Are Virgin Births Biologically Possible?

Virgin births are not only biologically possible but documented in dozens of animal species, from sharks and snakes to turkeys and stick insects. The scientific term is parthenogenesis, literally “virgin creation,” and it describes an egg developing into a viable offspring without fertilization by sperm. In mammals, though, a molecular barrier called genomic imprinting has so far made natural parthenogenesis functionally impossible, which is why the phenomenon still carries such surprise when it shows up in a zoo aquarium or a remote reptile population.

Where Virgin Births Have Been Confirmed

The list of vertebrates known to reproduce without mating keeps growing. Among sharks, the first genetically confirmed case involved a bonnethead hammerhead in captivity: DNA fingerprinting showed the pup carried only its mother’s genetic material, ruling out stored sperm from a prior encounter with a male.¹ Since then, parthenogenesis has been confirmed in the smooth-hound shark, with offspring showing complete homozygosity at every genetic marker tested.² Most shark cases come from females held in captivity with no access to males, but wild-caught smalltooth sawfish have also turned out to be parthenogens, demonstrating that these offspring can survive in natural settings.³

Snakes and lizards have provided some of the most dramatic examples. The green anaconda, Komodo dragon, and Burmese python have all been documented reproducing parthenogenetically.⁴ Neotropical pitvipers in the genus Bothrops represent another confirmed group, with three species in a single evolutionary clade shown to produce all-female litters without any genetic contribution from a father.⁵ Birds round out the picture: turkeys are the best-studied avian example, with specific genes now identified as playing a role in triggering spontaneous embryo development from unfertilized eggs.⁶

How an Egg Develops Without Sperm

Normally, an egg cell carries half the mother’s chromosomes, and sperm delivers the other half to create a full set. In parthenogenesis, the egg somehow restores a complete chromosome count on its own. The most common route in vertebrates is called automixis: the egg goes through the normal division process that halves its chromosomes, but then two of the resulting products fuse back together, restoring the full count.⁷ A specific version of this, terminal fusion automixis, is what genetic analyses have confirmed in smooth-hound sharks and many reptiles.²

The offspring are not exact clones of the mother. Because the chromosome-halving process shuffles genes before the products fuse, the result is typically a highly homozygous individual, one that carries two identical copies of many gene variants. Think of it as drawing from only one parent’s genetic deck and ending up with a lot of matching pairs. This is biologically significant because it means hidden harmful gene variants that a mother carried silently (masked by a healthy second copy) can suddenly be exposed in the offspring.

In some insects and lizards, a different mechanism exists: premeiotic endoreplication, where the cell duplicates its entire genome before the chromosome-halving division, guaranteeing a full set at the end. Research on rock lizards of the genus Darevskia confirmed this mechanism operates in all independently evolved lineages of obligate parthenogenetic vertebrates studied so far.⁸ Unlike automixis, this approach preserves more of the mother’s original genetic diversity because it starts from a pre-shuffled genome copy.

Facultative Versus Obligate Parthenogenesis

An important distinction runs through the research. Some species can only reproduce parthenogenetically. Certain whiptail lizard species, for instance, are entirely female and have no choice in the matter. These are obligate parthenogens. But the cases making headlines in zoos and aquariums involve facultative parthenogenesis: species that normally reproduce sexually but can switch to virgin birth under certain conditions, most often when males are absent.

Whether facultative parthenogenesis is merely a reproductive accident or a genuine adaptive strategy is still debated. The fact that parthenogenetic offspring from sharks and sawfish have been found surviving in the wild, not just dying shortly after birth in a tank, provides real support for the adaptive interpretation.³ The smooth-hound shark case is particularly striking because the same female reproduced parthenogenetically on multiple occasions, suggesting it can be a recurrent strategy rather than a one-off fluke.²

Research in fruit flies has started to identify the genetic machinery behind the switch. A study in Drosophila mercatorum, a species with natural parthenogenetic strains, pinpointed three genes that, when their expression levels were altered in a normally sexual species, enabled those flies to produce offspring without mating.⁹ The researchers proposed that this relatively simple genetic switch could evolve as a last-resort reproductive strategy when a female finds herself isolated from mates. That framing has obvious implications for endangered species with dwindling populations.

The Fitness Cost of Going It Alone

If virgin birth is possible, why don’t more species do it all the time? The short answer is that the offspring tend to be less fit. Because automixis produces highly homozygous individuals, harmful recessive variants get unmasked. Work on desert locusts showed that parthenogenetic offspring hatched at far lower rates than sexually produced ones and that the gap was too large to be explained by inbreeding depression alone.¹⁰ The researchers estimated the locust genome carries several lethal equivalents that become exposed under full homozygosity, making parthenogenetic development a gamble even when the egg successfully activates.

Beyond immediate survival, parthenogenetic lineages lose the genetic shuffling that sexual reproduction provides. Over generations, harmful mutations accumulate without the corrective mechanism of recombination between two different parents’ genomes. This is one reason obligate parthenogens tend to be evolutionary dead ends on geological timescales, even though they can persist for thousands or millions of years in the right ecological niche.

