title: Keloids: A viral hypothesis.
abstract: The triggering cause of keloid formation on a healing wound remains an enigma. In fact, the hypotheses put forward so far to explain this phenomenon seem inconsistent with some clinical features of the disease. The recently established bonds between infectious agents and some pathologies of unknown origin such as peptic ulcer disease, Kaposi's sarcoma or cervical cancer among others led us to consider a potential infectious origin for keloids. This paper presents an infection-based hypothesis (specifically, a viral hypothesis) intended to account for most of their clinical features. Essentially, we hypothesize that healthy individuals carrying a virus, whether known or unknown, associated to some adjuvant, and having some genetic susceptibility, may develop keloids during the scar maturation process in the following manner: the virus would make the bone marrow or lymphatic system its reservoir, residing there in a silent state, and reach the wound via two different mechanisms. The primary mechanism might use an internal circuit through which the viral genome would be transported from its myeloid reservoir to the wound via bone marrow or circulating fibrocytes chemotactically attracted to the damaged skin region. The secondary mechanism might involve an external circuit by which infecting virions via saliva would be shed in the wound directly (preferentially in the sternal or deltoid region) or indirectly (other satellite regions) via the hands or some fomites. A combination of both mechanisms might also be possible. Once in the wound, the virus would switch from a silent state to a latent state by effect of some chemical stimulus probably generated during the tissue repair process; in the new state, the transcription of some of the powerful viral proteins might cause thorough derailment of the normal repair process. As a result, keloid growth might depend both on individual susceptibility and on the viral load deposited into the wound; the greater the susceptibility and viral load were, the more markedly the keloid would develop and the more aggressive it would be.
authors.affiliation: Plastic Surgery Unit, Hospital USP Marbella, Avda. Severo Ochoa, 22, Marbella, Málaga, Spain. pedroe.alonso@usphospitales.com
authors.forename: Pedro E
authors.initials: PE
authors.lastname: Alonso
authors.forename: Luis F
authors.initials: LF
authors.lastname: Rioja
authors.forename: Carlos
authors.initials: C
authors.lastname: Pera
mesh_terms: D000293:Adolescent; D002921:Cicatrix / Q000473:pathology / Q000821:virology; D004197:Disease Reservoirs; D005260:Female; D006801:Humans; D007627:Keloid / Q000821:virology*; D008297:Male; D008954:Models, Biological; D012008:Recurrence; D014780:Viruses / Q000302:isolation & purification*; D014945:Wound Healing / Q000502:physiology*