【摘 要】
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During human immunodeficiency virus (HIV) infection,type Ⅰ interferon (IFN-Ⅰ) signaling induces an antiviral state that includes the production of restriction factors that inhibit virus replication,thereby limiting the infection.As seen in other viral inf
【机 构】
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Institute of Clinical and Molecular Virology, University Hospital Erlangen, Erlangen 91054, Germany;
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During human immunodeficiency virus (HIV) infection,type Ⅰ interferon (IFN-Ⅰ) signaling induces an antiviral state that includes the production of restriction factors that inhibit virus replication,thereby limiting the infection.As seen in other viral infections,type Ⅰ IFN can also increase systemic immune activation which,in HIV disease,is one of the strongest predictors of disease progression to acquired immune deficiency syndrome (AIDS) and non-AIDS morbidity and mortality.Moreover,IFN-Ⅰ is associated with CD4 T cell depletion and attenuation of antigen-specific T cell responses.Therefore,therapeutic manipulation of IFN-Ⅰ signaling to improve HIV disease outcome is a source of much interest and debate in the field.Recent studies have highlighted the importance of timing (acute vs.chronic infection) and have suggested that specific targeting of type Ⅰ IFNs and their subtypes may help harness the beneficial roles of the IFN-Ⅰ system while avoiding its deleterious activities.
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