Mathematical models of the interrelated dynamics of hepatitis D and B
被引:16
作者:
Packer, Aaron
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机构:
Arizona State Univ, Sch Math & Stat Sci, Tempe, AZ 85287 USAArizona State Univ, Sch Math & Stat Sci, Tempe, AZ 85287 USA
Packer, Aaron
[1
]
Forde, Jonathan
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Hobart & William Smith Coll, Dept Math & Comp Sci, Geneva, NY 14456 USAArizona State Univ, Sch Math & Stat Sci, Tempe, AZ 85287 USA
Forde, Jonathan
[2
]
Hews, Sarah
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机构:
Hampshire Coll, Sch Nat Sci, Amherst, MA 01002 USAArizona State Univ, Sch Math & Stat Sci, Tempe, AZ 85287 USA
Hews, Sarah
[3
]
Kuang, Yang
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Arizona State Univ, Sch Math & Stat Sci, Tempe, AZ 85287 USA
King Abdulaziz Univ, Dept Math, Jeddah 21589, Saudi ArabiaArizona State Univ, Sch Math & Stat Sci, Tempe, AZ 85287 USA
Kuang, Yang
[1
,4
]
机构:
[1] Arizona State Univ, Sch Math & Stat Sci, Tempe, AZ 85287 USA
[2] Hobart & William Smith Coll, Dept Math & Comp Sci, Geneva, NY 14456 USA
[3] Hampshire Coll, Sch Nat Sci, Amherst, MA 01002 USA
[4] King Abdulaziz Univ, Dept Math, Jeddah 21589, Saudi Arabia
The hepatitis delta virus (HDV) is a rarest form of viral hepatitis, but has the worst outcomes for patients. It is a subviral satellite dependent on coinfection with hepatitis B (HBV) to replicate within the host liver. To date, there has been little to no modeling effort for HDV. Deriving and analyzing such a mathematical model poses difficulty as it requires the inclusion of (HBV). Here we begin with a well-studied HBV model from the literature and expand it to incorporate HDV. We investigate two models, one with and one without infected hepatocyte replication. Additionally, we consider treatment by the drug lamivudine. Comparison of model simulations with experimental results of lamivudine treatment indicate that infected cell proliferation may play a significant role in chronic HDV infection. Our results also shed light on several questions surrounding HDV and illustrate the need for more data. (C) 2013 Elsevier Inc. All rights reserved.