Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Retrovirology cung cấp cho các bạn kiến thức về ngành y đề tài: Modulation of the virus-receptor interaction by mutations in the V5 loop of feline immunodeficiency virus (FIV) following in vivo escape from neutralising antibody. | Willett etal. Retrovirology 2010 7 38 http content 7 1 38 gtr RETR0VIR0L0GY RESEARCH Open Access Modulation of the virus-receptor interaction by mutations in the V5 loop of feline immunodeficiency virus FIV following in vivo escape from neutralising antibody Brian J Willett Martin Kraase Nicola Logan Elizabeth L McMonagle Ayman Samman and Margaret J Hosie Abstract Background In the acute phase of infection with feline immunodeficiency virus FIV the virus targets activated CD4 T cells by utilising CD134 OX40 as a primary attachment receptor and CXCR4 as a co-receptor. The nature of the virusreceptor interaction varies between isolates strains such as GL8 and CPGammer recognise a complex determinant on CD134 formed by cysteine-rich domains CRDs 1 and 2 of the molecule while strains such as PPR and B2542 require a more simple determinant comprising CRD1 only for infection. These differences in receptor recognition manifest as variations in sensitivity to receptor antagonists. In this study we ask whether the nature of the virus-receptor interaction evolves in vivo. Results Following infection with a homogeneous viral population derived from a pathogenic molecular clone a quasispecies emerged comprising variants with distinct sensitivities to neutralising antibody and displaying evidence of conversion from a complex to a simple interaction with CD134. Escape from neutralising antibody was mediated primarily by length and sequence polymorphisms in the V5 region of Env and these alterations in V5 modulated the virus-receptor interaction as indicated by altered sensitivities to antagonism by both anti-CD134 antibody and soluble CD134. Conclusions The FIV-receptor interaction evolves under the selective pressure of the host humoral immune response and the V5 loop contributes to the virus-receptor interaction. Our data are consistent with a model whereby viruses with distinct biological properties are present in early versus late infection and with a .
