Pathology and Histopathology

In the molluscum contagiosum lesion, the epidermis grows down into the dermis and projects above the surface as a papule. The basement membrane remains intact. The basal cells are larger and more columnar than usual and intracytoplasmic inclusion bodies (Henderson-Paterson or molluscum bodies), the site of virus assembly, appear first in the cells of the

Figure 2 Molluscum contagiosum lesion. Skin section showing lobules of keratinocytes containing large intracytoplasmic inclusions (molluscum bodies). The stratum comeum has disintegrated in the center of the lesion, releasing the molluscum bodies and generating a central crater. Hematoxylin and eosin; x 100. (Reproduced with permission from Dr D Woodrow and R Bamett, Charing Cross Hospital, London.)

Figure 2 Molluscum contagiosum lesion. Skin section showing lobules of keratinocytes containing large intracytoplasmic inclusions (molluscum bodies). The stratum comeum has disintegrated in the center of the lesion, releasing the molluscum bodies and generating a central crater. Hematoxylin and eosin; x 100. (Reproduced with permission from Dr D Woodrow and R Bamett, Charing Cross Hospital, London.)

stratum spinosum. The molluscum bodies expand and fill the cytoplasm as the affected cells migrate through the stratum granulosum towards the surface (Fig. 2). Viral particles are present exclusively in the cytoplasm of infected cells and do not occur in basal cells or in uninfected cells adjacent to the lesion: the latter continue to develop normally. The virion colony is enclosed by a sac within each infected keratinocyte. In the stratum corneum, the degenerating keratinocytes with their inclusion bodies become enmeshed in the keratin network. The central core of the lesion is an expressible soft material consisting of husks of epidermal cells packed with the elementary bodies of the virus.

The molluscum contagiosum tumor results both from hypertrophy of epidermal cells, due to the presence of the virus-packed inclusion bodies, and from hyperplasia of basal cells, which show a twofold reduction in their division time. Infected cells migrate through the epidermis at a more uniform rate of 9-15 days to reach the stratum granulosum, compared with 9-30 days for uninfected cells. Viral DNA replication occurs within the first 4—5 days, and host transcription is inhibited. Some hyperplasia of the dermal fibroblasts subjacent to the lesion has been reported, although these cells, like the basal cells, do not contain virus. It has been proposed that MCV-infected keratinocytes may secrete a virus-encoded growth factor, analogous to vaccinia virus growth factor, which stimulates the proliferation of adjacent cells. Analysis of the MCV genomic sequence reveals no such coding capability (see above) and so this stimulation may be a secondary effect, mediated by a cellular product induced by infection of keratinocytes.

0 0

Post a comment