitis B Virus

“…Prompt diagnosis and treatment of chronic hepatitis B (CHB) disease are significant for the avoidance of complications such as liver fibrosis, cirrhosis and hepatocellular cancer (Kaya et al, 2023). The host immune response is not only essential to control the spread of virus infection, but it is also responsible for the inflammatory events causing liver pathologies (Walter et al, 2022, Lopez-Scarim et al, 2023, Nevola et al, 2023. C-reactive protein-toalbumin ratio (CAR), aspartate-to-platelet ratio index (APRI) and Globulin-to-platelet ratio index (GPI) are noninvasive models derived from simple routine laboratory tests used in the evaluation of liver fibrosis in patients with chronic hepatitis B virus infection with reference to liver biopsy: the gold standard for detecting and grading liver fibrosis (Huang et al, 2017).…”