Optimization of the algorithm diagnosis chronic hepatitis B markers in patients with newly diagnosed HIV infection

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.