Abstract
Primary cytomegalovirus (CMV) infection leads to strong innate and adaptive immune responses against the virus, which prevents serious disease. However, CMV infection can cause serious morbidity and mortality in individuals who are immunocompromised. The adaptive immune response to CMV is characterized by large populations of effector-memory (EM) T cells that are maintained lifelong, a process termed memory inflation. Recent findings indicate that infection with CMV leads to continuous differentiation of CMV-specific EM-like T cells and that high-dose infection accelerates this progression. Whether measures that counteract CMV infection, such as anti-viral drugs, targeting of latently infected cells, adoptive transfer of CMV-specific T cells, and vaccination strategies, are able to impact the progressive differentiation of CMV-specific EM-like cells is discussed.
Highlights
Human cytomegalovirus (HCMV) is a highly prevalent virus that establishes a state of persistent infection[1]
During primary HCMV infection, there is a strong natural killer cell response, which is succeeded by the formation of humoral and cellular immunity[5]
With the use of novel computational tools that allow the analysis of cytometry data with much finer detail[22,23], we recently discovered that CMV infection continuously affects the differentiation of the virus-specific EM-like cells[24]
Summary
Human cytomegalovirus (HCMV) is a highly prevalent virus that establishes a state of persistent infection[1]. Measures to counteract cytomegalovirusassociated perturbations and their impact on T-cell differentiation In cases where CMV-associated perturbations are known to be a negative factor (for example, in congenital infection and viral reactivation after transplantation), measures to reduce the burden of CMV infection are being investigated Several approaches, such as anti-viral drugs, treatments targeting latently infected cells, adoptive transfer of CMV-specific T cells, and (prophylactic) vaccines, have been developed. Administration of valaciclovir to mice with an established MCMV infection resulted in a reduction of the magnitude of the MCMV-specific CD8+ T-cell response This was accompanied by a less-differentiated phenotype of the residual CD8+ T cells compared with mice that received no anti-viral treatment. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
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