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Purpose <p>Occult hepatitis B infection (OBI) can sustain residual transfusion risk because HBV DNA may persist at very low levels while HBsAg remains undetectable by routine serology. We assessed OBI among anti-HBc–reactive, HBsAg-negative (anti-HBc+/HBsAg−) donors in Bucaramanga, Colombia and characterized small-S variation within genotype F3.</p> Methods <p>In 2021, we analyzed 61,188 donations in three licensed blood banks using routine serology. From anti-HBc+/HBsAg− donations, 219 randomly selected sera underwent nested PCR targeting the small-S/reverse-transcriptase overlap, followed by Sanger sequencing. Genotyping and phylogeny used a curated 960-nt small-S fragment. Associations with OBI were estimated by logistic regression.</p> Results <p>HBsAg reactivity was 0.21% and anti-HBc prevalence was 1.77%. OBI occurred in 16/219 anti-HBc+/HBsAg− donations (7.3%; 95% CI, 4.5–11.5), approximately 130 per 100,000 donations (95% CI, 80–204). Among the 16 OBI cases, 12 were anti-HBs reactive. Sex, age, and anti-HBs were not associated with OBI after adjustment. All sequences clustered within genotype F3. Small-S amino acid variation at positions previously linked to altered HBsAg detectability was observed in 11/16 (68.8%): A166G (5/16) outside “a”; “a” substitutions L127R, K141N, N146Y, C147S; variants at the pre-“a” boundary K122R/T123A; loop-proximal cysteine changes C149S/C149F and S117C; stop codons W156 and L216*; additional MHR changes included V106D, T118S, I150V, P151R, I152S, K160I.</p> Conclusions <p>All OBI cases belonged to genotype F3 and showed small-S variants at positions previously associated with HBsAg detectability, which may contribute to reduced detection rather than classical antigenic escape. Among anti-HBc+/HBsAg− donations, targeted NAT identified donors with detectable HBV DNA within this serologic profile that routine screening alone could not resolve, indicating a residual risk that may be reduced through selective NAT where universal implementation is not feasible.</p>

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Occult HBV among anti-HBc–reactive blood donors in Colombia: low HBsAg prevalence, genotype F3, and small-S variation relevant to HBsAg detectability

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月9日

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  • Henry Bautista-Amorocho,
  • Jorge Alexander Silva-Sayago,
  • Yeny Zulay Castellanos-Domínguez

摘要

Purpose

Occult hepatitis B infection (OBI) can sustain residual transfusion risk because HBV DNA may persist at very low levels while HBsAg remains undetectable by routine serology. We assessed OBI among anti-HBc–reactive, HBsAg-negative (anti-HBc+/HBsAg−) donors in Bucaramanga, Colombia and characterized small-S variation within genotype F3.

Methods

In 2021, we analyzed 61,188 donations in three licensed blood banks using routine serology. From anti-HBc+/HBsAg− donations, 219 randomly selected sera underwent nested PCR targeting the small-S/reverse-transcriptase overlap, followed by Sanger sequencing. Genotyping and phylogeny used a curated 960-nt small-S fragment. Associations with OBI were estimated by logistic regression.

Results

HBsAg reactivity was 0.21% and anti-HBc prevalence was 1.77%. OBI occurred in 16/219 anti-HBc+/HBsAg− donations (7.3%; 95% CI, 4.5–11.5), approximately 130 per 100,000 donations (95% CI, 80–204). Among the 16 OBI cases, 12 were anti-HBs reactive. Sex, age, and anti-HBs were not associated with OBI after adjustment. All sequences clustered within genotype F3. Small-S amino acid variation at positions previously linked to altered HBsAg detectability was observed in 11/16 (68.8%): A166G (5/16) outside “a”; “a” substitutions L127R, K141N, N146Y, C147S; variants at the pre-“a” boundary K122R/T123A; loop-proximal cysteine changes C149S/C149F and S117C; stop codons W156 and L216*; additional MHR changes included V106D, T118S, I150V, P151R, I152S, K160I.

Conclusions

All OBI cases belonged to genotype F3 and showed small-S variants at positions previously associated with HBsAg detectability, which may contribute to reduced detection rather than classical antigenic escape. Among anti-HBc+/HBsAg− donations, targeted NAT identified donors with detectable HBV DNA within this serologic profile that routine screening alone could not resolve, indicating a residual risk that may be reduced through selective NAT where universal implementation is not feasible.