In the prenatal period, virilization refers to closure of the
perineum, thinning and wrinkling (rugation) of the
scrotum, growth of the penis, and closure of the
urethral groove to the tip of the
penis. In this context,
masculinization is synonymous with
virilization. Prenatal virilization of XX fetuses and undervirilization of XY fetuses are common causes of
ambiguous genitalia such as in conditions like
Congenital adrenal hyperplasia and
5α-Reductase 2 deficiency. For many years, it was widely believed that in
mammals, the female is the "default" developmental pathway, and the
SRY gene on the
Y chromosome is responsible for suppressing the development of female characteristics and stimulating males characteristics. In this scenario, an
embryo would passively develop female sexual characteristics without intervention by the SRY gene. However, in the early 2000s, other genes, such as
WNT4 and
RSPO1, were discovered that perform the opposite function – i.e., genes which suppress masculinization and stimulate feminization. Two processes:
defeminization, and masculinization, are involved in producing
male typical morphology and behavior.
High Prenatal virilization of a genetically female fetus can occur when an excessive amount of androgen is produced by the fetal
adrenal glands or is present in maternal blood, resulting in virilization of the female genitalia such as an
enlarged clitoris. It can also be associated with
progestin-induced virilisation.
Low Undervirilization can occur if a genetic male cannot produce enough androgen or the body tissues cannot respond to it. Extreme undervirilization occurs when no significant androgen hormones can be produced or the body is completely insensitive to androgens, in which case a female phenotype will develop. Partial undervirilization produces ambiguous genitalia part-way between male and female. Examples of undervirilization in fetuses with a 46,XY karyotype are
androgen insensitivity syndrome and
5 alpha reductase deficiency. ==Normal virilization==