immunosuppressed patients, MC lesions are classically located on the genitalia, abdomen, and thighs, and the lesions can be more widespread.17 Diagnosis is made via clinical course.1 The methods of transmitting MCV include autoinoculation, direct contact, and fomites.6 Individuals with skin barrier dysfunction, such as in atopic dermatitis, are more susceptible to MC.7 The infection and replication of MC is confined to the epidermal layer and does not permeate the basement membrane.7,8 Consequently, MCV doesn't disseminate systemically, nor does it stay dormant in human body to inflict latent infection.5 This might be the main reason why recurrence is rarely observed clinically. Microscopically, MC is confirmed by the presence of molluscum bodies or Henderson-Paterson bodies - eosinophilic inclusion bodies in the cytoplasm of the epidermal cells.2 During infection, the virion can be identified in the stratum basale.7 As the keratinocytes differentiate from the stratum basale to the stratum corneum, the virus replicates and forms an inclusion body within the cytoplasm. The virus is released from the stratum corneum layer (Figure 2).7 MCV upregulates epidermal growth factor receptors (EGFR) and augments cell division.7
There are no FDA-approved treatments for MC; however, cryotherapy, curettage, pulsed dye laser, cantharidin, benzoyl peroxide, salicylic acid, interferon alpha, and imiquimod have been used.6 Currently, there is no vaccine for MCV, although there are anecdotal reports of MCV being treated successfully with intralesional measles, mumps, and rubella (MMR) vaccine.9
Lending to the failure of effective MCV therapeutics is the fact that MCV does not grow in cell culture or outside a human host, thus most of research of MC must be conducted by immunohistochemical analysis of infected tissues or through surrogate investigations of the VV.1,8,10,11 Even though MCV is serologically distinct from VV, the sequencing of MCV has shown several homologues of the VV for signaling proteins, an RNA polymerase subunit, and structural proteins.12 Hence, VV can be used as a surrogate to study MC proteins in vivo.11
The genome of the MCV type I was decoded in 1997.10 The genetics of MCV consists of 180 proteins with 105 traceable to other orthopoxvirus counterparts.13 However, MCV encodes 50 distinct proteins not found in other poxviruses including major histocompatibility complex class I (MHC-I), chemokine, and glutathione peroxidase homologs.14,15 The duration of symptoms is variable in the literature. Molluscum lesions are usually present for weeks to months but may persist up
