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Author Spotlight: Advancements and Challenges in Hepatitis B Virus Detection
Published on: December 15, 2023
Optimization of the algorithm diagnosis chronic hepatitis B markers in patients with newly diagnosed HIV infection
A V Semenov1,2,3, Yu V Ostankova1, E N Serikova1
1Saint-Petersburg Pasteur Institute.
Insights
Diagnosing chronic hepatitis B in HIV patients requires updated lab methods. Detecting occult hepatitis B virus (HBV) in co-infected individuals is crucial for effective treatment and managing complications.
Area of Science:
- Hepatology
- Virology
- Infectious Diseases
Background:
- Hepatitis B virus (HBV) and human immunodeficiency virus (HIV) co-infection is common.
- Standard laboratory diagnostics for chronic hepatitis B (CHB) may be insufficient in HIV-infected individuals.
- Occult HBV infection, characterized by the absence of HBsAg, poses diagnostic challenges.
Purpose of the Study:
- To analyze the possibility of modifying laboratory diagnostic algorithms for CHB in newly diagnosed HIV patients.
- To evaluate the prevalence of HBV infection and its genetic characteristics in this population.
- To assess the utility of detecting occult HBV infection for optimizing anti-HBV therapy.
Main Methods:
- Analysis of plasma samples from 196 HIV-infected patients in the Northwestern Federal District.
- Serological testing for HBV markers (HBsAg, anti-HBcore IgG, anti-HBe IgG, anti-HBs IgG).
- HBV DNA detection using a commercial kit and a newly developed method.
- Genotyping and subtyping of HBV.
- Detection of mutations in HBV genes (RT, S, Core, Precore regions), including drug resistance and vaccine escape mutations.
Main Results:
- Serological HBV markers were present in 79.6% of patients, with HBsAg detected in only 5.6%.
- The newly developed method detected HBV DNA in 18.36% of HIV-infected individuals, including 12.75% with HBsAg-negative (occult) infection.
- HBV genotype D (91.7%) predominated, with specific subgenotype distributions.
- High prevalence of mutations in HBV genes (RT, S, Core, Precore regions) was observed.
- Drug resistance mutations (to lamivudine, entecavir, telbivudine, tenofovir) and vaccine escape mutations were detected in significant proportions of patients.
- The double mutation A1762T/G1764A and G1896A were identified in the basal nucleus promoter, Precore, and Core regions.
Conclusions:
- Current CHB laboratory diagnostic algorithms need modification for HIV-infected individuals.
- Detection of occult HBV infection is essential for accurate diagnosis and management.
- The high prevalence of mutations, including drug resistance and vaccine escape variants, highlights the need for early genetic analysis.
- Integrating occult HBV detection into diagnostic algorithms can reduce the burden of HIV/HBV co-infection and guide appropriate anti-HBV therapy.
Abstract:
The possibility of modifying the algorithms for chronic viral hepatitis B laboratory diagnosis in individuals with newly diagnosed HIV infection is analyzed. Plasma samples were used from 196 patients residing in the Northwestern Federal District. Serological HBV markers were found in 79.6% of cases. However, HBsAg was detected in 5.6% of patients. Anti-HBcore IgG antibodies are found in 62.24% of cases, anti-HBe IgG antibodies in 27.55%, anti-HBs IgG antibodies in 52.55% of cases. Using a commercial kit with a 100 IU / ml sensitivity, HBV DNA was detected in 4.6% of patients, that is, 81.8% of HBsAg-positive individuals. Using the method developed by us, HBV DNA was found in 18.36% of HIV-infected individuals, including 12.75% of cases was HBsAg-negative (latent) disease form. In the examined group, HBV of genotype D prevailed (91.7%), genotype A was detected in 8.3% of cases. The distribution of subgenotypes is presented in the following ratios: D2 - 55.6%, D1 - 22.2%, D3 - 13.9%, A2 - 8.3%. Mutations were detected in the reverse transcriptase (RT) region in 91.6% of patients, in the SHB region in 83.3%, in the Core and Precore regions in 72.2% and in 27.7% of patients, respectively. Three HBV isolates (8.3%) were identified with drug resistance mutations to lamivudine, entericavir, telbivudine and tenofovir, which are amino acid substitutions in the HBV polymerase gene at positions L180M, T184A, M204V. Vaccine escape mutations were detected in 61.1% of patients. In all samples with drug resistance mutations, escape-mutants were simultaneously present. When analyzing the basal nucleus promoter, Precore and Core regions, 22.2% of patients with the double mutation A1762T / G1764A, 25% with the mutation G1896A were identified. In one person, all three substitutions were found. In the Core region, 77.7% of patients showed mutations in one of the hot spots (codons 87, 97, 112, and 130 substitution), which can play a role in immunomodulation in CHB. Analysis of the HBV genetic structure, mutations detection early in the virus in patients with HBV can help predict the clinical course and disease progression, and ART complications. To reduce the HIV HBV co-infection burden and to appointer anti-HBV therapy, it is necessary to introduce detection the occult HBV to modify the algorithm for CHB laboratory diagnosis.

