AI Article Synopsis
- The study investigates how the host immune system affects the genetic variability of the hepatitis B virus (HBV), focusing on patients with different stages of infection.
- It analyzes DNA samples from 113 individuals to evaluate HBV genetic diversity, resistance to antiviral drugs, and mutations that help the virus evade detection by the immune system.
- Results show that most patients carry genotype A HBV and that those with lower viral loads exhibit higher genetic diversity, indicating they face greater selective pressure from the immune response.
Article Abstract
The selection pressure imposed by the host immune system impacts on hepatitis B virus (HBV) variability. This study evaluates HBV genetic diversity, nucleos(t)ide analogs resistance and HBsAg escape mutations in HBV patients under distinct selective pressures. One hundred and thirteen individuals in different phases of HBV infection were included: 13 HBeAg-positive chronic infection, 9 HBeAg-positive chronic hepatitis, 47 HBeAg-negative chronic infection (ENI), 29 HBeAg-negative chronic hepatitis (ENH) and 15 acute infected individuals. Samples were PCR amplified, sequenced and genetically analyzed for the overlapping POL/S genes. Most HBV carriers presented genotype A (84/113; 74.3%), subgenotype A1 (67/84; 79.7%), irrespective of group, followed by genotypes D (20/113; 17.7%), F (8/113; 7.1%) and E (1/113; 0.9%). Clinically relevant mutations in polymerase (tL180M/M204V) and in the Major Hydrophilic Region of HBsAg (sY100C, T118A/M, sM133T, sD144A and sG145R) were observed. Our findings, however, indicated that most polymorphic sites were located in the cytosolic loops (CYL1-2) and transmembrane domain 4 (TMD4) of HBsAg. Lower viral loads and higher HBV genetic diversity were observed in ENI and ENH groups (p < 0.001), suggesting that these groups are subjected to a higher selective pressure. Our results provide information on the molecular characteristics of HBV in a diverse clinical setting, and may guide future studies on the balance of HBV quasispecies at different stages of infection.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11087654 | PMC |
| http://dx.doi.org/10.1038/s41598-024-60900-2 | DOI Listing |
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