Why Mammals Are Different

Parthenogenesis has been observed across vertebrate groups, but mammals stand alone in their resistance to it. The reason is genomic imprinting, a system in which certain genes are chemically tagged during egg and sperm production so that only the copy from one parent is active. Both a mother’s and a father’s genetic contributions are required because each parent’s copies of imprinted genes are silenced or activated in complementary patterns.¹¹

In mice, embryos created with two maternal genomes and no paternal genome are growth-retarded and die early in development.¹² The placenta is especially affected: paternally expressed imprinted genes play a dominant role in placental growth and function, and without a father’s genetic contribution those genes stay silent.¹³ One leading explanation for why this system evolved frames it as a tug-of-war over resources. Genes inherited from the father push for more nutrients from the mother, while genes inherited from the mother restrain resource flow to protect her own health for future pregnancies.¹⁴ The result is that a mammalian embryo needs both sides of this tug-of-war to develop normally.

These chemical marks are maintained even through the extensive genomic reprogramming that occurs after fertilization.¹⁵ In practical terms, the mammalian genome is set up so that a single parent’s contribution is inherently incomplete. This is fundamentally different from, say, a shark or a snake, where both copies of a gene contributed by one parent can function interchangeably.

Getting Around the Mammalian Barrier in the Lab

Researchers have managed to produce live mice from two mothers, but it required precise genetic engineering. By manipulating just two imprinted regions on separate chromosomes, scientists were able to generate bimaternal mice at a relatively high rate.¹⁶ The trick was to delete or alter the imprinting control centers that normally silence paternal-type gene expression, effectively convincing one set of maternal chromosomes to behave as though they came from a father. These bimaternal mice could survive to adulthood and even reproduce, but the procedure required knowing exactly which imprinted regions to target, and the technology to edit them with precision. It is a proof of concept, not something that would happen spontaneously.

What About Humans?

No fully parthenogenetic human has ever been born, and the imprinting barrier makes spontaneous parthenogenesis in humans essentially impossible under normal circumstances. But there are a few biological curiosities worth knowing about.

One is ovarian teratomas, tumors found in ovaries that can contain teeth, hair, and other tissue types. These growths appear to arise from egg cells that began dividing on their own without fertilization, essentially a parthenogenetic activation event that goes nowhere developmentally but produces disorganized tissue.¹⁷ An IVF case report documented the retrieval of a parthenogenetically activated embryo from a patient with a history of ovarian teratomas, strengthening the connection between the two phenomena.¹⁸

A rarer and more startling finding involves chimerism. In a documented case published in Nature Genetics, a living child was found to be a parthenogenetic chimera: some of the child’s cells were derived from a parthenogenetically activated egg while others were derived from normal fertilization. The parthenogenetic cells were homozygous at every tested locus, while other tissues showed normal biparental inheritance.¹⁹ The child was viable, but only because of that mixture: the normally fertilized cells presumably provided the imprinted gene expression the parthenogenetic cells could not. This case demonstrates that human eggs can spontaneously activate and begin dividing, even if they cannot build a complete organism on their own.

When Bacteria Force the Issue

One of the strangest chapters in parthenogenesis research involves Wolbachia, a genus of bacteria that infects an enormous proportion of the world’s insects. Some Wolbachia strains have evolved the ability to convert would-be male offspring into asexually reproducing females, a trick known as parthenogenesis induction.²⁰ Because Wolbachia are transmitted from mother to offspring through eggs (not sperm), males are a dead end for the bacterium. By eliminating males and forcing females to reproduce without them, Wolbachia ensures maximum transmission of its own lineage.

Recent work has revealed how Wolbachia pulls this off at the molecular level, at least in parasitoid wasps. The bacterium carries a gene it appears to have stolen from its insect host, a copy of the host’s own sex-determination gene called transformer. The Wolbachia-encoded version is expressed constantly, locking the host’s developmental pathway into female mode regardless of whether the individual was genetically destined to become male.²¹ The host’s own copy of the gene appears to have degraded over evolutionary time, leaving the wasp dependent on Wolbachia for female development. This is one of the more remarkable examples of a parasite rewriting its host’s reproductive biology from the inside.

Gynogenesis and Other Gray Areas

Not every form of sperm-free reproduction qualifies as true parthenogenesis. In gynogenesis, a female still needs sperm to trigger egg development, but the sperm’s genetic material is discarded. The offspring end up with only the mother’s DNA.²² Certain fish, including some Carassius (goldfish relatives), use this strategy. These gynogenetic species face a peculiar conservation challenge: they depend on males of closely related sexual species to provide the sperm stimulus, even though none of that male’s genes make it into the next generation.²³ Protecting a gynogenetic species means also protecting the sexual species it parasitizes for sperm, an unusual wrinkle in conservation planning.

How Stick Insects Made It Easy

Some animal groups seem almost pre-adapted for parthenogenesis. In stick insects, the sperm cell normally does not contribute a key cellular structure called the centrosome during fertilization; the egg provides everything the embryo needs for its early cell divisions on its own.²⁴ Because the embryo was never depending on sperm for this machinery in the first place, dispensing with sperm entirely is a shorter evolutionary step. This helps explain why both facultative and obligate parthenogenesis are so widespread in the order Phasmatodea. It also illustrates a broader principle: the ease with which a species can evolve parthenogenesis depends heavily on what the sperm was contributing beyond DNA. In groups where sperm provides critical cellular components, the transition is harder.

Honeybees offer another window into the genetics of parthenogenesis. In the Cape honeybee subspecies, workers can produce female offspring without mating, a trait called thelytokous parthenogenesis. Researchers attempting to map the genetic basis of this ability found it was not controlled by a single gene, and a genetic marker once thought to be specific to thelytoky turned up in populations across Africa and the Americas where thelytokous reproduction has never been observed.²⁵ The genetics underlying the switch between sexual and asexual reproduction, even within a single species, appear more complicated than early models suggested.