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.