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Drug-resistant and immune-escape HBV mutants in HIV-infected hosts.

Abstract：

:HIV-HBV-coinfected patients require optimal control of viral replication in order to prevent the development of severe comorbidities, such as liver cirrhosis and hepatocellular carcinoma. The genetic diversity of HBV is a poorly investigated factor of such viral replication in HIV-infected hosts. HBV genome diversity can be differentiated into two major aspects: genotypic and phenotypic. Genotypic diversity is more related to the natural history of HBV infection and genotypes are mostly determined by geographical origin of the hosts. Phenotypic diversity arises from attempts to escape from host immune surveillance (that is, precore, core and basal core promoter mutants), selection resulting from the use of treatments with weak genetic barrier (that is, pol mutants), exposure to hepatitis B immunoglobulin (that is, 'immune-escape' S gene mutants) or treatment-induced mutations from overlapping genes (that is, pol mutants inducing 'vaccine-escape' S gene mutants). pol mutations typically lead to uncontrolled viral replication, whereas S gene mutations can significantly alter hepatitis B surface antigen synthesis and reduce binding to antibodies, which renders individuals who are vaccinated or cured of HBV infection susceptible to infection. For patients coinfected with HIV, hepatitis B treatment options that aim to reduce the risk of HBV mutations from emerging must be seriously considered, not only from clinical but also public health perspectives.

journal_name

Antivir Ther

journal_title

Antiviral therapy

authors

Lacombe K,Boyd A,Gozlan J,Lavocat F,Girard PM,Zoulim F

doi

10.3851/IMP1495

subject

Has Abstract

pub_date

2010-01-01 00:00:00

pages

493-7

issue

3 Pt B

eissn

1359-6535

issn

2040-2058

journal_volume

15

pub_type

杂志文章,评审

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