Abstract
Lifelong persistent infection by herpesviruses depends on the balance between host immune responses and viral immune evasion. CD4 T cells responding to antigens presented on major histocompatibility complex class II (MHC-II) molecules are known to play an important role in controlling herpesvirus infections. Here we review, with emphasis on human herpesvirus infections, the strategies evolved to evade CD4 T cell immunity. These viruses target multiple points on the MHC class II antigen presentation pathway. The mechanisms include: suppression of CIITA to inhibit the synthesis of MHC class II molecules, diversion or degradation of HLA-DR molecules during membrane transport, and direct targeting of the invariant chain chaperone of HLA-DR.
Highlights
Members of the family herpesviridae are large DNA viruses that commonly cause disease in animals
In mixed lymphocyte culture assays of T cell function, gp42 can inhibit antigen-driven PBMC proliferation. Both the viral entry function and the immune-evasion function of gp42 derive from its ability to bind to the MHC-IIDR β-chain, which occurs in a domain that participates in the formation of peptide binding pockets [85]
It has yet to be tested that this vhs protein or that of the gamma-herpesviruses can inhibit the recognition by CD4 T cells, in light of their effect on CD8 T cell recognition [95] it is reasonable to presume that the effect on major histocompatibility complex class II (MHC-II) expression could lead to escape from CD4 T cell recognition
Summary
Members of the family herpesviridae are large DNA viruses that commonly cause disease in animals. Whilst the potent cellular immune responses normally restrict the pathogenic potential of herpesviruses, it is evident that they fail to eliminate the virus completely from its host. This implies that herpesviruses have very effective immune evasion mechanisms. In the healthy infected host the establishment of an equilibrium between host immune responses and viral evasion mechanisms allows virus persistence with minimum pathogenic consequences. The identification and functional characterisation of immunevasins of herpesviruses targeting the major histocompatibility complex class I (MHC-I) antigen presentation pathways has been extensively studied (for reviews, see [10,11,12,13,14]). We will outline and discuss recent developments in the research on the interference by herpesvirus immunevasins with MHC-II antigen presentation pathways to CD4 T cells
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