Parthenogenesis, often called “virgin birth,” is a form of asexual reproduction where an embryo develops from an unfertilized egg cell. This mechanism is a natural reproductive strategy for many species. However, viable, full-term human parthenogenesis is biologically impossible. No documented case of a human successfully developing from an unfertilized egg exists, due to complex genetic requirements specific to mammalian development.
What Parthenogenesis Is
Parthenogenesis is a reproductive strategy found widely in the animal kingdom, allowing for the creation of offspring without the contribution of a male gamete. The process involves an unfertilized egg restoring the necessary diploid number of chromosomes. The resulting offspring are typically clones, or half-clones, of the mother.
This reproductive mode is common in lower plants and invertebrates (rotifers, aphids, and bees) and also appears in a few vertebrates. Certain species of lizards, snakes, fish, and birds, like the Komodo dragon, can reproduce asexually. Parthenogenesis can be obligate (reproduction is only asexual) or facultative (switching between sexual and asexual reproduction).
The Biological Blockade: Genomic Imprinting
The reason human parthenogenesis is not a viable option lies in a unique genetic process found in mammals called genomic imprinting. This is an epigenetic mechanism where certain genes are chemically “stamped” or silenced based on whether they are inherited from the mother or the father. For a small, important set of genes, only the copy from one parent is active, while the copy from the other is silenced.
For normal, full-term development, an embryo requires both a paternally imprinted set of genes and a maternally imprinted set. The paternal genome expresses genes that promote placental growth, while the maternal genome expresses genes that promote embryonic development. Without both contributions, the balance is severely disrupted.
An embryo attempting parthenogenesis would only possess maternal imprints, leading to a functional absence of the paternally expressed genes. This imbalance results in significant developmental defects, particularly in the formation of the placenta and associated tissues. In laboratory mice, parthenogenetic embryos consistently fail to survive past the early stages of gestation. This genetic barrier ensures all placental mammals require bi-parental reproduction.
Non-Viable Development: Parthenogenetic Human Cells
Though full human parthenogenesis is impossible, two specific medical phenomena represent the closest examples of unfertilized egg activation. These non-viable cellular developments highlight the failure of development without a paternal contribution. Ovarian teratomas, also known as dermoid cysts, are one such example.
Teratomas are tumors typically composed of tissues like hair, teeth, skin, and fat. These tumors originate from an unfertilized oocyte that has spontaneously activated and begun to develop. Genetic studies confirm that ovarian teratomas are parthenogenetic, arising from a single germ cell. They are a disorganized collection of differentiated cells that lack the viability to form a fetus.
A contrasting example is the complete hydatidiform mole, a type of abnormal pregnancy. This condition is genetically opposite to parthenogenesis, resulting from a conceptus having two sets of paternal chromosomes and no maternal contribution. The complete mole is characterized by an overgrowth of placental tissue that forms grape-like clusters, but it lacks any identifiable embryonic or fetal tissue. The failure of both the maternal-only parthenogenetic teratoma and the paternal-only hydatidiform mole underscores the strict requirement for both parental genomes in human development.