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TIGP -- Quasispecies Reset After Hepatitis B Virus (HBV) Transmission and its Implications on Long Term Evolution

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TIGP -- Quasispecies Reset After Hepatitis B Virus (HBV) Transmission and its Implications on Long Term Evolution

  • 講者王弘毅 教授 (國立台灣大學)
    邀請人:TIGP Bioinformatics Program
  • 時間2013-06-06 (Thu.) 14:00 ~ 15:10
  • 地點資訊所新館106演講廳
摘要

The lack of correlation between time of separation and sequence divergence of hepatitis B virus (HBV) has been shown in many previous studies. We hypothesize that this lack of correlation is partly due to limited host immune response to HBV during immune tolerance phase if acquired perinatally. Most variation observed at relative late stage of infection, e.g. after immune clearance phase, within HBV donors would not be transmitted or be outcompeted by viral strains with high replicative ability in recipients during immune tolerance phase. In other words, after motherto-infant transmission, the viral quasi-species “reset” to wild-type like sequences and most of mutations accumulated in previous host are lost. The “reset” hypothesis predicts that, for a given time, genetic distance of HBV between individuals would be negatively correlated with the number of mother-to-infant transmission. In addition, this negative correlation is mainly due to amino-acid altering instead of silent changes as the former may have stronger fitness consequences than the latter. To test this hypothesis, we selected a family of three generations including one grandmother, five siblings, and two granddaughters. All family members were presumably acquired HBV via perinatal transmission. For each patient, serial serum samples were collected and multiple full-length HBV sequences were recovered. As previous studies have shown, the correlation between HBV divergence and time of separation was limited. Nevertheless, our data showed significant negative correlation between HBV sequence divergence and number of transmission. Further analysis revealed that this negative correlation is due to amino acid altering rather than silent mutations, suggesting that different selection regimes among hosts play an important role in shaping long-term evolutionary dynamic of HBV.