Molluscum contagiosum virus (MCV)

Molluscum contagiosum virus (MCV) is a large, enveloped, double-stranded DNA virus within the Poxviridae family and the sole member of the Molluscipoxvirus genus [15, 16]. It causes molluscum contagiosum, a prevalent skin infection characterized by firm, dome-shaped, umbilicated papules that typically resolve spontaneously in immunocompetent individuals but can become chronic and disfiguring in immunocompromised patients [11, 12]. The virus replicates exclusively in the cytoplasm of human keratinocytes and utilizes a suite of specialized proteins, such as MC159 and MC160, to evade host immune detection by inhibiting apoptosis and inflammatory signaling pathways [4, 12]. Therapeutic strategies focus on the destruction of viral lesions or the inhibition of viral replication. Recently, pharmacological options have expanded beyond physical modalities like cryotherapy to include FDA-approved treatments such as the nitric oxide-releasing agent berdazimer and the topical vesicant cantharidin [1, 6]. Emerging research identifies specific viral proteins, notably the mD4 DNA processivity factor and the mE9 DNA polymerase, as high-priority molecular targets for the development of potent and specific antiviral agents [2, 9].

Other names

Molluscum contagiosum poxvirusMolluscipoxvirusMCV-1MCV-2MCV-3MCV-4

Drugs targeting the virus work through various mechanisms: Berdazimer releases nitric oxide which exerts broad antiviral effects and reduces early viral gene expression [4, 6]; Cantharidin acts as a vesicant, likely through protein phosphatase inhibition, to induce epidermal blistering and physical destruction of the infected lesion [10, 17]; Cidofovir acts as a nucleotide analog that inhibits the viral DNA polymerase (mE9) [2, 6]; and Imiquimod stimulates the local immune response via Toll-like receptor 7 (TLR7) agonism [8, 10].