His overseeing specialist Ebonie Vincent operated on him to manage the growths on his feet. References
Further reading
Yabe Y, Sadakane H (September 1975). "The virus of epidermodysplasia verruciformis: electron microscopic and fluorescent antibody studies". The Journal of Investigative Dermatology. 65 (3): 324–30. doi:10.1111/1523-1747.ep12598388. PMID 808576. Lewandowsky F, Lutz W (October 1922). "Ein Fall einer bisher nicht beschriebenen Hauterkrankung (Epidermodysplasia verruciformis)". Archiv für Dermatologie und Syphilis (in German). 141 (2): 193–203. doi:10.1007/BF01938833. S2CID 8585441. == External links ==
Letermovir (INN; trade name Prevymis) is an antiviral drug for the treatment of cytomegalovirus (CMV) infections. It has been tested in CMV infected patients with allogeneic stem cell transplants and may also be useful for other patients with a compromised immune system such as those with organ transplants or HIV infections. The drug was initially developed by the anti-infective division at Bayer, which became AiCuris Anti-infective Cures AG through a spin-out and progressed the development to end of Phase 2 before the project was sold to Merck & Co  for Phase 3 development and approval.The drug was granted fast track status by the US Food and Drug Administration (FDA) and orphan drug status by the European Medicines Agency. It is now approved for prevention of CMV infection and disease in recipients of an allogeneic stem cell transplant.The FDA considers it to be a first-in-class medication. Medical use
In the US as well as in the EU, letermovir is used for the prevention of cytomegalovirus infection and disease in adult CMV-seropositive recipients of an allogeneic stem cell transplant. The therapy is started shortly after the transplantation and typically lasts for 100 days. Although letermovir is a relatively new antiviral, CMV resistance has been documented in stem cell transplantation recipients; although rare, breakthrough infections of prophylactic treatment with letermovir underscores the ongoing selective pressure on CMVs viral evolution and its continued ability to evade therapeutic suppression through mutations in critical gene regions such as within the UL56 amplicon.