Over 60% of the world’s population carries human cytomegalovirus (HCMV) for life, and in transplant patients whose immune systems are suppressed, the virus can reactivate and cause severe multi-organ disease. Current drugs target the active, replicating virus, but resistance develops frequently, and 20–35% of transplant patients still face serious illness or death from HCMV. With more than 100,000 solid organ transplants performed each year worldwide, this places a heavy burden on healthcare systems. The core problem is that scientists do not yet understand the molecular and immunological mechanisms that keep the virus latent in healthy people, or what triggers it to reactivate. This project aims to uncover exactly how HCMV hides in the body and what a protective immune response looks like. If successful, the work could guide the design of better-targeted treatments—such as vaccines or immunotherapies—that prevent reactivation rather than just treating active infection. That would reduce drug resistance, lower mortality in transplant patients, and save the NHS significant costs. While the research is fundamental in nature, similar mechanistic studies of persistent viruses have previously led to breakthroughs in antiviral therapy and vaccine design.
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Human cytomegalovirus (HCMV) infection is a major cause of disease in infants infected in utero and also in immunosuppressed solid organ and bone marrow transplant patients. The cost associated with treating HCMV disease has placed this virus as one of the highest priorities for vaccine development. A defining feature of HCMV is that while healthy people initially infected with the virus recover quickly, the virus is never cleared from the body, instead it establishes a lifelong latent infection capable of reactivating in the future. Over 60% of the world population is currently infected with HCMV and, therefore, carrying the virus. Consequently there is a high risk of primary infection, reinfection and reactivation of latent HCMV in vulnerable patient groups. Reactivation is particularly problematic in the organ transplant setting where the immune-suppression required to stop organ rejection can allow the virus replicate and cause disease due to loss of immune control. While there are a number of current drug therapies which target HCMV lytic virus replication, patients often develop drug resistance and 20-35% of all transplant patients are still at risk of multi-organ disease with significant morbidity and mortality. With over 100,000 solid organ transplants performed each year this represents a substantial burden on an already stretched NHS transplant programme. Our long-term goal is that understanding the viral and immunological mechanisms that control the various stages of the virus lifecycle (latency, reactivation and lytic replication) have the potential to advance our understanding of how the virus can survive in the host and what a good immune response against HCMV looks like. This knowledge could help the design of better targeted treatments of HCMV which will have significant medical benefit to patients in addition to financial benefits to the NHS in a variety of clinical settings.
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