Viral Structure & Replication
How viruses are built (genome + capsid + envelope), the Baltimore classification, and the stages of the viral replication cycle.
Interactive Diagram
Tap a teal label to learn about each structure.
What a Virus Is
A virus is an obligate intracellular parasite: a genome (DNA or RNA) packaged in a protein capsid, sometimes surrounded by a lipid envelope. Viruses carry no ribosomes or metabolic machinery and must commandeer host cells to replicate. They range from 20 nm (parvovirus) to ~300 nm (poxvirus). Because they have no independent metabolism, antibiotics that target bacterial processes do not work; antivirals target virus-specific enzymes (e.g., polymerases, neuraminidase, protease).
Capsid, Envelope, and Genome
The capsid is built from repeating capsomere subunits in icosahedral or helical symmetry, an efficient way to enclose the genome with minimal genetic information. The envelope is acquired from host nuclear or cell membranes during budding and carries viral glycoproteins (spikes) responsible for attachment and fusion. Enveloped viruses (influenza, HIV, herpes) are sensitive to drying, detergent, and acid; non-enveloped viruses (norovirus, adenovirus, poliovirus) are hardier and survive the gut. The genome may be dsDNA, ssDNA, dsRNA, (+)ssRNA, (−)ssRNA, or retroviruses (RNA with reverse transcriptase).
Baltimore Classification
David Baltimore grouped viruses into seven classes by how their genome produces mRNA. Class I dsDNA (herpes, adenovirus) transcribes directly. Class III dsRNA (rotavirus) replicates via a replicase. Classes IV (+)ssRNA (polio, SARS-CoV-2) can serve as mRNA directly, while class V (−)ssRNA (influenza, rabies) must carry an RNA-dependent RNA polymerase. Class VI (retroviruses, HIV) uses reverse transcriptase to make DNA from RNA, integrating into the host genome. Class VII (hepadnaviruses, HBV) uses an RNA intermediate during replication. Knowing the class predicts replication location, polymerase needs, and drug targets.
The Replication Cycle
Replication follows: (1) attachment via receptor binding; (2) penetration/entry by fusion or endocytosis; (3) uncoating to release the genome; (4) macromolecular synthesis — early proteins (polymerases, regulatory), genome replication, then late structural proteins; (5) assembly of new virions; (6) release by budding (enveloped) or lysis (non-enveloped). Each step is a drug target: entry inhibitors (enfuvirtide), uncoating inhibitors (amantadine), polymerase inhibitors (acyclovir, remdesivir), integrase inhibitors (raltegravir), protease inhibitors, and neuraminidase inhibitors (oseltamivir).
Cytopathic Effects and Latency
Viruses damage cells in characteristic ways: cell lysis, syncytium formation (HIV, measles, RSV), inclusion bodies (Negri in rabies, owl-eye in CMV), and transformation (oncogenesis — HPV, EBV, HBV). Some viruses establish latency: herpesviruses persist in neurons (HSV) or B cells (EBV) and reactivate; retroviruses integrate permanently as provirus. This explains recurrent disease (cold sores, shingles) and the need for lifelong suppression in HIV.
