some variants of HIV-1, so MC148 may inhibit the entry of other viruses into human cells. CCR8 receptor antagonism broadly inhibits monocyte function. Taken together, MC148 prevents the recruitment of monocytes, lymphocytes, and neutrophils, and ultimately, the local inflammatory response.8,40,41 MC148 is expressed early in the life cycle of MCV to aid in immune evasion before subsequent processes take over.
MC infection induces benign growth of keratinocytes, thus viral proteins can control and promote cellular proliferation. MC007 inhibits the retinoblastoma/E2 factor (RB/E2F) complex.42 Normally, RB is an important regulator for cellular apoptosis and E2F is a family of transcriptional factors.43 MC007 may contribute to the tumor-like lesions of MCV. In mammals, the selenium-dependent glutathione peroxidase is a protector for programmed cell death.44,45 MCV also acquires a glutathione peroxidase homolog, MC66, which prevents cell death induced by oxidative stress or ultraviolet radiation.46,47
The MC80 protein plays a role in decreasing immune surveillance by inhibiting the acquired immune response. MHC-I plays a crucial role in cellular recognition of viral particles to aid in mourning an immune response. MC80 shares a moderate sequence similarity of MHC-I and binds with components of the MHC-I peptide-loading complex and targets it for destruction in the membrane of the endoplasmic reticulum. This action prevents the viral specific MHC-I-peptide complex from reaching the cell surface to be recognized by immune cells.48
DISCUSSION
MC lesions may persist several months to years, perhaps due in part to the immune evasion characteristics unique to the MCV. MC proteins 005 and 132, 159, 160, and 163 subvert host immunity by inhibiting the NF-κB pathway via several effector mechanisms and pathways. Cell death pathways are modulated by MC 007, 66, and 163. MC 148 inhibits immune cell chemotaxis, and MC80 inhibits MHC-1 peptide complex from reaching the cell surface to be recognized by immune cells. Thus, various MC proteins work synergistically through a variety of pathways to evade host immunity, making individual MC proteins a desirable therapeutic target.
Although MC causes persistent infection by evading immune surveillance, a therapeutic goal would be to initiate immune recognition to promote MC resolution by targeting one or more of the MC proteins. MC lesion redness and inflammation, known as the BOTE sign, is a predictor of resolution of MC and indicative of host immunity activation. However, the mechanism by which BOTE inflammation leads to MC resolution is unknown.19
Though MC is often a self-limiting condition, treatment may thwart associated complications, such as infection, contagiosity, or aesthetic concerns.3 There is currently no FDA-approved treatment for MC; however, 2 therapeutics are in phase 3 development.
Although MC causes persistent infection by evading immune surveillance, a therapeutic goal would be to initiate immune recognition to promote MC resolution by targeting one or more of the MC proteins. MC lesion redness and inflammation, known as the BOTE sign, is a predictor of resolution of MC and indicative of host immunity activation. However, the mechanism by which BOTE inflammation leads to MC resolution is unknown.19
Though MC is often a self-limiting condition, treatment may thwart associated complications, such as infection, contagiosity, or aesthetic concerns.3 There is currently no FDA-approved treatment for MC; however, 2 therapeutics are in phase 3 development.
