Recent work with selenium has demonstrated that a deficiency in this trace mineral will lead to increased viral pathogenesis. Selenium-deficient animals infected with a viral pathogen demonstrate immune dysfunction, including altered chemokine and cytokine expression patterns. A benign coxsackievirus infection of selenium-deficient mice leads to the development of myocarditis and further experiments demonstrated that the change in virulence was due to point mutations in the viral genome. Thus, replication in a selenium-deficient host led to a normally benign virus acquiring virulence due to viral mutations. A deficiency in selenium is also associated with disease progression in HIV-infected individuals and with hepatitis C virus-induced liver cancers. It appears that adequate levels of selenium help to protect the host against viral infection.