What Are Viruses?

By Yasin Ali Muhammad

Viruses are often spoken about as if they represent a well-defined form of life. In reality, their nature is anything but settled. Their evolutionary beginnings remain uncertain, and scientists still disagree on whether viruses should even be classified as living entities. Most discussions of viral origins revolve around three major frameworks: the progressive (or escape) hypothesis, the regressive (or reduction) hypothesis, and the virus-first hypothesis. Each offers useful insights, yet none fully resolves the puzzle. Before examining these ideas, it is necessary to clarify what we mean when we refer to a virus.
to a virus.

What Is a Virus?

In everyday language, the term “virus” usually refers to virions – the microscopic particles capable of entering cells and initiating infection. However, these particles represent only one phase of a virus’s existence. As emphasized by Nasir et al. (2020), a virus is better understood as a broader biological system rather than a single physical object. This system includes genetic material, replication strategies, interactions with host organisms, and multiple mechanisms for genetic transfer.

From this perspective, the virion functions primarily as a delivery mechanism. It is a transient structure that enables nucleic acids to move from one cellular environment to another. The virus itself encompasses much more: its genome, its dependence on host cellular machinery, its evolutionary adaptability, and even nontraditional modes of genetic movement, such as transfer via extracellular vesicles or plasmid-like elements.

This expanded definition helps explain why viruses resist conventional classifications of life. They do not grow or reproduce independently, possess no intrinsic metabolism, and cannot function without a host. Yet despite these limitations, viruses contribute profoundly to genetic innovation, horizontal gene transfer, and evolutionary change across all known domains of life. Rather than being simple parasites, they operate as powerful mediators of genetic exchange and diversification.

Adopting this broader framework provides a foundation for evaluating competing hypotheses about viral origins, including newer ideas that attempt to bridge the gaps left by classical models.

Models of Viral Origin

The Progressive (Escape) Hypothesis

The progressive hypothesis proposes that viruses originated from mobile genetic elements that once resided within cellular genomes. Over time, these elements may have acquired the ability to exit the cell and move between hosts. Retrotransposons offer a compelling parallel, as they replicate via reverse transcription in a manner reminiscent of retroviruses.

Despite its appeal, this model faces unresolved questions. Viral capsids are intricate and highly specialized protein structures with no clear counterparts in cellular biology. While proteins such as neuronal Arc show partial similarities, the evolutionary leap from a simple genetic element to a fully formed infectious particle remains difficult to explain.

The Regressive (Reduction) Hypothesis

The regressive model takes the opposite stance, suggesting that viruses are descendants of ancient cellular organisms that gradually lost complexity as they became dependent on host cells. Support for this idea comes from giant viruses such as mimiviruses, which possess unusually large genomes and retain genes associated with translation and other cellular processes. These features resemble those seen in obligate intracellular bacteria like Rickettsia prowazekii.

However, this hypothesis also encounters challenges. A large proportion of viral genes lack identifiable homologs in cellular organisms, indicating the emergence of novel genetic material rather than simple degradation. Furthermore, most viruses are far more minimalistic than even the most reduced parasitic bacteria, lacking essential metabolic and structural components.

The Virus-First Hypothesis

The virus-first hypothesis suggests that viruses may have existed before modern cells or emerged alongside them during early evolution. This idea is often linked to the RNA world hypothesis, which posits that early life relied on RNA for both information storage and catalysis. In such a setting, self-replicating RNA entities could have spread independently before becoming parasitic once cellular life arose. Some theorists have even proposed that early DNA viruses contributed to the development of eukaryotic cells.

A major conceptual issue remains, however: without cells, the concept of infection becomes meaningless. It is more likely that early replicators existed within membrane-bound compartments rather than functioning as true viruses in the modern sense.

The Bubble Theory

To reconcile these limitations, Piast (2024) proposed the Bubble Theory. This framework envisions early Earth as an environment rich in spontaneously forming lipid vesicles that enclosed replicating molecules. These vesicles were neither fully cellular nor viral, but rather protocellular structures that provided protection and spatial organization for nucleic acids.

Within such compartments, primitive genetic systems could replicate, compete, and spread in ways that resemble viral behavior, even in the absence of true cells. This intermediary stage suggests that viral strategies such as genome packaging and transmission may have originated before the emergence of fully developed organisms.

A contemporary parallel can be seen in extremophilic microorganisms. For instance, an Antarctic haloarchaeon has been shown to spread a plasmid using specialized membrane vesicles that infect plasmid-free cells (Erdmann et al., 2017). These extracellular vesicles function as carriers of genetic material, blurring the distinction between plasmids, vesicles, and viruses. Their existence provides a modern example of how early proto-viral systems may have operated.

Such observations lend credibility to the Bubble Theory by demonstrating that vesicle-mediated genetic transfer is not merely theoretical but actively occurs in living systems today. This mechanism may reflect an ancient evolutionary strategy that predates classical viruses.

Why This Matters

No single hypothesis fully accounts for the diversity and evolutionary complexity of viruses. Their genomes contain unique genes, their replication strategies defy simple categorization, and their evolutionary histories do not align neatly with traditional definitions of life. What is increasingly evident is that viruses are not evolutionary anomalies, but fundamental participants in the history of biology.

This raises a provocative question: is the term “virus” itself sufficient? What we currently label as viruses may represent only one segment of a broader continuum that includes early vesicle-bound replicators, mobile plasmids, extracellular vesicles, and modern infectious particles. If so, viruses are less a discrete category and more a phase in an ongoing evolutionary narrative – one that has shaped life from its earliest origins to the present day.

References

Erdmann, S., Tschitschko, B., Zhong, L., Raftery, M. J., & Cavicchioli, R. (2017). A plasmid from an Antarctic haloarchaeon uses specialized membrane vesicles to disseminate and infect plasmid-free cells. Nature Microbiology, 2(10), 1446–1455. https://doi.org/10.1038/s41564-017-0009-2

Nasir, A., Romero-Severson, E., & Claverie, J. M. (2020). Investigating the concept and origin of viruses. Trends in Microbiology, 28(12), 959–967. https://doi.org/10.1016/j.tim.2020.08.003

Piast, R. W. (2024). The bubble theory: Exploring the transition from first replicators to cells and viruses in a landscape-based scenario. Theory in Biosciences, 143(2), 153–160. https://doi.org/10.1007/s12064-024-00417-4