CD8 T-Cell Response to Respiratory Syncytial Virus Infection

Abstract

Respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract infection and hospitalization among infants. Despite the significant healthcare burden, there is no licensed RSV vaccine currently available. This problem is further exacerbated as a natural RSV infection fails to elicit the development of long-lived immunity. It is well established that RSV-specific antibodies play a critical role in mediating protection from severe disease. The CD8 T-cell response is critical for mediating virus clearance following an acute RSV infection. However, the relative contribution of memory CD8 T cells in providing protection against secondary RSV infections remains unclear. In addition, data from animal models indicate that memory CD8 T-cell responses can be pathogenic under certain conditions. Herein, we provide an overview of the CD8 T-cell response elicited by RSV infection and how our current knowledge may impact future studies and vaccine development.

Targeting CD40 enhances antibody- and CD8-mediated protection against respiratory syncytial virus infection

“…Following RSV infection, antigen-specific CD8 T cells exhibit an activated phenotype and gain effector functions 41 corroborating the common theory that inflammatory responses increase with antigen encounters 40 . Notably, in humans, an increase in TEM population can be seen following resolution of infection 44 .…”

“…Over time following infection or vaccination, as the antigen load decreases, the population of mature CD8 T cells contracts to form a stable memory CD8 T cell pool whose functional activities evolve with time 40 . As is the role of immune memory, RSV-specific CD8 T cells expand in magnitude and effector functions following infection 41 . However, FIRSV has been shown to elicit no memory CD8 T cell response in mice adding another facet to its ineffectiveness 42 , 43 .…”

PD-1 of Sigmodon hispidus: Gene identification, characterization and preliminary evaluation of expression in inactivated RSV vaccine-induced enhanced respiratory disease

“…Indeed, the engagement of PD-1 with inflammatory DC-derived PD-L1 is crucial for regulation of pro-inflammatory cytokine release by effector CD4 and CD8 T cells, resulting in control of effector T cell activities in the lungs. In addition, they showed that blocking PD-L1 following RSV infection enhanced weight loss and lung histopathology in mice 22,59 . Taken together, our observations are in good agreement with severe RSV infection in the murine model where low levels of PD-1 induction accompany enhanced respiratory disease.…”