An Update on the Clinical Management of Cutaneous Molluscum Contagiosum

Harrison P. Nguyen, BA; Stephen K. Tyring, MD, PhD, MBA

Disclosures

Skin Therapy Letter. 2014;19(2) 

In This Article

Biology and Pathogenesis of MCV

MCV is one of the largest human viruses. It is a member of the genus Molluscipoxvirus and contains a non-segmented single molecule of linear, double-stranded DNA 200–300 nm in length. The genome is covalently linked at both ends and encodes redundant, repeating sequences at both ends.[15] Restriction endonuclease digestion is used to differentiate among the four subypes of molluscum contagiosum – MCV-1, MCV-1a, MCV-2, and MCV-3 – which all appear to cause very similar disease presentations.[16] The genome of MCV-1 has been completely sequenced and several novel gene products involved in its pathogenesis and evasion of the immune system have been identified: MC54L, MC148, MC013L, MC159, and glutathione peroxidase.[17–19] The protein MC54L prevents inflammation by binding the pro-inflammatory cytokine human interleukin-18.20 MC148 promotes viral replication by preventing infected keratinocytes from differentiating.[21] MC159 interacts with Fas (CD95; a member of the tumor necrosis factor receptor family), tumor necrosis factor (TNF), and TNF-related apoptosisinducing ligand (TRAIL) to inhibit apoptosis.[22] MC80R, a major histocompatibility complex (MHC) class I homolog, interferes with the host presentation of peptides specific to MCV and inhibits cell-mediated cytotoxicity of infected cells.[23] Finally, infected cells express glutathione peroxidase to prevent leukocyte-mediated oxidative damage.[17] Together, these viral gene products are able to maintain active infection until the host immune system gradually prevails.

MCV likely enters the skin through small abrasions; this explains why eczema-prone and atopic individuals, who typically scratch inflamed areas on their skin, are more susceptible. Once MCV has penetrated the lower layers of the epidermis it begins to replicate, extending upwards, in the lower layers of the epidermis.[24] The estimated incubation period varies from 14 days to 6 months. When active infection commences, the epidermis hypertrophies, extending into the underlying dermis, and characteristic molluscum bodies (also known as Henderson-Paterson bodies) form inside cells of the stratum spinosum. As infection progresses, the molluscum bodies enlarge, causing the spinosa cells to migrate upwards while hyperplasia of the basal cell layer simultaneously replaces the migrating spinosa cells. Viral structures are rarely observed in the stratum basale, and the structure of the basal lamina remains intact. The hypertrophied epidermal cells project above the skin, which forms the characteristic tumor observed in molluscum contagiosum.[25] Interestingly, an inflammatory infiltrate is not observed until shortly before natural resolution of the lesion.[26]

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