Arne Schneidewind

TL;DR: The functional ability of NK cells to differentially control HIV-1 replication in vitro based on their KIR and HLA types is examined, providing the first functional evidence that variation at the KIR locus influences the effectiveness of NK cell activity in the containment of viral replication.

TL;DR: Naturally occurring dominant STAT‐C resistance mutations are common in treatment‐naïve patients infected with HCV genotype 1, and their influence on treatment outcome should be characterized to evaluate possible benefits of drug resistance testing for individual tailoring of drug combinations when treatment options are limited due to previous nonresponse to peginterferon and ribavirin.

TL;DR: It is demonstrated that KIR-positive NK cells can place immunological pressure on HIV-1, and that the virus can evade such NK-cell-mediated immune pressure by selecting for sequence polymorphisms, as was previously described for virus-specific T cells and neutralizing antibodies.

TL;DR: It is concluded that the impact of the R264K substitution on capsid structure constrains viral escape and enables long-term maintenance of the dominant CTL response against B27-KK10, providing an explanation for the protective effect of HLA-B27 during HIV infection.

TL;DR: A dual mechanism for durable control of HIV replication is suggested, consisting of viral fitness loss resulting from CTL escape mutations together with strong CD8 T-cell immune responses to the arising variant epitopes.