Viruses are microscopic entities defined by their inability to reproduce independently. As obligate intracellular parasites, they must invade a living host cell to complete their life cycle and generate new virus particles. This process involves hijacking the host cell’s machinery to create multiple copies of themselves. Unlike bacteria or other cells, viruses do not grow or divide; instead, they are assembled from newly manufactured components inside the infected cell, propagating the viral genome to new hosts.
Attachment and Entry into the Host Cell
The viral life cycle begins with attachment, a highly specific process where the virus recognizes and binds to receptor molecules on the host cell surface. This interaction, often described as a lock-and-key mechanism, requires viral surface proteins to match specific host cell receptors. The presence or absence of these compatible receptors determines the host range, or tropism, of the virus. For instance, the human immunodeficiency virus (HIV) specifically targets immune cells because its gp120 protein recognizes the CD4 molecule on their surface.
Following attachment, the virus must penetrate the cell membrane to deliver its genetic material inside, a step called entry. Enveloped viruses, which possess an outer lipid layer, often enter through membrane fusion, where the viral envelope merges directly with the host cell membrane. This releases the internal components into the cytoplasm. Non-enveloped viruses and some enveloped ones often enter via endocytosis, where the host cell engulfs the virus in a membrane-bound vesicle.
Once inside the vesicle, the virus must escape into the cytoplasm, often triggered by the acidic environment of the endosome. Other viruses use direct penetration, injecting their genetic material straight through the membrane, a method common among bacteriophages. The entry phase concludes when the viral genetic material, either DNA or RNA, is successfully delivered into the host cell’s interior.
Replication and Synthesis of Viral Components
With the genetic material inside the cell, the next step is uncoating, where the protective protein shell, or capsid, is shed to expose the viral genome. This release of the genetic blueprint marks the beginning of the manufacturing phase, where the virus completely commandeers the host cell’s machinery. The viral genome uses the host’s resources, including ribosomes and enzymes, to perform two main functions: replicating the viral genome and synthesizing viral proteins.
Viral proteins are produced in two main categories: structural proteins, which form the new capsids and surface components, and non-structural proteins, which are typically enzymes required for genome replication. The strategy for genome replication varies significantly depending on whether the virus uses DNA or RNA as its genetic material. DNA viruses generally move their genome to the host cell’s nucleus and use host enzymes to replicate their DNA and transcribe messenger RNA (mRNA).
RNA viruses typically replicate entirely in the cytoplasm and must supply their own enzymes, specifically RNA-dependent RNA polymerase, as host cells lack this enzyme. Positive-sense RNA viruses can use their genome directly as mRNA for immediate protein synthesis. Negative-sense RNA viruses must first transcribe a complementary positive-sense strand using their own polymerase before protein synthesis can begin. This diverse range of replication strategies ensures the production of new viral genomes and proteins, setting the stage for the next phase.
Assembly and Release of New Viruses
The assembly phase involves packaging the newly synthesized genetic material into structural proteins to form complete, infectious virus particles, known as virions. This is often a self-assembly phenomenon where structural proteins spontaneously come together around the viral genome. The assembly location varies by virus type; for example, many DNA viruses assemble in the nucleus, while most RNA viruses assemble in the cytoplasm.
Once assembled, the new virions must exit the host cell to spread the infection, a process known as release. Viruses use two primary methods depending on whether they are enveloped or non-enveloped. Non-enveloped viruses typically exit through lysis, or the bursting of the host cell. The virus produces enzymes that weaken the cell membrane, leading to its destruction and the rapid release of all newly formed virus particles.
Enveloped viruses are released by budding. The virion pushes against the cell membrane, acquiring a section of the host’s lipid bilayer as its outer envelope. Viral proteins, previously inserted into the host membrane, become embedded in this new envelope. Budding allows the virus to exit without immediately causing cell death, often leading to a slower, continuous release of virions.
Two Strategies: Lytic vs. Lysogenic Cycles
The choice of release mechanism relates to two broader strategies for viral propagation: the lytic cycle and the lysogenic cycle. The lytic cycle is characterized by rapid replication and a destructive outcome. Viruses following this path immediately take over the host cell’s machinery, mass-produce new virions, and then cause the cell to lyse, releasing the progeny viruses to infect surrounding cells. This cycle is associated with acute, fast-acting infections.
The lysogenic cycle represents a more temperate, long-term strategy, particularly well-studied in bacteriophages. In this cycle, the viral genetic material integrates directly into the host cell’s chromosome, becoming a silent passenger called a prophage or provirus. The host cell continues to live and divide normally, replicating the integrated viral genome along with its own DNA. The virus remains dormant until an environmental trigger, such as cellular stress or UV radiation, causes the viral genome to excise itself and switch into the destructive lytic cycle. This allows the virus to spread its genetic material widely through host cell division before initiating an aggressive phase.