A virus is a submicroscopic infectious agent defined as an obligate intracellular parasite, meaning it cannot replicate or carry out metabolic functions outside a living host cell. The basic viral particle, known as a virion, consists of genetic material—either DNA or RNA—encased within a protective protein shell called a capsid. Some viruses also possess an outer lipid envelope derived from a host cell membrane. The viral life cycle’s sole purpose is to commandeer the host cell’s machinery to produce thousands of copies of the original virus. This process requires a precise sequence of events for successful multiplication and spread.
Attachment and Entry
The life cycle begins with attachment, a highly specific recognition process where proteins on the virion surface bind to complementary receptor molecules on the host cell membrane. This specificity determines the host range, as a virus can only infect cells possessing the correct receptor. For instance, HIV specifically targets immune cells by binding to the CD4 molecule and a co-receptor.
Following attachment, the virus must penetrate the host cell membrane to deliver its genetic payload. Enveloped viruses, such as HIV, often achieve entry through membrane fusion, where the viral envelope merges directly with the host cell membrane. Viral fusion proteins mediate this event, undergoing conformational changes that create a pore allowing the capsid to enter the cytoplasm.
Other viruses, both enveloped and non-enveloped, exploit the host cell’s natural uptake processes, primarily endocytosis. The virus is engulfed by the host cell membrane, forming an endosome. Inside this vesicle, the virus often relies on the acidic environment to trigger uncoating, releasing the viral genetic material into the cytoplasm. Bacteriophages use a specialized mechanism involving direct injection, where the virus remains outside and threads its genome through the cell envelope.
Genome Replication
Once the viral genome is released into the host cell, the next stage focuses on copying this genetic blueprint. DNA viruses typically transport their genome to the host cell’s nucleus to utilize the host’s DNA polymerases for replication. Smaller DNA viruses rely heavily on host enzymes, while larger viruses, like poxviruses, replicate in the cytoplasm and must encode most of their own replication enzymes.
RNA viruses present a challenge because host cells lack the enzymes needed to copy an RNA template. These viruses must encode their own specialized polymerase, known as RNA-dependent RNA polymerase (RdRp). This enzyme synthesizes new RNA genomes and messenger RNA (mRNA) from the viral template, and its error-prone nature contributes to the high mutation rate observed in many RNA viruses, such as influenza.
Retroviruses, a unique class of RNA viruses including HIV, use reverse transcriptase (RT) to convert their single-stranded RNA genome into a double-stranded DNA copy. This viral DNA then integrates into the host cell’s chromosome, ensuring the viral genome is replicated every time the host cell divides. These specialized polymerases are frequently co-packaged within the virion to be immediately available upon entry.
Component Synthesis
With the genome successfully replicated, the cell must manufacture the physical building blocks of new viruses. This stage involves transcribing viral genomes into messenger RNA (mRNA) and subsequently translating that mRNA into viral proteins. All viruses are entirely dependent on the host cell’s ribosomes, the protein synthesis factories, to carry out translation.
The viral mRNA competes with host mRNA to seize control of the ribosomes and translation factors. Viruses employ strategies to prioritize their own proteins, sometimes actively degrading host mRNA in a process known as “host shut-off.” The proteins produced fall into two categories: non-structural proteins, which are enzymes needed for replication, and structural proteins, which form the physical components of the new virions.
Many viruses utilize genetic mechanisms to maximize protein yield from their small genomes. For instance, some viral mRNAs are translated into a single, long, non-functional polyprotein chain. Viral proteases, among the first non-structural proteins produced, then precisely cleave this chain into multiple functional proteins. Other viruses use ribosomal frameshifting, where the ribosome shifts its reading frame mid-translation, allowing a single stretch of RNA to encode two different proteins.
Assembly and Maturation
Once all necessary genomes and proteins have been synthesized, the components must be organized into new infectious virions. This assembly process is efficient and often relies on the principle of self-assembly. Structural proteins, such as the capsid subunits, possess inherent chemical properties that cause them to spontaneously associate around the replicated genome.
The viral genome must be accurately packaged into the forming capsid shell. For many viruses, this packaging involves specific recognition signals on the genome that ensure only the correct viral nucleic acid is enclosed. Assembly often begins with the formation of a precursor particle called a procapsid.
The final step is maturation, which converts the newly assembled, non-infectious particle into a fully functional virion. Maturation frequently involves a structural transition, often triggered by viral proteases that modify the capsid or envelope proteins. For example, in retroviruses like HIV, the final cleavage of precursor proteins often occurs after the particle has been released, making it a target for certain antiviral drugs.
Release from the Host Cell
The cycle concludes with the release of progeny virions, enabling them to spread and infect other cells. Viruses generally employ one of two distinct strategies for exiting the host cell, depending on whether they possess a lipid envelope.
Non-enveloped viruses, such as poliovirus, typically exit via lysis, a process that involves the destruction of the host cell. Viral proteins disrupt the host cell membrane, causing it to rupture and release thousands of virions simultaneously. This method is rapid and destructive, leading to the death of the infected cell.
Enveloped viruses, including influenza and HIV, use a process called budding. The assembled nucleocapsid moves to the host cell membrane (or an internal membrane) where viral envelope proteins have already been inserted. The nucleocapsid pushes outward, acquiring a piece of the host cell’s lipid membrane as its envelope while exiting. Budding is a gradual process that may allow the host cell to survive longer, acting as a continuous factory for virus production.