Immune control of herpesvirus latency

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Abstract
The mechanism of herpesvirus latency, viral transmission and the immune response to infection are reviewed. The immune response may influence the state of latency. The viral genome may be maintained in a latent state by humoral antibody (Ab) directed against viral-coded membrane antigens. Fluctuations in specific Ab or weakening of immunoglobulin G binding may result in virus reactivation. Immediately after replication occurs, a rapid infiltration of polymorphonuclear leukocytes, lymphocytes and macrophages and secretion of lymphokines may limit infection by killing infected cells or limiting virus replication.